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factoid
|
Abnormality in which vertebral region is important in the Bertolotti's syndrome?
|
['lumbosacral']
|
[
"lumbosacral",
"lumbosacral region",
"lumbosacral plexus",
"lumbosacral spine",
"lumbosacral junction"
] |
Lumbosacral vertebral region is implicated in the Bertolotti's syndrome. Lumbosacral transitional vertebra is an anatomical variation of the fifth lumbar vertebra in which an enlarged transverse process can form a joint or fusion with the sacrum or ilium. Patients often complain of intractable sciatica that arises from impingement of the nerve root extraforaminally by compression caused by the enlarged transverse process.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24156003",
"http://www.ncbi.nlm.nih.gov/pubmed/21511940",
"http://www.ncbi.nlm.nih.gov/pubmed/20624239",
"http://www.ncbi.nlm.nih.gov/pubmed/19830065",
"http://www.ncbi.nlm.nih.gov/pubmed/19646556",
"http://www.ncbi.nlm.nih.gov/pubmed/19547821",
"http://www.ncbi.nlm.nih.gov/pubmed/19037900",
"http://www.ncbi.nlm.nih.gov/pubmed/18596536",
"http://www.ncbi.nlm.nih.gov/pubmed/16943469",
"http://www.ncbi.nlm.nih.gov/pubmed/11154546",
"http://www.ncbi.nlm.nih.gov/pubmed/8457417",
"http://www.ncbi.nlm.nih.gov/pubmed/2533403",
"http://www.ncbi.nlm.nih.gov/pubmed/23969004",
"http://www.ncbi.nlm.nih.gov/pubmed/23096483"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24156003",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 155,
"text": "Bertolotti's syndrome (BS), a form of lumbago in lumbosacral transitional vertebrae, is an important cause of low back pain in young patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24156003",
"endSection": "abstract",
"offsetInBeginSection": 728,
"offsetInEndSection": 850,
"text": " Common causes of back pain were the ipsilateral L5-S1 facet joint, neoarticulation, the SI joint, and disc degeneration. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21511940",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Patients with Bertolotti's syndrome have characteristic lumbosacral anomalies and often have severe sciatica. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21511940",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 475,
"text": "We suggest that the intractable sciatica in this syndrome could arise from impingement of the nerve root extraforaminally by compression caused by the enlarged transverse process."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20624239",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Radiofrequency sensory ablation as a treatment for symptomatic unilateral lumbosacral junction pseudarticulation (Bertolotti's syndrome): a case report."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20624239",
"endSection": "abstract",
"offsetInBeginSection": 410,
"offsetInEndSection": 534,
"text": "She was found to have an elongated right L5 transverse process that articulated with the sacral ala (Bertolotti's syndrome)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19830065",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 348,
"text": "Lumbosacral transitional vertebra is an anatomical variation of the fifth lumbar vertebra in which an enlarged transverse process can form a joint or fusion with the sacrum or ilium. The association of that variant with low back pain and the change in the biomechanical properties of the lumbar spine is called Bertolotti's syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19830065",
"endSection": "abstract",
"offsetInBeginSection": 517,
"offsetInEndSection": 703,
"text": "Radiographic investigation revealed an anomalous enlargement of the left transverse process of the fifth lumbar vertebra forming a pseudarthrosis with the infrajacent ala of the sacrum. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19547821",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Transitional lumbosacral vertebrae and low back pain: diagnostic pitfalls and management of Bertolotti's syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19547821",
"endSection": "abstract",
"offsetInBeginSection": 10,
"offsetInEndSection": 227,
"text": " Bertolotti's syndrome is a spine disorder characterized by the occurrence of a congenital lumbar transverse mega-apophysis in a transitional vertebral body that usually articulates with the sacrum or the iliac bone. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18596536",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 488,
"text": "It is characterized by an enlarged transverse process at the most caudal lumbar vertebra with a pseudoarticulation of the transverse process and the sacral ala. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16943469",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "Bertolotti's syndrome is characterised by anomalous enlargement of the transverse process(es) of the most caudal lumbar vertebra which may articulate or fuse with the sacrum or ilium and cause isolated L4/5 disc disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11154546",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 184,
"text": "Case report of surgically treated mechanical low back pain from the facet joint contralateral to a unilateral anomalous lumbosacral articulation (Bertolotti's syndrome). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11154546",
"endSection": "abstract",
"offsetInBeginSection": 530,
"offsetInEndSection": 624,
"text": "Bertolotti's syndrome is mechanical low back pain associated with these transitional segments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11154546",
"endSection": "abstract",
"offsetInBeginSection": 944,
"offsetInEndSection": 1087,
"text": "Repeated fluoroscopically guided injections implicated a symptomatic L6-S1 facet joint contralateral to an anomalous lumbosacral articulation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8457417",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "We surgically treated 16 patients with Bertolotti's syndrome (chronic, persistent low back pain and radiographically diagnosed transitional lumbar vertebra)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2533403",
"endSection": "title",
"offsetInBeginSection": 33,
"offsetInEndSection": 76,
"text": "Transitional vertebrae of the lumbar spine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2533403",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Bertolotti's syndrome refers to the association of back pain with lumbosacral transitional vertebrae. "
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013131",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013577",
"http://www.disease-ontology.org/api/metadata/DOID:225"
] |
[
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/13767955"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/14432659"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/13716899"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/13700654"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/13305927"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/14445302"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/13580681"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/14902269"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/13642924"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/20254848"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/13574281"
},
{
"o": "http://linkedlifedata.com/resource/pubmed/keyword/LUMBOSACRAL+REGION%2Fabnormalities",
"p": "http://linkedlifedata.com/resource/pubmed/keyword",
"s": "http://linkedlifedata.com/resource/pubmed/id/14493837"
}
] |
5313058de3eabad02100000e
|
bioasq_factoid
|
yesno
|
Can the Micro-C XL method achieve mononucleosome resolution?
|
['yes']
|
[
"yes"
] |
['Yes. Micro-C XL is an improved method for analysis of chromosome folding at mononucleosome resolution.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27723753"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27723753",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "We present Micro-C XL, an improved method for analysis of chromosome folding at mononucleosome resolution"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27723753",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "We present Micro-C XL, an improved method for analysis of chromosome folding at mononucleosome resolution."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27723753",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Micro-C XL: assaying chromosome conformation from the nucleosome to the entire genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27723753",
"endSection": "abstract",
"offsetInBeginSection": 413,
"offsetInEndSection": 538,
"text": "Micro-C XL provides a single assay to interrogate chromosome folding at length scales from the nucleosome to the full genome."
}
] | 6
|
BioASQ-training6b
| null | null |
587dfde9ae05ffb474000001
|
bioasq_yesno
|
factoid
|
What is commotio cordis?
|
['blunt thoracic impact causing sudden death']
|
[
"blunt thoracic impact causing sudden death",
"blunt chest trauma leading to sudden death",
"blunt chest impact resulting in sudden death",
"blunt thoracic trauma causing sudden death",
"blunt force trauma to the chest leading to sudden death"
] |
Commotio cordis is a term used to describe cases of blunt thoracic impact causing sudden death without structural damage of the heart
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22816548",
"http://www.ncbi.nlm.nih.gov/pubmed/14646469",
"http://www.ncbi.nlm.nih.gov/pubmed/11879111",
"http://www.ncbi.nlm.nih.gov/pubmed/10894918",
"http://www.ncbi.nlm.nih.gov/pubmed/10498299",
"http://www.ncbi.nlm.nih.gov/pubmed/9703576",
"http://www.ncbi.nlm.nih.gov/pubmed/6496438",
"http://www.ncbi.nlm.nih.gov/pubmed/17957272",
"http://www.ncbi.nlm.nih.gov/pubmed/23107651",
"http://www.ncbi.nlm.nih.gov/pubmed/22869311",
"http://www.ncbi.nlm.nih.gov/pubmed/22027166",
"http://www.ncbi.nlm.nih.gov/pubmed/21699851",
"http://www.ncbi.nlm.nih.gov/pubmed/20086611",
"http://www.ncbi.nlm.nih.gov/pubmed/18691236",
"http://www.ncbi.nlm.nih.gov/pubmed/19749607",
"http://www.ncbi.nlm.nih.gov/pubmed/17229310",
"http://www.ncbi.nlm.nih.gov/pubmed/15744544",
"http://www.ncbi.nlm.nih.gov/pubmed/15331287",
"http://www.ncbi.nlm.nih.gov/pubmed/11555799",
"http://www.ncbi.nlm.nih.gov/pubmed/11334832",
"http://www.ncbi.nlm.nih.gov/pubmed/11208236",
"http://www.ncbi.nlm.nih.gov/pubmed/11048776",
"http://www.ncbi.nlm.nih.gov/pubmed/10392228",
"http://www.ncbi.nlm.nih.gov/pubmed/10338239",
"http://www.ncbi.nlm.nih.gov/pubmed/9930916"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22816548",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "Commotio cordis is a rare type of blunt cardiac injury in which low impact chest trauma causes sudden cardiac arrest, usually occurs from being struck by a projectile during sports."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14646469",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 323,
"text": "Commotio cordis due to blunt trauma to the precordium is a rare cause of death in young athletes, occurring less frequently than all of the other athletics-related deaths. Commotio cordis is a term used to describe cases of blunt thoracic impact causing fatality without structural damage of the heart and internal organs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11879111",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 223,
"text": "Although blunt, nonpenetrating chest blows causing sudden cardiac death (commotio cordis) are often associated with competitive sports, dangers implicit in such blows can extend into many other life activities. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10894918",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Sudden death following blunt chest trauma is a frightening occurrence known as 'commotio cordis' or 'concussion of the heart'."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10498299",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 169,
"text": "Commotio cordis is a term used to describe cases of blunt thoracic impact causing fatality without gross structural damage of the heart and internal organs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9703576",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 303,
"text": "Cardiac concussion, previously known as commotio cordis, occurs in structurally normal hearts without gross or microscopic injury to the myocardium, cardiac valves, or coronary arteries, as opposed to other sports-related deaths known to occur more frequently in structural or congenital heart disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6496438",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Nonpenetrating cardiac injuries due to direct precordial blunt impacts are a commonly encountered phenomenon in medicolegal offices."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6496438",
"endSection": "abstract",
"offsetInBeginSection": 279,
"offsetInEndSection": 472,
"text": "less commonly occurring manifestation of nonpenetrating injury is a concussion of the heart (commotio cordis), often with dramatic physiological consequences but no morphologic cardiac injury. "
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D056104"
] |
[] |
53035d7c2059c6d71c000085
|
bioasq_factoid
|
factoid
|
What is the incidence of Facioscapulohumeral Muscular Dystrophy?
|
['1:8000 to 1:20000']
|
[
"1:8000 to 1:20000",
"1:8000-1:20000",
"1:8000-20000",
"1:8000 to 20000",
"1:8000 - 1:20000"
] |
['Facioscapulohumeral Muscular Dystrophy has and incidence of 1:8000 to 1:20000.', 'The incidence of Facioscapulohumeral Muscular Dystrophy (FSHD) is approximately 1 in 8000 individuals.', 'The incidence of Facioscapulohumeral Muscular Dystrophy is approximately 1 in 8,000.', 'The incidence of Facioscapulohumeral Muscular Dystrophy is approximately 1 in 8000 people.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34315378",
"http://www.ncbi.nlm.nih.gov/pubmed/21496633"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34315378",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Facioscapulohumeral Muscular Dystrophy (FSHD) is in the top three list of all dystrophies with an approximate 1:8000 incidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21496633",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 322,
"text": "It is present worldwide, with a prevalence of around 4 per 100000 and an incidence of about 1 in 20000. Overall lifespan is not affected significantly."
}
] | 12
|
BioASQ-training12b
| null | null |
64425ce357b1c7a315000059
|
bioasq_factoid
|
factoid
|
Which disease was studied in the CADISS trial?
|
['carotid and vertebral artery dissection']
|
[
"carotid and vertebral artery dissection",
"CVA dissection",
"carotid artery dissection",
"vertebral artery dissection",
"cervical artery dissection",
"cervical artery dissection syndrome",
"carotid and vertebral artery injury"
] |
['CADISS was a prospective multicentre randomised-controlled trial in acute (within 7 days of onset) carotid and vertebral artery dissection.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28087823",
"http://www.ncbi.nlm.nih.gov/pubmed/18705933",
"http://www.ncbi.nlm.nih.gov/pubmed/22855862",
"http://www.ncbi.nlm.nih.gov/pubmed/22110554",
"http://www.ncbi.nlm.nih.gov/pubmed/19386884",
"http://www.ncbi.nlm.nih.gov/pubmed/30801621",
"http://www.ncbi.nlm.nih.gov/pubmed/25684164"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28087823",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "Prognosis of carotid dissecting aneurysms: Results from CADISS and a systematic review."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28087823",
"endSection": "abstract",
"offsetInBeginSection": 262,
"offsetInEndSection": 497,
"text": "METHODS: We included 264 patients with extracranial cervical artery dissection (CAD) from the Cervical Artery Dissection in Stroke Study (CADISS), a multicenter prospective study that compared antiplatelet with anticoagulation therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28087823",
"endSection": "abstract",
"offsetInBeginSection": 1451,
"offsetInEndSection": 1602,
"text": "CONCLUSIONS: The results of CADISS provide evidence suggesting that DAs may have benign prognosis and therefore medical treatment should be considered."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25684164",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25684164",
"endSection": "abstract",
"offsetInBeginSection": 379,
"offsetInEndSection": 540,
"text": "We compared their efficacy in the Cervical Artery Dissection in Stroke Study (CADISS), with the additional aim of establishing the true risk of recurrent stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22855862",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 365,
"text": "OBJECTIVE: To present the results of the nonrandomized arm of the Cervical Artery Dissection in Stroke Study (CADISS-NR) trial, comparing anticoagulation and antiplatelets for prevention of recurrent stroke after carotid and vertebral dissection, and perform a meta-analysis of these results with previously published studies comparing the 2 therapeutic strategies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19386884",
"endSection": "abstract",
"offsetInBeginSection": 555,
"offsetInEndSection": 823,
"text": "Although optimal treatment for VAD is unknown, the Cervical Artery Dissection in Stroke Study (CADISS) is an ongoing randomised multicentre prospective study comparing antiplatelet therapy with anticoagulation for patients with both carotid artery dissection and VAD. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22110554",
"endSection": "abstract",
"offsetInBeginSection": 620,
"offsetInEndSection": 720,
"text": "We use dual antiplatelets for the management of cervical dissections as a part of the CADISS trial. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18705933",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Antiplatelet therapy vs. anticoagulation in cervical artery dissection: rationale and design of the Cervical Artery Dissection in Stroke Study (CADISS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18705933",
"endSection": "abstract",
"offsetInBeginSection": 535,
"offsetInEndSection": 679,
"text": "AIMS: CADISS is a prospective multicentre randomised-controlled trial in acute (within 7 days of onset) carotid and vertebral artery dissection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18705933",
"endSection": "abstract",
"offsetInBeginSection": 537,
"offsetInEndSection": 681,
"text": "AIMS\n\nCADISS is a prospective multicentre randomised-controlled trial in acute (within 7 days of onset) carotid and vertebral artery dissection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22110554",
"endSection": "abstract",
"offsetInBeginSection": 620,
"offsetInEndSection": 719,
"text": "We use dual antiplatelets for the management of cervical dissections as a part of the CADISS trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18705933",
"endSection": "abstract",
"offsetInBeginSection": 535,
"offsetInEndSection": 678,
"text": "AIMS CADISS is a prospective multicentre randomised-controlled trial in acute (within 7 days of onset) carotid and vertebral artery dissection."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30801621",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "Antiplatelet Therapy vs Anticoagulation Therapy in Cervical Artery Dissection: The Cervical Artery Dissection in Stroke Study ( CADISS ) Randomized Clinical Trial Final Results ."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18705933",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Antiplatelet therapy vs. anticoagulation in cervical artery dissection: rationale and design of the Cervical Artery Dissection in Stroke Study ( CADISS ) ."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25684164",
"endSection": "abstract",
"offsetInBeginSection": 369,
"offsetInEndSection": 533,
"text": "We compared their efficacy in the Cervical Artery Dissection in Stroke Study ( CADISS) , with the additional aim of establishing the true risk of recurrent stroke ."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25684164",
"endSection": "abstract",
"offsetInBeginSection": 378,
"offsetInEndSection": 540,
"text": "We compared their efficacy in the Cervical Artery Dissection in Stroke Study (CADISS), with the additional aim of establishing the true risk of recurrent stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22855862",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 365,
"text": "OBJECTIVE\nTo present the results of the nonrandomized arm of the Cervical Artery Dissection in Stroke Study (CADISS-NR) trial, comparing anticoagulation and antiplatelets for prevention of recurrent stroke after carotid and vertebral dissection, and perform a meta-analysis of these results with previously published studies comparing the 2 therapeutic strategies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22110554",
"endSection": "abstract",
"offsetInBeginSection": 620,
"offsetInEndSection": 720,
"text": "We use dual antiplatelets for the management of cervical dissections as a part of the CADISS trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18705933",
"endSection": "abstract",
"offsetInBeginSection": 537,
"offsetInEndSection": 681,
"text": "AIMS\nCADISS is a prospective multicentre randomised-controlled trial in acute (within 7 days of onset) carotid and vertebral artery dissection."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18705933",
"endSection": "title",
"offsetInBeginSection": 25,
"offsetInEndSection": 152,
"text": "anticoagulation in cervical artery dissection: rationale and design of the Cervical Artery Dissection in Stroke Study (CADISS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30801621",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Antiplatelet Therapy vs Anticoagulation Therapy in Cervical Artery Dissection: The Cervical Artery Dissection in Stroke Study (CADISS) Randomized Clinical Trial Final Results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19386884",
"endSection": "abstract",
"offsetInBeginSection": 555,
"offsetInEndSection": 822,
"text": "Although optimal treatment for VAD is unknown, the Cervical Artery Dissection in Stroke Study (CADISS) is an ongoing randomised multicentre prospective study comparing antiplatelet therapy with anticoagulation for patients with both carotid artery dissection and VAD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18705933",
"endSection": "abstract",
"offsetInBeginSection": 525,
"offsetInEndSection": 663,
"text": "CADISS is a prospective multicentre randomised-controlled trial in acute (within 7 days of onset) carotid and vertebral artery dissection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22855862",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 354,
"text": "To present the results of the nonrandomized arm of the Cervical Artery Dissection in Stroke Study (CADISS-NR) trial, comparing anticoagulation and antiplatelets for prevention of recurrent stroke after carotid and vertebral dissection, and perform a meta-analysis of these results with previously published studies comparing the 2 therapeutic strategies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25684164",
"endSection": "abstract",
"offsetInBeginSection": 367,
"offsetInEndSection": 528,
"text": "We compared their efficacy in the Cervical Artery Dissection in Stroke Study (CADISS), with the additional aim of establishing the true risk of recurrent stroke."
}
] | 11
|
BioASQ-training11b
| null | null |
5e4604d83f54159529000003
|
bioasq_factoid
|
yesno
|
Does an interferon (IFN) signature exist for SLE patients?
|
['yes']
|
[
"yes"
] |
['Interferon type I (IFN-I) plays a pivotal role in the pathogenesis of SLE. An IFN-I score (positive or negative), as a measure of IFN-I activation, is assessed using the expression values of IFN-I signature genes (IFI44, IFI44L, IFIT1, Ly6e, MxA, IFITM1) in CD14+ monocytes of cSLE patients and healthy controls (HCs).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29850618",
"http://www.ncbi.nlm.nih.gov/pubmed/21576205",
"http://www.ncbi.nlm.nih.gov/pubmed/29321042",
"http://www.ncbi.nlm.nih.gov/pubmed/28830352"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21576205",
"endSection": "title",
"offsetInBeginSection": 69,
"offsetInEndSection": 167,
"text": "Interferon regulatory factor 7 activation correlates with the IFN signature and recurrent disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21576205",
"endSection": "abstract",
"offsetInBeginSection": 801,
"offsetInEndSection": 941,
"text": "In SLE post-transplant, recurrent disease activity and induction of IRF7 protein expression correlated with activation of the IFN signature."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28830352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28830352",
"endSection": "abstract",
"offsetInBeginSection": 1068,
"offsetInEndSection": 1329,
"text": "We also detected decreased expression of several IFN-signature genes Ifit3 and Isg15 in CD4+ from SLE-prone mice following TOFA and DEXA treatment, and IFIT3 in CD3+ T cells from human patients following immunosuppressant therapy including steroid, respectively"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29850618",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 992,
"text": "We found that cDCs from prediseased TCSle male mice express the IFN signature as female TCSle cDCs do. Estrogens are necessary but not sufficient to express this IFN signature, but high doses of E2 can compensate for other steroidal components."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29850618",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Conventional DCs from Male and Female Lupus-Prone B6.NZM Sle1/Sle2/Sle3 Mice Express an IFN Signature and Have a Higher Immunometabolism That Are Enhanced by Estrogen."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29321042",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "Type I IFN signature in childhood-onset systemic lupus erythematosus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29321042",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 190,
"text": " Interferon type I (IFN-I) plays a pivotal role in the pathogenesis of SLE. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29321042",
"endSection": "abstract",
"offsetInBeginSection": 401,
"offsetInEndSection": 677,
"text": "The IFN-I score (positive or negative), as a measure of IFN-I activation, was assessed using real-time quantitative PCR (RT-PCR) expression values of IFN-I signature genes (IFI44, IFI44L, IFIT1, Ly6e, MxA, IFITM1) in CD14+ monocytes of cSLE patients and healthy controls (HCs)"
}
] | 11
|
BioASQ-training11b
| null | null |
5c7019557c78d6947100005f
|
bioasq_yesno
|
yesno
|
Are variants in FHF2 (also known as FGF13) associated with encephalopathy?
|
['yes']
|
[
"yes"
] |
['Yes. FHF2 (also known as FGF13) variants are a cause of infantile-onset developmental and epileptic encephalopathy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33245860"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33245860",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Missense variants in the N-terminal domain of the A isoform of FHF2/FGF13 cause an X-linked developmental and epileptic encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33245860",
"endSection": "abstract",
"offsetInBeginSection": 390,
"offsetInEndSection": 1418,
"text": "Whole-exome sequencing identified hemi- and heterozygous variants in the N-terminal domain of the A isoform of FHF2 (FHF2A). The X-linked FHF2 gene (also known as FGF13) has alternative first exons which produce multiple protein isoforms that differ in their N-terminal sequence. The variants were located at highly conserved residues in the FHF2A inactivation particle that competes with the intrinsic fast inactivation mechanism of Nav channels. Functional characterization of mutant FHF2A co-expressed with wild-type Nav1.6 (SCN8A) revealed that mutant FHF2A proteins lost the ability to induce rapid-onset, long-term blockade of the channel while retaining pro-excitatory properties. These gain-of-function effects are likely to increase neuronal excitability consistent with the epileptic potential of FHF2 variants. Our findings demonstrate that FHF2 variants are a cause of infantile-onset developmental and epileptic encephalopathy and underline the critical role of the FHF2A isoform in regulating Nav channel function."
}
] | 11
|
BioASQ-training11b
| null | null |
61f9605f882a024a1000004f
|
bioasq_yesno
|
yesno
|
Is overexpression of LY6K associated with better prognosis for non-small cell lung cancer patients?
|
['no']
|
[
"no"
] |
['No, LY6K overexpression is associated with poor prognosis for patients with NSCLC.', 'No, overexpression of LY6K has been found to be associated with poor prognosis for non-small cell lung cancer patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18089789"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18089789",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 570,
"text": "Gene expression profile analyses of non-small cell lung carcinomas (NSCLC) and esophageal squamous cell carcinomas (ESCC) revealed that lymphocyte antigen 6 complex locus K (LY6K) was specifically expressed in testis and transactivated in a majority of NSCLCs and ESCCs. Immunohistochemical staining using 406 NSCLC and 265 ESCC specimens confirmed that LY6K overexpression was associated with poor prognosis for patients with NSCLC (P = 0.0003), as well as ESCC (P = 0.0278), and multivariate analysis confirmed its independent prognostic value for NSCLC (P = 0.0035). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18089789",
"endSection": "abstract",
"offsetInBeginSection": 271,
"offsetInEndSection": 569,
"text": "Immunohistochemical staining using 406 NSCLC and 265 ESCC specimens confirmed that LY6K overexpression was associated with poor prognosis for patients with NSCLC (P = 0.0003), as well as ESCC (P = 0.0278), and multivariate analysis confirmed its independent prognostic value for NSCLC (P = 0.0035)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18089789",
"endSection": "abstract",
"offsetInBeginSection": 271,
"offsetInEndSection": 570,
"text": "Immunohistochemical staining using 406 NSCLC and 265 ESCC specimens confirmed that LY6K overexpression was associated with poor prognosis for patients with NSCLC (P = 0.0003), as well as ESCC (P = 0.0278), and multivariate analysis confirmed its independent prognostic value for NSCLC (P = 0.0035)."
}
] | 11
|
BioASQ-training11b
| null | null |
5e49c5336d0a277941000011
|
bioasq_yesno
|
yesno
|
Are there randomised controlled trials on sevoflurane?
|
['yes']
|
[
"yes"
] |
['Yes. There are < 10 studies reported, answering questions like : how to improve speed of recovery, relationship to dreaming and anesthetic experience, effect on cardiac troponin release, effect on myocardial injury, postoperative delirium, haemodynamics & emergence and recovery characteristics of total intravenous anaesthesia, costs of postoperative nausea and vomiting, pediatric conscious sedation for dental procedures']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23452265",
"http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"http://www.ncbi.nlm.nih.gov/pubmed/22103571",
"http://www.ncbi.nlm.nih.gov/pubmed/21733178",
"http://www.ncbi.nlm.nih.gov/pubmed/21675061",
"http://www.ncbi.nlm.nih.gov/pubmed/20683334",
"http://www.ncbi.nlm.nih.gov/pubmed/16867087",
"http://www.ncbi.nlm.nih.gov/pubmed/15310345",
"http://www.ncbi.nlm.nih.gov/pubmed/12693995",
"http://www.ncbi.nlm.nih.gov/pubmed/11966554"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23452265",
"endSection": "sections.0",
"offsetInBeginSection": 459,
"offsetInEndSection": 641,
"text": "After Ethics Review Board approval, 44 ASA I-III patients undergoing elective gynaecological surgery were randomised after surgery to either hypercapnic hyperpnoea or control groups."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23452265",
"endSection": "sections.0",
"offsetInBeginSection": 1471,
"offsetInEndSection": 1617,
"text": "Hypercapnic hyperpnoea in spontaneously breathing patients halves the time of recovery from sevoflurane-induced anaesthesia in the operating room."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"endSection": "sections.0",
"offsetInBeginSection": 329,
"offsetInEndSection": 569,
"text": "A total of 200 women undergoing first trimester abortion (American Society of Anesthesiologists physical status I) participated in the study. Patients were randomly assigned to receive either sevoflurane or propofol for short-term sedation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"endSection": "sections.0",
"offsetInBeginSection": 650,
"offsetInEndSection": 841,
"text": "The results showed the incidence of dreaming was significantly different between anaesthesia groups with 60% (60/100) of the sevoflurane group and 33% (33/100) of the propofol group (P=0.000)"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"endSection": "sections.0",
"offsetInBeginSection": 1269,
"offsetInEndSection": 1569,
"text": "Anaesthesia administered had no effect on patient satisfaction. The results suggest that the incidence of dreaming was not affected by recovery time. Patient satisfaction was not influenced by choice of sedative and/or by the occurrence of dreaming during sevoflurane or propofol short-term sedation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Prior reports suggest that dreaming during anaesthesia is dependent on recovery time. Dreaming during sedation may impact patient satisfaction"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22103571",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Sevoflurane vs. propofol in patients with coronary disease undergoing mitral surgery: a randomised study."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22103571",
"endSection": "sections.0",
"offsetInBeginSection": 197,
"offsetInEndSection": 373,
"text": "We therefore performed a randomised controlled trial (sevoflurane vs. propofol) to compare cardiac troponin release in patients with coronary disease undergoing mitral surgery."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21675061",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Myocardial injury in remifentanil-based anaesthesia for off-pump coronary artery bypass surgery: an equipotent dose of sevoflurane versus propofol"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21675061",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 340,
"text": "This randomised controlled trial compared the effect of equipotent anaesthetic doses of sevoflurane (S group) versus propofol (P group), during remifentanil-based anaesthesia for off-pump coronary artery bypass surgery, on myocardial injury. Either sevoflurane or propofol was titrated to maintain bispectral index values between 40 and 50."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20683334",
"endSection": "sections.0",
"offsetInBeginSection": 365,
"offsetInEndSection": 545,
"text": "This randomised, multicentre, parallel-group trial included 98 adult patients. Patients received intravenous propofol for induction followed by sevoflurane maintenance anaesthesia."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20683334",
"endSection": "sections.0",
"offsetInBeginSection": 654,
"offsetInEndSection": 747,
"text": "Patients were randomly allocated to receive sugammadex 2.0 mg kg(-1) or neostigmine 50 microg"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16867087",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "We compared the haemodynamics, emergence and recovery characteristics of total intravenous anaesthesia using propofol/remifentanil with sevoflurane/remifentanil anaesthesia, under bispectral index guidance, in 103 patients undergoing surgical procedures lasting > 3.5 h"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15310345",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "A randomised controlled trial of paediatric conscious sedation for dental treatment using intravenous midazolam combined with inhaled nitrous oxide or nitrous oxide/sevoflurane"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15310345",
"endSection": "sections.0",
"offsetInBeginSection": 1403,
"offsetInEndSection": 1643,
"text": "Intravenous midazolam, especially in combination with inhaled nitrous oxide or sevoflurane and nitrous oxide, are effective techniques, with the combination of midazolam and sevoflurane the one most likely to result in successful treatment."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12693995",
"endSection": "sections.0",
"offsetInBeginSection": 114,
"offsetInEndSection": 244,
"text": "We randomly assigned 1063 adult and 322 paediatric elective patients to one of four (adult) or two (paediatric) anaesthesia groups"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12693995",
"endSection": "sections.0",
"offsetInBeginSection": 842,
"offsetInEndSection": 1174,
"text": "In both studies, there was no difference in postdischarge outcomes at Day 7. Sevoflurane/sevoflurane was more costly with higher PONV rates in both studies. In adults, the cost per extra episode of PONV avoided was pound 296 (propofol/propofol vs. propofol/ sevoflurane) and pound 333 (propofol/sevoflurane vs. propofol/isoflurane)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11966554",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "Comparison of sevoflurane and nitrous oxide mixture with nitrous oxide alone for inhalation conscious sedation in children having dental treatment: a randomised controlled trial."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11966554",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "We studied 411 children aged 3-10 years who were referred for dental treatment. They were randomly allocated to have inhalation conscious sedation with either sevoflurane/nitrous oxide mixture or nitrous oxide alone"
}
] | 5
|
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4252326"
] | null |
515d9e5c298dcd4e5100000e
|
bioasq_yesno
|
yesno
|
Has ivosidenib been FDA approved for use against acute myeloid leukemia?
|
['yes']
|
[
"yes"
] |
['The FDA approved ivosidenib for patients with IDH1-mutant relapsed/refractory acute myeloid leukemia.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30093505"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30093505",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "The FDA approved ivosidenib for patients with IDH1-mutant relapsed/refractory acute myeloid leukemia. "
}
] | 11
|
BioASQ-training11b
| null | null |
5c65495be842deac67000021
|
bioasq_yesno
|
yesno
|
Is ocrelizumab effective for primary progressive multiple sclerosis?
|
['yes']
|
[
"yes"
] |
['Yes, ocrelizumab is effective and approved for primary progressive multiple sclerosis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35583174",
"http://www.ncbi.nlm.nih.gov/pubmed/35590041",
"http://www.ncbi.nlm.nih.gov/pubmed/35192158"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35192158",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "Ocrelizumab (Ocrevus®) is an intravenously administered, humanized anti-CD20 monoclonal antibody approved for the treatment of adults with relapsing forms of multiple sclerosis (RMS) or primary progressive multiple sclerosis (PPMS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35590041",
"endSection": "abstract",
"offsetInBeginSection": 2194,
"offsetInEndSection": 2363,
"text": "When using the anti-CD20 monoclonal antibodies ocrelizumab and ofatumumab in the treatment of MS, it is not necessary to test for NAbs as these occur very infrequently. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35583174",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 35,
"text": "Ocrelizumab for multiple sclerosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35583174",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 318,
"text": "BACKGROUND: Ocrelizumab is a humanised anti-CD20 monoclonal antibody developed for the treatment of multiple sclerosis (MS). It was approved by the Food and Drug Administration (FDA) in March 2017 for using in adults with relapsing-remitting multiple sclerosis (RRMS) and primary progressive multiple sclerosis (PPMS)."
}
] | 12
|
BioASQ-training12b
| null | null |
6404199d201352f04a000019
|
bioasq_yesno
|
factoid
|
What does the gene symbol EREG stand for?
|
['epiregulin']
|
[
"epiregulin",
"EREG",
"epiregulin precursor",
"epiregulin protein",
"epiregulin isoform"
] |
['The gene symbol EREG stands for the gene epiregulin.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34667080"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34667080",
"endSection": "abstract",
"offsetInBeginSection": 268,
"offsetInEndSection": 569,
"text": "We found that epidermal growth factor (EGF)-deficient cells exhibited lower basal ERK activity than the cells deficient in heparin-binding EGF (HBEGF), transforming growth factor alpha (TGFα) or epiregulin (EREG), but all cell lines deficient in a single EGFR ligand retained the ERK activation waves."
}
] | 11
|
BioASQ-training11b
| null | null |
6237a5513a8413c6530000b0
|
bioasq_factoid
|
yesno
|
Do brown fat cells produce heat?
|
['yes']
|
[
"yes"
] |
['Yes, brown fat cells produce heat.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23834768",
"http://www.ncbi.nlm.nih.gov/pubmed/26910308",
"http://www.ncbi.nlm.nih.gov/pubmed/22796012",
"http://www.ncbi.nlm.nih.gov/pubmed/21196229",
"http://www.ncbi.nlm.nih.gov/pubmed/23818608",
"http://www.ncbi.nlm.nih.gov/pubmed/6148836",
"http://www.ncbi.nlm.nih.gov/pubmed/3083882",
"http://www.ncbi.nlm.nih.gov/pubmed/26496384",
"http://www.ncbi.nlm.nih.gov/pubmed/26322018",
"http://www.ncbi.nlm.nih.gov/pubmed/15058310",
"http://www.ncbi.nlm.nih.gov/pubmed/6819159",
"http://www.ncbi.nlm.nih.gov/pubmed/21982742",
"http://www.ncbi.nlm.nih.gov/pubmed/24567786",
"http://www.ncbi.nlm.nih.gov/pubmed/27528872",
"http://www.ncbi.nlm.nih.gov/pubmed/8042786",
"http://www.ncbi.nlm.nih.gov/pubmed/25642708",
"http://www.ncbi.nlm.nih.gov/pubmed/962510",
"http://www.ncbi.nlm.nih.gov/pubmed/27528697",
"http://www.ncbi.nlm.nih.gov/pubmed/27552974",
"http://www.ncbi.nlm.nih.gov/pubmed/1550210",
"http://www.ncbi.nlm.nih.gov/pubmed/25068090",
"http://www.ncbi.nlm.nih.gov/pubmed/2039657",
"http://www.ncbi.nlm.nih.gov/pubmed/21123942",
"http://www.ncbi.nlm.nih.gov/pubmed/9277366",
"http://www.ncbi.nlm.nih.gov/pubmed/24129212",
"http://www.ncbi.nlm.nih.gov/pubmed/5262992",
"http://www.ncbi.nlm.nih.gov/pubmed/24046370",
"http://www.ncbi.nlm.nih.gov/pubmed/26912151",
"http://www.ncbi.nlm.nih.gov/pubmed/6315457",
"http://www.ncbi.nlm.nih.gov/pubmed/541897",
"http://www.ncbi.nlm.nih.gov/pubmed/25466254",
"http://www.ncbi.nlm.nih.gov/pubmed/16594742",
"http://www.ncbi.nlm.nih.gov/pubmed/26749900",
"http://www.ncbi.nlm.nih.gov/pubmed/22654830",
"http://www.ncbi.nlm.nih.gov/pubmed/19641492"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24567786",
"endSection": "abstract",
"offsetInBeginSection": 271,
"offsetInEndSection": 512,
"text": "WAT and BAT are both involved in energy balance. WAT is mainly involved in the storage and mobilization of energy in the form of triglycerides, whereas BAT specializes in dissipating energy as heat during cold- or diet-induced thermogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25466254",
"endSection": "abstract",
"offsetInBeginSection": 76,
"offsetInEndSection": 288,
"text": "Because brown adipose tissue (BAT) dissipates energy in the form of heat, increasing energy expenditure by augmenting BAT-mediated thermogenesis may represent an approach to counter obesity and its complications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23818608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "Classic brown fat and inducible beige fat both dissipate chemical energy in the form of heat through the actions of mitochondrial uncoupling protein 1. This nonshivering thermogenesis is crucial for mammals as a defense against cold and obesity/diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22654830",
"endSection": "abstract",
"offsetInBeginSection": 105,
"offsetInEndSection": 245,
"text": "Mitochondrial uncoupling protein 1 in brown fat cells produces heat by dissipating the energy generated by fatty acid and glucose oxidation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21196229",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 36,
"text": "Brown fat biology and thermogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21196229",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Brown fat (brown adipose tissue, BAT) primary function is to produce heat. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 353,
"text": "Brown fat cells were classified into 6 types: Type 1 cells are fat-depleted cells filled with granular cytoplasm and are believed to be produced after oxidation of fat for heat production."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9277366",
"endSection": "abstract",
"offsetInBeginSection": 1226,
"offsetInEndSection": 1487,
"text": "Calorimetric measurements from cell suspensions showed that ATP increased basal heat production of isolated brown fat cells by approximately 40% but had no effect on the greater than fivefold increase in heat production seen with maximal adrenergic stimulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23818608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Classic brown fat and inducible beige fat both dissipate chemical energy in the form of heat through the actions of mitochondrial uncoupling protein 1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21982742",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Brown adipocytes oxidize fatty acids to produce heat in response to cold or to excessive energy intake; stimulation of brown fat development and function may thus counteract obesity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1285,
"text": "The occurrence of Types 1 and/or 6 cells that has been revealed in 65 out of the total 180 samples (36%), suggests that the oxidation of fat for the thermogenesis proceeds in the brown fat tissue and that brown fat cells partially undergo fat depletion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 354,
"text": "Brown fat cells were classified into 6 types: Type 1 cells are fat-depleted cells filled with granular cytoplasm and are believed to be produced after oxidation of fat for heat production."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26322018",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 333,
"text": "In response to cold, both classical brown fat and the newly identified \"beige\" or \"brite\" cells are activated by β-adrenergic signaling and catabolize stored lipids and carbohydrates to produce heat via UCP1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26496384",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "The ability of brown adipocytes (fat cells) to dissipate energy as heat shows great promise for the treatment of obesity and other metabolic disorders"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24046370",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Inappropriate heat dissipation ignites brown fat thermogenesis in mice with a mutant thyroid hormone receptor α1"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25068090",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Brown fat and vascular heat dissipation: The new cautionary tail"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21123942",
"endSection": "abstract",
"offsetInBeginSection": 255,
"offsetInEndSection": 458,
"text": "Brown adipose produces heat as a defense against hypothermia and obesity, and the appearance of brown-like adipocytes within white adipose tissue depots is associated with improved metabolic phenotypes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 1764,
"offsetInEndSection": 1902,
"text": "In the same manner, marked ability to produce a considerable amount of heat was evidenced in brown fat tissue of children and teenagers. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 355,
"text": "Brown fat cells were classified into 6 types: Type 1 cells are fat-depleted cells filled with granular cytoplasm and are believed to be produced after oxidation of fat for heat production. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8042786",
"endSection": "abstract",
"offsetInBeginSection": 1616,
"offsetInEndSection": 1739,
"text": "It is inferred that brown-adipose-tissue heat production is reduced during (and probably also some time after) anesthesia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3083882",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Parallel measurements of heat production and thermogenin content in brown fat cells during cold acclimation of rats."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27528872",
"endSection": "abstract",
"offsetInBeginSection": 39,
"offsetInEndSection": 287,
"text": "The classical white adipose tissue builds up energy in the form of triglycerides and is useful for preventing fatigue during periods of low caloric intake and the brown adipose tissue instead of inducing fat accumulation can produce energy as heat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26322018",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 334,
"text": "In response to cold, both classical brown fat and the newly identified \"beige\" or \"brite\" cells are activated by β-adrenergic signaling and catabolize stored lipids and carbohydrates to produce heat via UCP1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23834768",
"endSection": "abstract",
"offsetInBeginSection": 103,
"offsetInEndSection": 245,
"text": "White adipose tissue stores energy reserves as fat, whereas the metabolic function of brown adipose tissue is lipid oxidation to produce heat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6148836",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "The main function of brown adipose tissue (BAT) is to produce heat in response to cold."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129212",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Brown adipocytes oxidize fatty acids to produce heat in response to cold or caloric overfeeding."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21196229",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Brown fat (brown adipose tissue, BAT) primary function is to produce heat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15058310",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 293,
"text": "Adipose tissue plays an active role in energy balance because it is not only a lipid storing and mobilizing tissue but consists of functionally specialized tissues able to produce heat (in brown adipose tissue) and to produce or release a vast number of so called adipokines or adipocytokines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25642708",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Brown adipose tissue (BAT), a specialized fat that dissipates energy to produce heat, plays an important role in the regulation of energy balance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19641492",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Brown adipose cells are specialized to dissipate chemical energy in the form of heat, as a physiological defence against cold and obesity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 1286,
"offsetInEndSection": 1430,
"text": "In the present study, the thermogenesis of human brown fat tissue was suggested chiefly with regard to the occurrence of Types 1 and/or 6 cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 1764,
"offsetInEndSection": 1901,
"text": "In the same manner, marked ability to produce a considerable amount of heat was evidenced in brown fat tissue of children and teenagers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26749900",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Adult humans have heat-producing and energy-consuming brown adipose tissue in the clavicular region of the neck."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27552974",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Brown and beige adipocytes expend chemical energy to produce heat and are therefore important in regulating body temperature and body weight."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2039657",
"endSection": "abstract",
"offsetInBeginSection": 2005,
"offsetInEndSection": 2203,
"text": "In human perirenal brown fat tissue, darkly stained fat-depleted cells (D) occupy, with other cell types (CR, CR'), an important part in the reversible heat production cycle of the brown fat tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26912151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Brown fat is a specialized fat depot that can increase energy expenditure and produce heat."
}
] | 6
|
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002477",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002001",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D052437",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006359",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005223"
] |
[
{
"o": "Heat",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0018837"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0066521",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0018837"
},
{
"o": "Heat",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0066521"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A18591807",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0018837"
},
{
"o": "heat",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A18591807"
}
] |
58ca906a02b8c6095300002e
|
bioasq_yesno
|
yesno
|
Is OXLUMO (lumasiran) used for the treatment of primary hyperoxaluria?
|
['yes']
|
[
"yes"
] |
['Yes, OXLUMO (lumasiran) is approved for the treatment of primary hyperoxaluria type 1 (PH1) in adults and children aged 6 years and older.', 'Yes, OXLUMO (lumasiran) is used for the treatment of primary hyperoxaluria.', 'OXLUMO (lumasiran) for the treatment of primary hyperoxaluria', 'Lumasiran (Oxlumo™) is a subcutaneously administered small interfering RNA (siRNA) targeting the mRNA for hydroxyacid oxidase 1 gene (HAO1; encodes glycolate oxidase) and was developed by Alnylam Pharmaceuticals for the treatment of primary hyperoxaluria type 1 (PH1).', 'Lumasiran (Oxlumo) is a subcutaneously administered small interfering RNA (siRNA) targeting the mRNA for hydroxyacid oxidase 1 gene (HAO1; encodes glycolate oxidase) and was developed by Alnylam Ph', 'Is OXLUMO (lumasiran) used for the treatment of primary hyperoxaluria ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33789010",
"http://www.ncbi.nlm.nih.gov/pubmed/34154993",
"http://www.ncbi.nlm.nih.gov/pubmed/34022071",
"http://www.ncbi.nlm.nih.gov/pubmed/33985991",
"http://www.ncbi.nlm.nih.gov/pubmed/35237473",
"http://www.ncbi.nlm.nih.gov/pubmed/35747094",
"http://www.ncbi.nlm.nih.gov/pubmed/33497125",
"http://www.ncbi.nlm.nih.gov/pubmed/34906487",
"http://www.ncbi.nlm.nih.gov/pubmed/35731461",
"http://www.ncbi.nlm.nih.gov/pubmed/33513899",
"http://www.ncbi.nlm.nih.gov/pubmed/35843439",
"http://www.ncbi.nlm.nih.gov/pubmed/33405070",
"http://www.ncbi.nlm.nih.gov/pubmed/35015123"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33405070",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 268,
"text": "Lumasiran (Oxlumo™) is a subcutaneously administered small interfering RNA (siRNA) targeting the mRNA for hydroxyacid oxidase 1 gene (HAO1; encodes glycolate oxidase) and was developed by Alnylam Pharmaceuticals for the treatment of primary hyperoxaluria type 1 (PH1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34154993",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 388,
"text": "OXLUMO (lumasiran) for the treatment of primary hyperoxaluria,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34154993",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 506,
"text": "Conjugation of oligonucleotide therapeutics, including small interfering RNAs (siRNAs) or antisense oligonucleotides, to N-acetylgalactosamine (GalNAc) ligands has become the primary strategy for hepatocyte-targeted delivery, and with the recent approvals of GIVLAARI (givosiran) for the treatment of acute hepatic porphyria, OXLUMO (lumasiran) for the treatment of primary hyperoxaluria, and Leqvio (inclisiran) for the treatment of hypercholesterolemia, the technology has been well validated clinically."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34022071",
"endSection": "abstract",
"offsetInBeginSection": 901,
"offsetInEndSection": 1240,
"text": "In this context we discuss nedosiran (Dicerna Pharmaceuticals, Inc.) and lumasiran (Alnylam Pharmaceuticals), which are both novel RNAi therapies for primary hyperoxaluria that selectively reduce hepatic expression of lactate dehydrogenase and glycolate oxidase respectively, reducing hepatic oxalate production and urinary oxalate levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33405070",
"endSection": "abstract",
"offsetInBeginSection": 622,
"offsetInEndSection": 737,
"text": "On 23 November 2020, lumasiran was approved in the USA for the treatment of adult and paediatric patients with PH1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33789010",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Lumasiran, an RNAi Therapeutic for Primary Hyperoxaluria Type 1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33405070",
"endSection": "abstract",
"offsetInBeginSection": 502,
"offsetInEndSection": 621,
"text": "On 19 November 2020, lumasiran received its first global approval in the EU for the treatment of PH1 in all age groups."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33513899",
"endSection": "abstract",
"offsetInBeginSection": 507,
"offsetInEndSection": 712,
"text": "Efforts made to develop pharmacological treatments succeeded with the biotechnological agent lumasiran, a siRNA product against glycolate oxidase, which has become the first effective therapy to treat PH1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34906487",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Phase 3 trial of lumasiran for primary hyperoxaluria type 1: A new RNAi therapeutic in infants and young children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33497125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 246,
"text": "Several new drugs have been approved to treat rare genetic disorders: setmelanotide for certain conditions causing obesity; lumasiran for primary hyperoxaluria type 1, a kidney disorder; and lonafarnib for two diseases that cause premature aging."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35747094",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Lumasiran in the Management of Patients with Primary Hyperoxaluria Type 1: From Bench to Bedside."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35015123",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "The effect of lumasiran therapy for primary hyperoxaluria type 1 in small infants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35731461",
"endSection": "abstract",
"offsetInBeginSection": 956,
"offsetInEndSection": 1079,
"text": " Lumasiran was recently approved in the treatment of primary hyperoxaluria type 1 and nedosiran is in the approval process."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33985991",
"endSection": "abstract",
"offsetInBeginSection": 1919,
"offsetInEndSection": 2084,
"text": "SIONS: Lumasiran had an acceptable safety profile and reduced urinary oxalate excretion in all patients with primary hyperoxaluria type 1 to near-normal levels.CLINI"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35237473",
"endSection": "abstract",
"offsetInBeginSection": 315,
"offsetInEndSection": 472,
"text": "Lumasiran is an RNA interference (RNAi) therapeutic agent that reduces hepatic oxalate production, which has been recently approved for the treatment of PH1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35843439",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 291,
"text": "RATIONALE & OBJECTIVE: Lumasiran reduces urinary and plasma oxalate (POx) in patients with primary hyperoxaluria type 1 (PH1) and relatively preserved kidney function. ILLUMINATE-C evaluates the efficacy, safety, pharmacokinetics, and pharmacodynamics of lumasiran in patients with PH1 and a"
}
] | 12
|
BioASQ-training12b
| null | null |
64281a47690f196b5100004f
|
bioasq_yesno
|
yesno
|
Is Mycobacterium avium less susceptible to antibiotics than Mycobacterium tuberculosis?
|
['yes']
|
[
"yes"
] |
['Mycobacterium avium causes disseminated infection in patients with acquired immune deficiency syndrome. M tuberculosis disease is preventable and curable and yet communicable, physicians should maintain a high degree of suspicion for tuberculosis in HIV-infected adults. In comparison, the goal of treating M avium complex in patients with advanced HIV disease is to reduce constitutional symptoms and improve survival. Patients who were suspected to have disseminated mycobacterial infection, presenting fever and (preferably) a CD4 T cell count<100.0 cell/mL were investigated. Twelve (15%) of the 80 blood cultures were positive for mycobacteria, with Mycobacterium avium being identified in 7 (8.8%) samples and M. tuberculosis in 5 (6.2%). The antimycobacterial activities of RS-112997, RS-124922 and RS-118641, three capuramycin analogues that inhibit phospho-N-acetylmuramyl-pentapeptide translocase, were tested against clinical isolates of Mycobacterium tuberculosis, Mycobacterium avium and Mycobacterium intracellulare. The MIC50/90 (mg/L) results for RS-118641 were: M. tuberculosis, 1/2; multidrug-resistant (MDR) M. tuberculosis, 0.5/2; M. avium, 4/8; and M. intracellulare, 0.06/0.5']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21258569",
"http://www.ncbi.nlm.nih.gov/pubmed/19302308",
"http://www.ncbi.nlm.nih.gov/pubmed/16410940",
"http://www.ncbi.nlm.nih.gov/pubmed/15347635",
"http://www.ncbi.nlm.nih.gov/pubmed/12355367",
"http://www.ncbi.nlm.nih.gov/pubmed/10988097",
"http://www.ncbi.nlm.nih.gov/pubmed/1441463",
"http://www.ncbi.nlm.nih.gov/pubmed/19956964",
"http://www.ncbi.nlm.nih.gov/pubmed/15328105",
"http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"http://www.ncbi.nlm.nih.gov/pubmed/17897062",
"http://www.ncbi.nlm.nih.gov/pubmed/17548640"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21258569",
"endSection": "abstract",
"offsetInBeginSection": 1447,
"offsetInEndSection": 1550,
"text": "The prevalence of MAC lung infection in two inner city hospitals was four times higher than that of TB."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21258569",
"endSection": "abstract",
"offsetInBeginSection": 1792,
"offsetInEndSection": 1908,
"text": "Most patients with combined infection were clinically consistent with MTB and responded to anti MTB treatment alone."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19302308",
"endSection": "abstract",
"offsetInBeginSection": 1719,
"offsetInEndSection": 1868,
"text": "The triplex PCR developed by us could be used to detect and differentiate M. tuberculosis, M. avium and other mycobacteria in a single reaction tube."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16410940",
"endSection": "abstract",
"offsetInBeginSection": 402,
"offsetInEndSection": 567,
"text": "Twelve (15%) of the 80 blood cultures were positive for mycobacteria, with Mycobacterium avium being identified in 7 (8.8%) samples and M. tuberculosis in 5 (6.2%). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15347635",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 296,
"text": "The antimycobacterial activities of RS-112997, RS-124922 and RS-118641, three capuramycin analogues that inhibit phospho-N-acetylmuramyl-pentapeptide translocase, were tested against clinical isolates of Mycobacterium tuberculosis, Mycobacterium avium and Mycobacterium intracellulare"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15347635",
"endSection": "abstract",
"offsetInBeginSection": 461,
"offsetInEndSection": 627,
"text": "The MIC50/90 (mg/L) results for RS-118641 were: M. tuberculosis, 1/2; multidrug-resistant (MDR) M. tuberculosis, 0.5/2; M. avium, 4/8; and M. intracellulare, 0.06/0.5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15347635",
"endSection": "abstract",
"offsetInBeginSection": 1456,
"offsetInEndSection": 1692,
"text": "These results suggest that capuramycin analogues exhibit strong antimycobacterial potential and should be considered for further evaluation in the treatment of M. tuberculosis and M. avium-M. intracellulare complex infections in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12355367",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Mycobacterium avium causes disseminated infection in patients with acquired immune deficiency syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10988097",
"endSection": "abstract",
"offsetInBeginSection": 421,
"offsetInEndSection": 694,
"text": "Overall incidences of Mycobacterium tuberculosis (TB) and Mycobacterium avium complex (MAC) were 0.8 and 1.4 cases/100 person-years of follow-up (PYF), decreasing from 1.8 (TB) and 3.5 cases/100 PYF (MAC) before September 1995 to 0.3 and 0.2 cases/100 PYF after March 1997."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1441463",
"endSection": "abstract",
"offsetInBeginSection": 427,
"offsetInEndSection": 750,
"text": "Because M tuberculosis disease is preventable and curable and yet communicable, physicians should maintain a high degree of suspicion for tuberculosis in HIV-infected adults. In comparison, the goal of treating M avium complex in patients with advanced HIV disease is to reduce constitutional symptoms and improve survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19956964",
"endSection": "abstract",
"offsetInBeginSection": 1210,
"offsetInEndSection": 1385,
"text": "MAC pulmonary disease should be considered in the differential diagnosis of SPNs, even when encountered in geographic regions with a high prevalence of pulmonary tuberculosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16410940",
"endSection": "abstract",
"offsetInBeginSection": 186,
"offsetInEndSection": 400,
"text": "From April 2001 to February 2002, 80 blood samples from patients who were suspected to have disseminated mycobacterial infection, presenting fever and (preferably) a CD4 T cell count<100.0 cell/mL were investigated"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17548640",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "IL-10 underlies distinct susceptibility of BALB/c and C57BL/6 mice to Mycobacterium avium infection and influences efficacy of antibiotic therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Clinical utility of rifabutin 1 (RBT), a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC), has been hampered due to dose-limiting toxicity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Clinical utility of rifabutin 1 (RBT), a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC), has been hampered due to dose-limiting toxicity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12355367",
"endSection": "abstract",
"offsetInBeginSection": 214,
"offsetInEndSection": 364,
"text": "Effective therapeutic regimens exist that are limited by the emergence of drug resistance and the inability of antibiotics to kill dormant organisms. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17548640",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "IL-10 underlies distinct susceptibility of BALB/c and C57BL/6 mice to Mycobacterium avium infection and influences efficacy of antibiotic therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Clinical utility of rifabutin 1 (RBT), a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC), has been hampered due to dose-limiting toxicity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Clinical utility of rifabutin 1 (RBT), a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC), has been hampered due to dose-limiting toxicity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "Clinical utility of rifabutin 1 (RBT), a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC), has been hampered due to dose-limiting toxicity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 40,
"offsetInEndSection": 179,
"text": "a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC),"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Clinical utility of rifabutin 1 (RBT), a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC), has been hampered due to dose-limiting toxicity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Clinical utility of rifabutin 1 (RBT), a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC), has been hampered due to dose-limiting toxicity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Clinical utility of rifabutin 1 (RBT), a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC), has been hampered due to dose-limiting toxicity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19119013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Clinical utility of rifabutin 1 (RBT), a potent antibiotic used in multidrug regimens for tuberculosis (TB) as well as for infections caused by Mycobacterium avium complex (MAC), has been hampered due to dose-limiting toxicity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15328105",
"endSection": "abstract",
"offsetInBeginSection": 1048,
"offsetInEndSection": 1214,
"text": "tuberculosis appear to have different genetic mechanisms for resisting the effects of these antibiotics, with pks12 playing a relatively more significant role in MAC."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
5710a650cf1c32585100002b
|
bioasq_yesno
|
yesno
|
Is there a relationship between thyroid hormone altered metabolism and coronary artery disease?
|
['yes']
|
[
"yes"
] |
The major part of the studies and metaanalysis data show that hypothyroidism, both primary and secondary forms, is associated with higher incidence and severity of coronary artery disease.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23470525",
"http://www.ncbi.nlm.nih.gov/pubmed/22877896",
"http://www.ncbi.nlm.nih.gov/pubmed/22724581",
"http://www.ncbi.nlm.nih.gov/pubmed/21745107",
"http://www.ncbi.nlm.nih.gov/pubmed/19650571",
"http://www.ncbi.nlm.nih.gov/pubmed/19609889",
"http://www.ncbi.nlm.nih.gov/pubmed/18497453",
"http://www.ncbi.nlm.nih.gov/pubmed/17434631",
"http://www.ncbi.nlm.nih.gov/pubmed/17222925",
"http://www.ncbi.nlm.nih.gov/pubmed/14677810",
"http://www.ncbi.nlm.nih.gov/pubmed/16649727",
"http://www.ncbi.nlm.nih.gov/pubmed/16524858",
"http://www.ncbi.nlm.nih.gov/pubmed/16507804",
"http://www.ncbi.nlm.nih.gov/pubmed/21789282",
"http://www.ncbi.nlm.nih.gov/pubmed/17614771",
"http://www.ncbi.nlm.nih.gov/pubmed/9117915",
"http://www.ncbi.nlm.nih.gov/pubmed/9709915",
"http://www.ncbi.nlm.nih.gov/pubmed/23086805",
"http://www.ncbi.nlm.nih.gov/pubmed/732079"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23470525",
"endSection": "abstract",
"offsetInBeginSection": 1516,
"offsetInEndSection": 1747,
"text": "The results showed that higher levels of TSH within the reference range were independently associated with the presence of CAD only among subjects less than or equal to 65 years old, suggesting age might influence the relationship."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22877896",
"endSection": "abstract",
"offsetInBeginSection": 1594,
"offsetInEndSection": 1829,
"text": "FT3 levels within the normal range were inversely correlated with the presence and severity of CAD. Moreover, lower FT3 concentrations were correlated with the Gensini score and independently predicted the presence and severity of CAD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22724581",
"endSection": "abstract",
"offsetInBeginSection": 922,
"offsetInEndSection": 1221,
"text": "High TSH within the reference range was associated with increased risk of coronary death in women (P(trend) 0·005), but not in men. The risk of coronary death was also increased among women with subclinical hypothyroidism or subclinical hyperthyroidism, compared to women with TSH of 0·50-1·4 mU/l. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21745107",
"endSection": "abstract",
"offsetInBeginSection": 1110,
"offsetInEndSection": 1186,
"text": " Prevalence of CHD was more common in hypothyroid and moderate SCH patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19650571",
"endSection": "abstract",
"offsetInBeginSection": 1657,
"offsetInEndSection": 2003,
"text": "The angiographic results were as follows: significant coronary disease (SH 28.1% vs. non-SH 43.8%; p=0.087); three-vessel disease (9.4% vs. 9.9%; p=0.919); two-vessel disease (12.5% vs. 13.4%; p=0.892); single-vessel disease (6.3% vs. 29.5%; p=0.051); minimal lesions (9.4% vs. 10.9%; p=0.794); and no coronary disease (62.4% vs, 45.3%; p=0.064)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19609889",
"endSection": "abstract",
"offsetInBeginSection": 687,
"offsetInEndSection": 962,
"text": "Lower fT3 levels were predictive of both single-vessel (p = 0.012) and multivessel (p = 0.009) CAD. Through a multivariate logistic regression analysis, fT3 was still linked to the presence of CAD (hazard ratio [HR]: 0.48, 95% confidence interval [CI]: 0.34-0.68, p < 0.001)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18497453",
"endSection": "abstract",
"offsetInBeginSection": 1556,
"offsetInEndSection": 1766,
"text": "Our study showed that FT(4) levels were associated with the presence and the severity of CAD. Also, this study suggests that elevated serum FT(4) levels even within normal range could be a risk factor for CAD. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17434631",
"endSection": "abstract",
"offsetInBeginSection": 2114,
"offsetInEndSection": 2263,
"text": "The present meta-analysis indicates that sub-clinical hypothyroidism is associated with both, a significant risk of CHD at baseline and at follow-up."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222925",
"endSection": "abstract",
"offsetInBeginSection": 916,
"offsetInEndSection": 1398,
"text": "The incidence of multi-vessel disease was higher in patients with high TSH level (p=0.026). TSH level showed a significant correlation with age (r=0.109, p=0.044) and Gensini's score (r=0.117, p=0.045). The multivariate analysis revealed that age (OR 2.39, p=0.001), diabetes (OR 3.74, p=0.001), creatinine (OR 2.06, p=0.008), and smoking (OR 1.85, p=0.045) were independent predictors for significant coronary artery disease, but TSH level did not predict coronary artery stenosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14677810",
"endSection": "abstract",
"offsetInBeginSection": 2580,
"offsetInEndSection": 2784,
"text": "These data in patients referred for coronary angiography suggest that variation of thyroid function within the statistical normal range may influence the presence and severity of coronary atherosclerosis."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003324",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013963",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D023921",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003331",
"http://www.disease-ontology.org/api/metadata/DOID:3393",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013959",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013974",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014284"
] |
[] |
531d1279b166e2b806000042
|
bioasq_yesno
|
yesno
|
Is poly (ADP- ribosylation) involved in transcriptional control?
|
['yes']
|
[
"yes"
] |
Yes, poly (ADP- ribosylation) plays a role in the maintenance of transcriptional fidelity.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18851700",
"http://www.ncbi.nlm.nih.gov/pubmed/18396434",
"http://www.ncbi.nlm.nih.gov/pubmed/17286852",
"http://www.ncbi.nlm.nih.gov/pubmed/17158748",
"http://www.ncbi.nlm.nih.gov/pubmed/9790974",
"http://www.ncbi.nlm.nih.gov/pubmed/1828533"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18851700",
"endSection": "abstract",
"offsetInBeginSection": 336,
"offsetInEndSection": 547,
"text": "Histone phosphorylation, ubiquitylation, SUMOylation and poly-ADP-ribosylation, as well as ATP-dependent nucleosome remodeling complexes, play equally pivotal roles in the maintenance of transcriptional fidelity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18396434",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 188,
"text": "oly(ADP-ribose) polymerase-1 (PARP-1; EC 2.4.2.30) is an abundant nuclear protein that is involved in DNA repair, cell cycle control, programmed cell death and transcriptional regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17286852",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 213,
"text": "Many lines of evidence suggest that poly(ADP-ribose) polymerase-1 (Parp-1) is involved in transcriptional regulation of various genes as a coactivator or a corepressor by modulating chromatin structure"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17286852",
"endSection": "abstract",
"offsetInBeginSection": 1631,
"offsetInEndSection": 1765,
"text": "These results suggest that Parp-1 is required to maintain transcriptional regulation of a wide variety of genes on a genome-wide scale"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17158748",
"endSection": "abstract",
"offsetInBeginSection": 480,
"offsetInEndSection": 602,
"text": "PARP-1 was identified as a part of the mH2A1.1 nucleosome complex and was found to be associated with the Hsp70.1 promoter"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17158748",
"endSection": "abstract",
"offsetInBeginSection": 1020,
"offsetInEndSection": 1174,
"text": "Upon heat shock, the Hsp70.1 promoter-bound PARP-1 is released to activate transcription through ADP-ribosylation of other Hsp70.1 promoter-bound proteins"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9790974",
"endSection": "abstract",
"offsetInBeginSection": 1028,
"offsetInEndSection": 1409,
"text": "Cycloheximide-induced cells were treated with two chemical inhibitors of poly(ADP-ribose) polymerase. 3-Aminobenzamide inhibited 75% of PAP gene induction and 4-hydroxyquinazolone, the highly specific inhibitor of the enzyme, blocked almost completely PAP expression, suggesting that ADP-ribosylation was indeed required for the upregulation of PAP gene expression by cycloheximide"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1828533",
"endSection": "abstract",
"offsetInBeginSection": 471,
"offsetInEndSection": 589,
"text": " inhibitors of poly(ADP-ribose) polymerase suppressed UV-induced HIV-1 gene expression but not tat-mediated expression"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1828533",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 110,
"text": "oly(ADP-ribose) polymerase inhibitors suppress UV-induced human immunodeficiency virus type 1 gene expression"
}
] | 5
|
BioASQ-training5b
|
[
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0070212",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0006351",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020727"
] |
[] |
53380000d6d3ac6a34000059
|
bioasq_yesno
|
factoid
|
What is molecular radiotherapy?
|
['Molecular radiotherapy is working through tumor-targeted radionuclides.']
|
[
"Molecular radiotherapy",
"Tumor-targeted radionuclides",
"Targeted radionuclide therapy",
"Radionuclide therapy",
"Radioimmunotherapy",
"Radionuclide-based therapy",
"Targeted molecular therapy"
] |
['Molecular radiotherapy is working through tumor-targeted radionuclides.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28747518",
"http://www.ncbi.nlm.nih.gov/pubmed/29043399"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28747518",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 405,
"text": "Molecular radiotherapy with tumor-targeted radionuclides may overcome some of these challenges"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29043399",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 437,
"text": "Neuroblastoma may be treated with molecular radiotherapy, 131I meta-Iodobenzylguanidine and 177Lu Lutetium DOTATATE, directed at distinct molecular targets: Noradrenaline Transporter Molecule (NAT) and Somatostatin Receptor (SSTR2), respectively. This study used immunohistochemistry to evaluate target expression in archival neuroblastoma tissue, to determine whether it might facilitate clinical use of molecular radiotherapy."
}
] | 11
|
BioASQ-training11b
| null | null |
5e499c636d0a27794100000a
|
bioasq_factoid
|
factoid
|
Which is the target of the drug Denosumab?
|
[['receptor activator of nuclear factor-κB ligand', 'RANKL']]
|
[
"receptor activator of nuclear factor-κB ligand",
"RANKL",
"RANK ligand",
"receptor activator of NF-kB ligand",
"TNFSF11",
"OPGL",
"osteoprotegerin ligand"
] |
['Denosumab (Dmab) is a fully human monoclonal antibody against the receptor activator of nuclear factor-κB ligand (RANKL).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26029270",
"http://www.ncbi.nlm.nih.gov/pubmed/26203221",
"http://www.ncbi.nlm.nih.gov/pubmed/26504466",
"http://www.ncbi.nlm.nih.gov/pubmed/26508890"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26029270",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Denosumab is a human monoclonal antibody which specifically blocks receptor activator of nuclear factor κB ligand and is a very potent antiresorptive drug. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26203221",
"endSection": "abstract",
"offsetInBeginSection": 560,
"offsetInEndSection": 606,
"text": "denosumab, a monoclonal antibody against RANKL"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26504466",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Denosumab is a human monoclonal antibody indicated for the treatment of osteoporosis in postmenopausal women with a high risk of fractures. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26508890",
"endSection": "abstract",
"offsetInBeginSection": 466,
"offsetInEndSection": 776,
"text": "Denosumab (Dmab) is a fully human monoclonal antibody against the receptor activator of nuclear factor-κB ligand (RANKL), which, through the prevention of the RANKL/RANK interaction, inhibits osteoclast-mediated bone resorption and significantly reduces the risk of vertebral, nonvertebral, and hip fractures. "
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
56e6ec49edfc094c1f000005
|
bioasq_factoid
|
factoid
|
Which transcription factor binding site is contained in Alu repeats?
|
['The NF-κB-binding site']
|
[
"NF-kappa B binding site",
"NF-κB binding site",
"Nuclear factor kappa-light-chain-enhancer of activated B cells binding site",
"NF-kB binding site",
"NFκB-binding site",
"NF-kappaB binding site",
"The NF-κB-binding site"
] |
['A novel abundant NF-κB-binding site resides in specialized Alu-repetitive elements having the potential for long range transcription regulation, thus suggesting that in addition to its known role, NF-κB has a primate-specific function and a role in human evolution.', 'Remarkably, we identified a novel abundant NF-κB-binding site residing in specialized Alu-repetitive elements having the potential for long range transcription regulation, thus suggesting that in addition to its known role, NF-κB has a primate-specific function and a role in human evolution.', 'Remarkably, we identified a novel abundant NF-κB-binding site residing in specialized Alu-repetitive elements having the potential for long range transcription regulation, thus suggesting that in addition to its known role, NF-κB has a primate-specific function and a role in human evolution. A de novo motif enrichment analysis uncovers secondary TFBSs (AP1, SP1) at characteristic distances from NF-κB/RelA TFBSs.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23771139",
"http://www.ncbi.nlm.nih.gov/pubmed/21896491"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21896491",
"endSection": "abstract",
"offsetInBeginSection": 502,
"offsetInEndSection": 794,
"text": "Remarkably, we identified a novel abundant NF-κB-binding site residing in specialized Alu-repetitive elements having the potential for long range transcription regulation, thus suggesting that in addition to its known role, NF-κB has a primate-specific function and a role in human evolution."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23771139",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 551,
"text": "A de novo motif enrichment analysis uncovers secondary TFBSs (AP1, SP1) at characteristic distances from NF-κB/RelA TFBSs."
}
] | 11
|
BioASQ-training11b
| null | null |
5c74111f7c78d694710000a1
|
bioasq_factoid
|
factoid
|
The small molecule SEA0400 is an inhibitor of which ion antiporter/exchanger?
|
[['Na(+)/Ca(2+) exchanger', 'NCX']]
|
[
"Na(+)/Ca(2+) exchanger",
"NCX",
"sodium/calcium exchanger",
"sodium calcium exchanger",
"Na+/Ca2+ exchanger",
"Na+/Ca2+ antiporter",
"Na+/Ca2+ exchange protein"
] |
['SEA0400 is a selective inhibitor of the Na(+)/Ca(2+) exchanger having equal potencies to suppress both the forward and reverse mode operation of the Na(+)/Ca(2+) exchanger. SEA0400 (2-[4-[(2,5-difluorophenyl)methoxy] phenoxy]-5-ethoxyaniline), is a selective NCX inhibitor in vivo.', 'The effects of SEA0400, a selective inhibitor of the Na(+)/Ca(2+) exchanger (NCX), on Na(+)-dependent Ca(2+) uptake and catecholamine (CA) release were examined in bovine adrenal chromaffin cells that were loaded with Na(+) by treatment with ouabain and veratridine. SEA0400 inhibited Na(+)-dependent (45)Ca(2+) uptake and CA release, with the IC(50) values of 40 and 100 nM, respectively. ', 'The effects of SEA0400, a selective inhibitor of the Na(+)/Ca(2+) exchanger (NCX), on Na(+)-dependent Ca(2+) uptake and catecholamine (CA) release were examined in bovine adrenal chromaffin cells that were loaded with Na(+) by treatment with ouabain and veratridine. SEA0400 inhibited Na(+)-dependent (45)Ca(2+) uptake and CA release, with the IC(50) values of 40 and 100 nM, respectively. ', 'The effects of SEA0400, a selective inhibitor of the Na(+)/Ca(2+) exchanger (NCX), on Na(+)-dependent Ca(2+) uptake and catecholamine (CA) release were examined in bovine adrenal chromaffin cells that were loaded with Na(+) by treatment with ouabain and veratridine. SEA0400 inhibited Na(+)-dependent (45)Ca(2+) uptake and CA release, with the IC(50) values of 40 and 100 nM, respectively. ', 'The effects of SEA0400, a selective inhibitor of the Na(+)/Ca(2+) exchanger (NCX), on Na(+)-dependent Ca(2+) uptake and catecholamine (CA) release were examined in bovine adrenal chromaffin cells that were loaded with Na(+) by treatment with ouabain and veratridine. SEA0400 inhibited Na(+)-dependent (45)Ca(2+) uptake and CA release, with the IC(50) values of 40 and 100 nM, respectively. ', 'The effects of SEA0400, a selective inhibitor of the Na(+)/Ca(2+) exchanger (NCX), on Na(+)-dependent Ca(2+) uptake and catecholamine (CA) release were examined in bovine adrenal chromaffin cells that were loaded with Na(+) by treatment with ouabain and veratridine. SEA0400 inhibited Na(+)-dependent (45)Ca(2+) uptake and CA release, with the IC(50) values of 40 and 100 nM, respectively. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23441899",
"http://www.ncbi.nlm.nih.gov/pubmed/22119380",
"http://www.ncbi.nlm.nih.gov/pubmed/22075452",
"http://www.ncbi.nlm.nih.gov/pubmed/21903118",
"http://www.ncbi.nlm.nih.gov/pubmed/21672583",
"http://www.ncbi.nlm.nih.gov/pubmed/20447431",
"http://www.ncbi.nlm.nih.gov/pubmed/19593760",
"http://www.ncbi.nlm.nih.gov/pubmed/19423954",
"http://www.ncbi.nlm.nih.gov/pubmed/18855935",
"http://www.ncbi.nlm.nih.gov/pubmed/17727839",
"http://www.ncbi.nlm.nih.gov/pubmed/17310075",
"http://www.ncbi.nlm.nih.gov/pubmed/16960421",
"http://www.ncbi.nlm.nih.gov/pubmed/16497099",
"http://www.ncbi.nlm.nih.gov/pubmed/15878358",
"http://www.ncbi.nlm.nih.gov/pubmed/16495765",
"http://www.ncbi.nlm.nih.gov/pubmed/16842776",
"http://www.ncbi.nlm.nih.gov/pubmed/15703202",
"http://www.ncbi.nlm.nih.gov/pubmed/15678087",
"http://www.ncbi.nlm.nih.gov/pubmed/15556149",
"http://www.ncbi.nlm.nih.gov/pubmed/15231867",
"http://www.ncbi.nlm.nih.gov/pubmed/11877314",
"http://www.ncbi.nlm.nih.gov/pubmed/11408549"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23441899",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 341,
"text": "The plasma membrane Na(+)/Ca(2+) exchanger (NCX) is a bidirectional ion transporter that couples the translocation of Na(+) in one direction with that of Ca(2+) in the opposite direction. This system contributes to the regulation of intracellular Ca(2+) concentration via the forward mode (Ca(2+) efflux) or the reverse mode (Ca(2+) influx)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23441899",
"endSection": "abstract",
"offsetInBeginSection": 891,
"offsetInEndSection": 1161,
"text": "Concerning the role of NCX in NO cytotoxicity, we have found, using the specific inhibitor of NCX 2-[4-[(2,5-difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline (SEA0400), that NCX is involved in NO-induced cytotoxicity in cultured microglia, astrocytes, and neuronal cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22119380",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 496,
"text": "The Na(+)/Ca(2+)exchanger (NCX) principal function is taking 1 Ca(2+) out of the cytoplasm and introducing 3 Na(+). The increase of cytoplasmic Na(+) concentration induces the NCX reverse mode (NCX(REV)), favoring Ca(2+) influx. NCX(REV) can be inhibited by: KB-R7943 a non-specific compound that blocks voltage-dependent and store-operated Ca(2+) channels; SEA0400 that appears to be selective for NCX(REV), but difficult to obtain and SN-6, which efficacy has been shown only in cardiomyocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22075452",
"endSection": "abstract",
"offsetInBeginSection": 1050,
"offsetInEndSection": 1187,
"text": "SEA0400 (1 μM), a pharmacological inhibitor of NCX, significantly shortened the MAP duration (P < .01) and reduced dispersion (P < .05). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21903118",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 575,
"text": "We have recently shown that the Na(+)/Ca(2+) exchanger (NCX) is involved in nitric oxide (NO)-induced cytotoxicity in cultured astrocytes and neurons. However, there is no in vivo evidence suggesting the role of NCX in neurodegenerative disorders associated with NO. NO is implicated in the pathogenesis of neurodegenerative disorders such as Parkinson's disease. This study examined the effect of SEA0400, the specific NCX inhibitor, on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity, a model of Parkinson's disease, in C57BL/6J mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21672583",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 626,
"text": "The Na(+)/Ca(2+) exchanger (NCX) plays a role in the regulation of intracellular Ca(2+) levels, and nitric oxide (NO) is involved in many pathological conditions including neurodegenerative disorders. We have previously found that sodium nitroprusside (SNP), an NO donor, causes apoptotic-like cell death in cultured glial cells via NCX-mediated pathways and the mechanism for NO-induced cytotoxicity is cell type-dependent. The present study examined using the specific NCX inhibitor 2-[4-[(2,5-difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline (SEA0400) whether NCX is involved in NO-induced injury in cultured neuronal cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20447431",
"endSection": "abstract",
"offsetInBeginSection": 396,
"offsetInEndSection": 690,
"text": "In view of the previous observation that NO stimulates the activity of the Na(+)/Ca(2+) exchanger (NCX), this study examines the involvement of NCX in cytotoxicity. The specific NCX inhibitor SEA0400 blocked SNP-induced phosphorylation of ERK, JNK and p38 MAPK, and decrease in cell viability. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19593760",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 533,
"text": "The sodium-calcium exchanger (NCX) is one of the transporters contributing to the control of intracellular calcium (Ca(2+)) concentration by normally mediating net Ca(2+) efflux. However, the reverse mode of the NCX can cause intracellular Ca(2+) concentration overload, which exacerbates the myocardial tissue injury resulting from ischemia. Although the NCX inhibitor SEA0400 has been shown to therapeutically reduce myocardial injury, no in vivo technique exists to monitor intracellular Ca(2+) fluctuations produced by this drug."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19423954",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "We examined the involvement of the Na(+)/Ca(2+) exchanger in the automaticity of the pulmonary vein myocardium with a specific inhibitor, SEA0400."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18855935",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "We investigated the expression of Na(+)/Ca(2+) exchanger (NCX) and the functional role of NCX in retinal damage by using NCX1-heterozygous deficient mice (NCX1(+/-)) and SEA0400 (2-[4-[(2,5-difluorophenyl)methoxy] phenoxy]-5-ethoxyaniline), a selective NCX inhibitor in vivo. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17727839",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "SEA0400 is a selective inhibitor of the Na(+)/Ca(2+) exchanger having equal potencies to suppress both the forward and reverse mode operation of the Na(+)/Ca(2+) exchanger."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17310075",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Involvement of the Na+/Ca2+ exchanger in ouabain-induced inotropy and arrhythmogenesis was examined with a specific inhibitor, SEA0400."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17310075",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 431,
"text": "In right ventricular papillary muscle isolated from guinea-pig ventricle, 1 microM SEA0400, which specifically inhibits the Na+/Ca2+ exchanger by 80%, reduced the ouabain (1 microM)-induced positive inotropy by 40%, but had no effect on the inotropy induced by 100 microM isobutyl methylxantine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16960421",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 389,
"text": "The effects of SEA0400, a selective inhibitor of the Na(+)/Ca(2+) exchanger (NCX), on Na(+)-dependent Ca(2+) uptake and catecholamine (CA) release were examined in bovine adrenal chromaffin cells that were loaded with Na(+) by treatment with ouabain and veratridine. SEA0400 inhibited Na(+)-dependent (45)Ca(2+) uptake and CA release, with the IC(50) values of 40 and 100 nM, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16497099",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 482,
"text": "Given the potential clinical benefit of inhibiting Na+/Ca2+ exchanger (NCX) activity during myocardial ischemia reperfusion (I/R), pharmacological approaches have been pursued to both inhibit and clarify the importance of this exchanger. SEA0400 was reported to have a potent NCX selectivity. Thus, we examined the effect of SEA0400 on NCX currents and I/R induced intracellular Ca2+ overload in mouse ventricular myocytes using patch clamp techniques and fluorescence measurements."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16497099",
"endSection": "abstract",
"offsetInBeginSection": 1207,
"offsetInEndSection": 1349,
"text": "The results suggested that SEA0400 is a potent NCX inhibitor, which can protect mouse cardiac myocytes from Ca2+ overload during I/R injuries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15878358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 233,
"text": "The effect of SEA0400, a novel Na+-Ca2+ exchanger inhibitor, on mechanical and electrophysiological parameters of coronary-perfused guinea-pig right ventricular tissue preparation was examined during no-flow ischemia and reperfusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16495765",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 286,
"text": "The Ca2+ overload by Ca2+ influx via Na+/Ca2+ exchanger (NCX) is a critical mechanism in myocardial ischemia/reperfusion injury. We investigated protective effects of a novel selective inhibitor of NCX, SEA0400, on cardiac function and energy metabolism during ischemia and reperfusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16842776",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "The cardioprotective effects of SEA0400, a novel Na(+)-Ca(2+) exchanger inhibitor, were examined in isolated guinea pig myocardial tissue and ventricular myocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15703202",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 403,
"text": "The effects of a new, potent, and selective inhibitor of the Na(+)/Ca(2+) exchange, SEA-0400 (SEA), on steady-state outward (forward exchange), inward (reverse exchange), and Ca(2+)/Ca(2+) transport exchange modes were studied in internally dialyzed squid giant axons from both the extra- and intracellular sides. Inhibition by SEA takes place preferentially from the intracellular side of the membrane."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15678087",
"endSection": "abstract",
"offsetInBeginSection": 3,
"offsetInEndSection": 256,
"text": "Using SEA0400, a potent and selective inhibitor of the Na+-Ca2+ exchanger (NCX), we examined whether NCX is involved in nitric oxide (NO)-induced disturbance of endoplasmic reticulum (ER) Ca2+ homeostasis followed by apoptosis in cultured rat microglia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15556149",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 327,
"text": "Activation of the Na+/Ca2+ exchanger may contribute to Ca2+ overload during reperfusion after transient ischemia. We examined the effects of 2-[4-[(2,5-difluorophenyl) methoxy]phenoxy]-5-ethoxyaniline (SEA0400), a selective inhibitor of Na+/Ca2+ exchange, on a canine model of ischemia/reperfusion injury (myocardial stunning)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15231867",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 392,
"text": "SEA0400 (2-[4-[(2,5-difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline) has recently been described as a potent and selective inhibitor of Na(+)-Ca(2+) exchange in cardiac, neuronal, and renal preparations. The inhibitory effects of SEA0400 were investigated on the cloned cardiac Na(+)-Ca(2+) exchanger, NCX1.1, expressed in Xenopus laevis oocytes to gain insight into its inhibitory mechanism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11877314",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 780,
"text": "The effects of 2-[4-[(2,5-difluorophenyl) methoxy]phenoxy]-5-ethoxyaniline (SEA0400), a newly synthesized Na(+)-Ca(2+) exchanger (NCX) inhibitor, on the NCX current and other membrane currents were examined in isolated guinea-pig ventricular myocytes and compared with those of 2-[2-[4-(4-nitrobenzyloxy) phenyl]ethyl]isothiourea (KB-R7943). SEA0400 concentration-dependently inhibited the NCX current with a 10 fold higher potency than that of KB-R7943; 1 microM SEA0400 and 10 microM KB-R7943 inhibited the NCX current by more than 80%. KB-R7943, at 10 microM, inhibited the sodium current, L-type calcium current, delayed rectifier potassium current and inwardly rectifying potassium current by more than 50%, but SEA0400 (1 microM) had no significant effect on these currents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11877314",
"endSection": "abstract",
"offsetInBeginSection": 781,
"offsetInEndSection": 997,
"text": "These results indicate that SEA0400 is a potent and highly selective inhibitor of NCX, and would be a powerful tool for further studies on the role of NCX in the heart and the therapeutic potential of its inhibition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11408549",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "The effect of the newly synthesized compound 2-[4-[(2,5-difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline (SEA0400) on the Na+-Ca2+ exchanger (NCX) was investigated and compared against that of 2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea (KB-R7943)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11408549",
"endSection": "abstract",
"offsetInBeginSection": 255,
"offsetInEndSection": 850,
"text": "In addition, the effects of SEA0400 on reperfusion injury in vitro and in vivo were examined. SEA0400 was extremely more potent than KB-R7943 in inhibiting Na+-dependent Ca2+ uptake in cultured neurons, astrocytes, and microglia: IC50s of SEA0400 and KB-R7943 were 5 to 33 nM and 2 to 4 microM, respectively. SEA0400 at the concentration range that inhibited NCX exhibited negligible affinities for the Ca2+ channels, Na+ channels, K+ channels, norepinephrine transporter, and 14 receptors, and did not affect the activities of the Na+/H+ exchanger, Na+,K+-ATPase, Ca2+-ATPase, and five enzymes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11408549",
"endSection": "abstract",
"offsetInBeginSection": 1340,
"offsetInEndSection": 1515,
"text": "These results indicate that SEA0400 is the most potent and selective inhibitor of NCX, and suggest that the compound may exert protective effects on postischemic brain damage."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
5506c3e38e1671127b00000a
|
bioasq_factoid
|
factoid
|
What is the prevalence of intellectual developmental disorders in Becker Muscular Dystrophy?
|
['8%']
|
[
"8 percent",
"eight percent",
"0.08",
"0.08 fraction",
"8/100"
] |
['The global prevalence of intellectual developmental disorder (IDD) is 8% in Becker muscular dystrophy.', 'The global prevalence of intellectual developmental disorder (IDD) in Becker muscular dystrophy (BMD) is 8%.', 'The prevalence of intellectual developmental disorders in Becker Muscular Dystrophy is 8%.', 'The global prevalence of intellectual developmental disorder (IDD) was 8% in Becker muscular dystrophy.', 'The global prevalence of intellectual developmental disorder (IDD) in Becker muscular dystrophy is 8%.', 'The prevalence of intellectual developmental disorders in Becker Muscular Dystrophy is 8%', 'The prevalence of intellectual developmental disorders in Becker Muscular Dystrophy is estimated to be 8.3%.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36440509"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36440509",
"endSection": "abstract",
"offsetInBeginSection": 1369,
"offsetInEndSection": 1471,
"text": "The global prevalence of intellectual developmental disorder (IDD) was 8% in Becker muscular dystrophy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36440509",
"endSection": "abstract",
"offsetInBeginSection": 655,
"offsetInEndSection": 727,
"text": "dies were included. The prevalence of IDD in BMD was 8.0% (95% confidenc"
}
] | 13
|
BioASQ-training13b
| null | null |
66300d3e187cba990d00001b
|
bioasq_factoid
|
factoid
|
Which deficiency is the cause of restless leg syndrome?
|
['iron']
|
[
"iron",
"ferrous",
"ferric",
"Fe",
"element 26",
"iron metal"
] |
It has been well-documented that iron deficiency is the cause of restless leg syndrome. Magnesium and ferritin were also associated with restless leg syndrome.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23940258",
"http://www.ncbi.nlm.nih.gov/pubmed/22486183",
"http://www.ncbi.nlm.nih.gov/pubmed/21358851",
"http://www.ncbi.nlm.nih.gov/pubmed/21211209",
"http://www.ncbi.nlm.nih.gov/pubmed/20814842",
"http://www.ncbi.nlm.nih.gov/pubmed/20598107",
"http://www.ncbi.nlm.nih.gov/pubmed/19935988",
"http://www.ncbi.nlm.nih.gov/pubmed/19467991",
"http://www.ncbi.nlm.nih.gov/pubmed/18360657",
"http://www.ncbi.nlm.nih.gov/pubmed/19039990",
"http://www.ncbi.nlm.nih.gov/pubmed/17804903",
"http://www.ncbi.nlm.nih.gov/pubmed/16982219",
"http://www.ncbi.nlm.nih.gov/pubmed/16828857",
"http://www.ncbi.nlm.nih.gov/pubmed/12530992",
"http://www.ncbi.nlm.nih.gov/pubmed/11863398",
"http://www.ncbi.nlm.nih.gov/pubmed/11799409",
"http://www.ncbi.nlm.nih.gov/pubmed/11310286",
"http://www.ncbi.nlm.nih.gov/pubmed/21779527",
"http://www.ncbi.nlm.nih.gov/pubmed/24101430",
"http://www.ncbi.nlm.nih.gov/pubmed/23257652",
"http://www.ncbi.nlm.nih.gov/pubmed/22377249",
"http://www.ncbi.nlm.nih.gov/pubmed/22258033",
"http://www.ncbi.nlm.nih.gov/pubmed/21398376",
"http://www.ncbi.nlm.nih.gov/pubmed/20303704",
"http://www.ncbi.nlm.nih.gov/pubmed/14643912",
"http://www.ncbi.nlm.nih.gov/pubmed/22096645",
"http://www.ncbi.nlm.nih.gov/pubmed/24267148"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23940258",
"endSection": "abstract",
"offsetInBeginSection": 438,
"offsetInEndSection": 775,
"text": "We describe a unique case of a 23-yr-old female patient affected by a homozygous loss of function mutation in the L-ferritin gene, idiopathic generalized seizures, and atypical restless leg syndrome (RLS). We show that L chain ferritin is undetectable in primary fibroblasts from the patient, and thus ferritin consists only of H chains."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23940258",
"endSection": "abstract",
"offsetInBeginSection": 1136,
"offsetInEndSection": 1369,
"text": "Our results demonstrate for the first time the pathophysiological consequences of L-ferritin deficiency in a human and help to define the concept for a new disease entity hallmarked by idiopathic generalized seizure and atypical RLS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21358851",
"endSection": "abstract",
"offsetInBeginSection": 1332,
"offsetInEndSection": 1562,
"text": "These results when viewed along with prior RLS SPECT and autopsy studies of DAT, and cell culture studies with iron deficiency and DAT, suggest that membrane-bound striatal DAT, but not total cellular DAT, may be decreased in RLS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21211209",
"endSection": "abstract",
"offsetInBeginSection": 690,
"offsetInEndSection": 860,
"text": " Compared with the PD or healthy group, the level of serum ferritin and the H-reflex latency of tibial nerve were significantly decreased in PD with RLS group (P < 0.05)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21211209",
"endSection": "abstract",
"offsetInBeginSection": 913,
"offsetInEndSection": 1031,
"text": "Deficiency of iron and decreased inhibition function of spinal cord may lead to the occurrence of RLS in PD patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20814842",
"endSection": "abstract",
"offsetInBeginSection": 538,
"offsetInEndSection": 691,
"text": "Association of iron deficiency with febrile seizures, pica, breath holding spells, restless leg syndrome and thrombosis is increasingly being recognized."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20598107",
"endSection": "abstract",
"offsetInBeginSection": 714,
"offsetInEndSection": 857,
"text": " Iron status was generally poor among regular blood donors, especially in women, with a high incidence of iron depletion (>20%) and RLS (18%). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20598107",
"endSection": "abstract",
"offsetInBeginSection": 1217,
"offsetInEndSection": 1350,
"text": "Iron status is poor in regular blood donors, restless legs syndrome is common, and the routine iron supplementation is insufficient. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19935988",
"endSection": "abstract",
"offsetInBeginSection": 1240,
"offsetInEndSection": 1366,
"text": "Furthermore, there appears to be an association between iron deficiency and those suffering from Restless Leg Syndrome (RLS). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19935988",
"endSection": "abstract",
"offsetInBeginSection": 1491,
"offsetInEndSection": 1784,
"text": "The authors propose that PPIs, such as omeprazole, may interfere with iron absorption in certain patients and that a subpopulation of patients who develop significant iron deficiency characterized by low serum ferritin levels while on PPIs may also develop RLS-like symptoms (including RLSAP)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19467991",
"endSection": "abstract",
"offsetInBeginSection": 56,
"offsetInEndSection": 211,
"text": "Clinical studies have implicated the dopaminergic system in RLS, while others have suggested that it is associated with insufficient levels of brain iron. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19467991",
"endSection": "abstract",
"offsetInBeginSection": 1674,
"offsetInEndSection": 1877,
"text": "The results are consistent with the hypothesis that a primary iron insufficiency produces a dopaminergic abnormality characterized as an overly activated dopaminergic system as part of the RLS pathology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18360657",
"endSection": "abstract",
"offsetInBeginSection": 466,
"offsetInEndSection": 608,
"text": "RLS may also be secondary to a number of conditions including iron deficiency, pregnancy and end-stage renal failure and, perhaps, neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18360657",
"endSection": "abstract",
"offsetInBeginSection": 692,
"offsetInEndSection": 860,
"text": "The pathogenesis of RLS probably involves the interplay of systemic or brain iron deficiency and impaired dopaminergic neurotransmission in the subcortex of the brain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19039990",
"endSection": "abstract",
"offsetInBeginSection": 861,
"offsetInEndSection": 958,
"text": "All patients showed low levels of ferritin and iron supplementation was effective in five cases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17804903",
"endSection": "abstract",
"offsetInBeginSection": 432,
"offsetInEndSection": 724,
"text": "Clinical and animal studies that support the benefits of iron supplementation, independent of increasing hemoglobin, such as those on immune function, physical performance, thermoregulation, cognition, and restless leg syndrome and aluminum absorption is the subject of this narrative review."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 454,
"text": "Restless leg syndrome (RLS) and periodic limb movement disorder (PLMD) are considered to be a continuum of a neurological sleep disorder associated with abnormal iron metabolism or deficiency. I describe a case of RLS and PLMD in a cystic fibrosis patient with iron deficiency from chronic hemoptysis. This is the first case that reports RLS and PLMD manifesting from iron deficiency caused by chronic hemoptysis in advanced cystic fibrosis lung disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982219",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Restless leg syndrome manifested by iron deficiency from chronic hemoptysis in cystic fibrosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16828857",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Diurnal effects on motor control are evident in the human disease of Restless Leg Syndrome (RLS), which is purported to be linked to brain iron deficiency as well as alterations in dopaminergic systems. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12530992",
"endSection": "abstract",
"offsetInBeginSection": 755,
"offsetInEndSection": 974,
"text": "Iron deficiency in the central nervous system is known to cause motor impairment and cognitive deficits; more recently, it has been suggested that it may play a role in the pathophysiology of the restless leg syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11799409",
"endSection": "abstract",
"offsetInBeginSection": 276,
"offsetInEndSection": 412,
"text": "Restless leg syndrome (RLS), aging, pregnancy, uraemia, iron deficiency, polyneuropathy are some of the common causes of secondary PLMD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11310286",
"endSection": "abstract",
"offsetInBeginSection": 479,
"offsetInEndSection": 662,
"text": "The syndrome is increasingly often diagnosed, particularly in association with iron deficiency, during pregnancy, in chronic renal failure and in patients with peripheral neuropathy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8363978",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Clinical, EEG, electromyographic and polysomnographic studies in restless legs syndrome caused by magnesium deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22486183",
"endSection": "abstract",
"offsetInBeginSection": 1191,
"offsetInEndSection": 1373,
"text": "A frequent polymorphism in BTBD9 was significantly associated with serum ferritin. This polymorphism has previously been associated with RLS, but not low iron stores in blood donors."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012148",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003677",
"http://www.disease-ontology.org/api/metadata/DOID:0050425"
] |
[] |
530cefaaad0bf1360c000012
|
bioasq_factoid
|
factoid
|
What is the role of DNA Repair Cofactors ATMIN and NBS1?
|
['Suppresion of T Cell Activation.']
|
[
"Suppression of T Cell Activation",
"T Cell Activation Suppression",
"Inhibition of T Cell Activation",
"T Cell Suppression",
"T Cell Inhibition"
] |
['The DNA double-strand break signaling kinase ATM and its cofactor NBS1 are required during T cell development and for the maintenance of genomic stability. The role of a second ATM cofactor, ATMIN (also known as ASCIZ) in T cells is much less clear, and whether ATMIN and NBS1 function in synergy in T cells is unknown.', 'The DNA Repair Cofactors ATMIN and NBS1 are required to suppress T Cell activation. Loss of NBS1 led to a developmental block at the double-positive stage of T cell development, as well as reduced TCRα recombination, that was unexpectedly neither exacerbated nor alleviated by concomitant loss of ATMIN. In contrast, loss of both ATMIN and NBS1 enhanced DNA damage that drove spontaneous peripheral T cell hyperactivation, proliferation as well as excessive production of proinflammatory cytokines and chemokines, leading to a highly inflammatory environment. Intriguingly, the disease causing T cells were largely proficient for both ATMIN and NBS1. In vivo this resulted in severe intestinal inflammation, colitis and premature death.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26544571"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "DNA Repair Cofactors ATMIN and NBS1 Are Required to Suppress T Cell Activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "abstract",
"offsetInBeginSection": 452,
"offsetInEndSection": 1366,
"text": "Here, we investigate the roles of ATMIN and NBS1, either alone or in combination, using murine models. We show loss of NBS1 led to a developmental block at the double-positive stage of T cell development, as well as reduced TCRα recombination, that was unexpectedly neither exacerbated nor alleviated by concomitant loss of ATMIN. In contrast, loss of both ATMIN and NBS1 enhanced DNA damage that drove spontaneous peripheral T cell hyperactivation, proliferation as well as excessive production of proinflammatory cytokines and chemokines, leading to a highly inflammatory environment. Intriguingly, the disease causing T cells were largely proficient for both ATMIN and NBS1. In vivo this resulted in severe intestinal inflammation, colitis and premature death. Our findings reveal a novel model for an intestinal bowel disease phenotype that occurs upon combined loss of the DNA repair cofactors ATMIN and NBS1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "abstract",
"offsetInBeginSection": 1208,
"offsetInEndSection": 1358,
"text": "Our findings reveal a novel model for an intestinal bowel disease phenotype that occurs upon combined loss of the DNA repair cofactors ATMIN and NBS1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "abstract",
"offsetInBeginSection": 778,
"offsetInEndSection": 1033,
"text": "In contrast, loss of both ATMIN and NBS1 enhanced DNA damage that drove spontaneous peripheral T cell hyperactivation, proliferation as well as excessive production of proinflammatory cytokines and chemokines, leading to a highly inflammatory environment."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "DNA Repair Cofactors ATMIN and NBS1 Are Required to Suppress T Cell Activation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "abstract",
"offsetInBeginSection": 1216,
"offsetInEndSection": 1365,
"text": "Our findings reveal a novel model for an intestinal bowel disease phenotype that occurs upon combined loss of the DNA repair cofactors ATMIN and NBS1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "abstract",
"offsetInBeginSection": 1216,
"offsetInEndSection": 1366,
"text": "Our findings reveal a novel model for an intestinal bowel disease phenotype that occurs upon combined loss of the DNA repair cofactors ATMIN and NBS1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "abstract",
"offsetInBeginSection": 783,
"offsetInEndSection": 1038,
"text": "In contrast, loss of both ATMIN and NBS1 enhanced DNA damage that drove spontaneous peripheral T cell hyperactivation, proliferation as well as excessive production of proinflammatory cytokines and chemokines, leading to a highly inflammatory environment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "abstract",
"offsetInBeginSection": 555,
"offsetInEndSection": 782,
"text": "We show loss of NBS1 led to a developmental block at the double-positive stage of T cell development, as well as reduced TCRα recombination, that was unexpectedly neither exacerbated nor alleviated by concomitant loss of ATMIN."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26544571",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "DNA Repair Cofactors ATMIN and NBS1 Are Required to Suppress T Cell Activation."
}
] | 6
|
BioASQ-training6b
|
[
"http://www.uniprot.org/uniprot/NBS1_SCHPO",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004260",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D045643",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D053843",
"http://www.uniprot.org/uniprot/NBS1_ARATH"
] |
[
{
"o": "DNA repair",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0012899"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A18609617",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0012899"
},
{
"o": "dna repair",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A18609617"
},
{
"o": "http://purl.uniprot.org/uniprot/O43070",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://purl.uniprot.org/uniprot/O43070"
},
{
"o": "nbs1",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://purl.uniprot.org/intact/EBI-2125045"
},
{
"o": "nbs1",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_4F34333037300013"
},
{
"o": "NBS1_SCHPO",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://purl.uniprot.org/uniprot/O43070"
},
{
"o": "http://linkedlifedata.com/resource/#_4F34333037300013",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/O43070"
}
] |
58853c56e56acf5176000018
|
bioasq_factoid
|
factoid
|
Which company produces Eligard?
|
['Astellas Pharma GmbH']
|
[
"Astellas Pharma GmbH",
"Astellas Pharma",
"Astellas",
"Astellas Pharma Inc.",
"Astellas Pharma Limited"
] |
['Eligard is produced by Astellas Pharma GmbH.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29197875"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29197875",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 242,
"text": "We evaluated the efficacy and tolerability of 3- and 6-month leuprorelin acetate (LA) depot formulations (Eligard®, Astellas Pharma GmbH) in patients with advanced prostate cancer treated in routine clinical practice in Germany."
}
] | 11
|
BioASQ-training11b
| null | null |
5e776443835f4e4777000008
|
bioasq_factoid
|
factoid
|
What is Apretude used for?
|
['HIV-1 pre-exposure prophylaxis']
|
[
"HIV-1 pre-exposure prophylaxis",
"PrEP",
"HIV pre-exposure prophylaxis",
"HIV pre-exposure prophylaxis medication",
"HIV prevention pill"
] |
['Cabotegravir extended-release (ER) injectable suspension (Apretude™) is the first long-acting injectable option to be approved for HIV-1 pre-exposure prophylaxis (PrEP).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36255686"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36255686",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Cabotegravir Extended-Release Injectable Suspension: A Review in HIV-1 Pre-Exposure Prophylaxis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36255686",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Cabotegravir extended-release (ER) injectable suspension (Apretude™) is the first long-acting injectable option to be approved for HIV-1 pre-exposure prophylaxis (PrEP). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36255686",
"endSection": "abstract",
"offsetInBeginSection": 465,
"offsetInEndSection": 694,
"text": "Cabotegravir ER injectable suspension is indicated in the USA for PrEP to reduce the risk of sexually acquired HIV-1 infection in at-risk adults and adolescents weighing ≥ 35 kg who have a negative HIV-1 test prior to initiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36255686",
"endSection": "abstract",
"offsetInBeginSection": 1086,
"offsetInEndSection": 1312,
"text": "With its convenient, less-frequent dosing schedule and its long-acting formulation enabling intramuscular administration, cabotegravir ER injectable suspension represents a novel and efficacious alternative to daily oral PrEP."
}
] | 12
|
BioASQ-training12b
| null | null |
6440420857b1c7a315000050
|
bioasq_factoid
|
factoid
|
Where are the orexigenic peptides synthesized?
|
[['The orexigenic peptides are sythesized in the hypothalamus.']]
|
[
"orexigenic peptides",
"appetite-stimulating peptides",
"hunger-inducing peptides",
"hypothalamic peptides",
"peptides synthesized in the hypothalamus",
"orexigenic neuropeptides"
] |
['The orexigenic peptides are sythesized in the hypothalamus.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25502749",
"http://www.ncbi.nlm.nih.gov/pubmed/25258168",
"http://www.ncbi.nlm.nih.gov/pubmed/25039297",
"http://www.ncbi.nlm.nih.gov/pubmed/24991043",
"http://www.ncbi.nlm.nih.gov/pubmed/25241055",
"http://www.ncbi.nlm.nih.gov/pubmed/25017744",
"http://www.ncbi.nlm.nih.gov/pubmed/25047666",
"http://www.ncbi.nlm.nih.gov/pubmed/23707377",
"http://www.ncbi.nlm.nih.gov/pubmed/22771813",
"http://www.ncbi.nlm.nih.gov/pubmed/21903140",
"http://www.ncbi.nlm.nih.gov/pubmed/22325091",
"http://www.ncbi.nlm.nih.gov/pubmed/22922128",
"http://www.ncbi.nlm.nih.gov/pubmed/21574955"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25502749",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Orexin A and B, orexigenic peptides produced primarily by the lateral hypothalamus t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25258168",
"endSection": "abstract",
"offsetInBeginSection": 1409,
"offsetInEndSection": 1528,
"text": "Telmisartin reduced hypothalamic mRNA levels of the orexigenic peptides melanin-concentrating hormone and prepro-orexin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25039297",
"endSection": "abstract",
"offsetInBeginSection": 1517,
"offsetInEndSection": 1636,
"text": "expression of the orexigenic peptides, enkephalin (ENK) and galanin (GAL), in developing embryonic hypothalamic neurons"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24991043",
"endSection": "abstract",
"offsetInBeginSection": 1503,
"offsetInEndSection": 1536,
"text": "hypothalamic orexigenic peptides,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25241055",
"endSection": "abstract",
"offsetInBeginSection": 264,
"offsetInEndSection": 418,
"text": " Such mechanisms may involve orexigenic peptides known to stimulate alcohol intake through their actions in the hypothalamic paraventricular nucleus (PVN)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25017744",
"endSection": "abstract",
"offsetInBeginSection": 1264,
"offsetInEndSection": 1296,
"text": "hypothalamus orexigenic peptides"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25047666",
"endSection": "abstract",
"offsetInBeginSection": 518,
"offsetInEndSection": 585,
"text": " the hypothalamic mRNA expression of endogenous orexigenic peptides"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23707377",
"endSection": "abstract",
"offsetInBeginSection": 239,
"offsetInEndSection": 329,
"text": "The hypothalamus integrates peripheral and central signals to generate satiety or hunger. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22771813",
"endSection": "abstract",
"offsetInBeginSection": 950,
"offsetInEndSection": 1054,
"text": "increase in mRNA expression of hypothalamic orexigenic peptides and a decrease of anorexigenic peptides;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21903140",
"endSection": "abstract",
"offsetInBeginSection": 605,
"offsetInEndSection": 772,
"text": "expression of the orexigenic peptides, galanin (GAL) in the hypothalamic paraventricular nucleus (PVN) and orexin (OX) in the perifornical lateral hypothalamus (PFLH)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22325091",
"endSection": "abstract",
"offsetInBeginSection": 642,
"offsetInEndSection": 883,
"text": "Expression of orexigenic peptides neuropeptide Y (NPY) and agouti-related protein (AgRP) decreased in the hypothalamus of metformin-treated diabetic rats, though anorexigenic peptides pro-opiomelanocortin (POMC) did not change significantly."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22922128",
"endSection": "title",
"offsetInBeginSection": 38,
"offsetInEndSection": 71,
"text": "hypothalamic orexigenic peptides "
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
56e47e0051531f7e3300001c
|
bioasq_factoid
|
yesno
|
Are Spinal Intradural Primary Malignant Peripheral Nerve Sheath Tumors(MPNST) rare in neurofibromatosis patients?
|
['no']
|
[
"no"
] |
['Spinal intradural primary malignant peripheral nerve sheath tumors (MPNST) are rare in patients without neurofibromatosis.', 'No, Spinal Intradural Primary Malignant Peripheral Nerve Sheath Tumors(MPNST) rare in patients without neurofibromatosis.', 'yes, Primary malignant peripheral nerve sheath tumors (MPNSTs) are extremely rare in patients without a history of neurofibromatosis; only 18 cases have been reported in the English-language literature to this point.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27593814",
"http://www.ncbi.nlm.nih.gov/pubmed/24926928"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27593814",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Spinal intradural primary malignant peripheral nerve sheath tumors (MPNST) are rare in patients without neurofibromatosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24926928",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Primary malignant peripheral nerve sheath tumors (MPNSTs) are extremely rare in patients without a history of neurofibromatosis; only 18 cases have been reported in the English-language literature to this point."
}
] | 11
|
BioASQ-training11b
| null | null |
5e67bc121af46fc13000001c
|
bioasq_yesno
|
yesno
|
Is JTV519 (K201) a potential drug for the prevention of arrhythmias?
|
['yes']
|
[
"yes"
] |
Yes, JTV519 has antiarrhythmic properties.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23144205",
"http://www.ncbi.nlm.nih.gov/pubmed/22563249",
"http://www.ncbi.nlm.nih.gov/pubmed/22001562",
"http://www.ncbi.nlm.nih.gov/pubmed/21291389",
"http://www.ncbi.nlm.nih.gov/pubmed/20581784",
"http://www.ncbi.nlm.nih.gov/pubmed/20080988",
"http://www.ncbi.nlm.nih.gov/pubmed/17994112",
"http://www.ncbi.nlm.nih.gov/pubmed/17644079",
"http://www.ncbi.nlm.nih.gov/pubmed/16672364",
"http://www.ncbi.nlm.nih.gov/pubmed/16185151",
"http://www.ncbi.nlm.nih.gov/pubmed/15584870",
"http://www.ncbi.nlm.nih.gov/pubmed/15073377",
"http://www.ncbi.nlm.nih.gov/pubmed/12890053",
"http://www.ncbi.nlm.nih.gov/pubmed/11090108"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23144205",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 636,
"text": "We compared the suppressive effect of K201 (JTV519), a multiple-channel blocker and cardiac ryanodine receptor-calcium release channel (RyR2) stabilizer, with that of diltiazem, a Ca(2+ )channel blocker, in 2 studies of isoproterenol-induced (n = 30) and ischemic-reperfusion-induced VAs (n = 38) in rats. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23144205",
"endSection": "abstract",
"offsetInBeginSection": 1055,
"offsetInEndSection": 1584,
"text": "After administration of isoproterenol under Ca(2+) loading, fatal VA frequently occurred in the vehicle (9 of 10 animals, 90%) and diltiazem (8 of 10, 80%) groups, and K201 significantly suppressed the incidences of arrhythmia and mortality (2 of 10, 20%). In the reperfusion study, the incidence and the time until occurrence of reperfusion-induced VA and mortality were significantly suppressed in the K201 (2 of 15 animals, 13%) and diltiazem (1 of 9 animals, 11%) groups compared to the vehicle group (8 of 14 animals, 57%). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23144205",
"endSection": "abstract",
"offsetInBeginSection": 1707,
"offsetInEndSection": 1860,
"text": "K201 markedly suppressed both the isoproterenol-induced and the reperfusion-induced VAs, whereas diltiazem did not suppress the isoproterenol-induced VA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22563249",
"endSection": "abstract",
"offsetInBeginSection": 1614,
"offsetInEndSection": 1876,
"text": "JTV519 (K201) is a newly developed 1,4-benzothiazepine drug with antiarrhythmic and cardioprotective properties. It appears to be very effective in not only preventing but also in reversing the characteristic myocardial changes and preventing lethal arrhythmias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22001562",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 389,
"text": "The novel antiarrhythmic drug K201 (4-[3-{1-(4-benzyl)piperidinyl}propionyl]-7-methoxy-2,3,4,5-tetrahydro-1,4-benzothiazepine monohydrochloride) is currently in development for treatment of atrial fibrillation. K201 not only controls intracellular calcium release by the ryanodine receptors, but also possesses a ventricular action that might predispose to torsade de pointes arrhythmias. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21291389",
"endSection": "abstract",
"offsetInBeginSection": 969,
"offsetInEndSection": 1152,
"text": "The RyR is currently used as a therapeutic target in malignant hyperthermia where dantrolene is effective and to relieve ventricular arrhythmia, with the use of JTV519 and flecainide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20581784",
"endSection": "abstract",
"offsetInBeginSection": 1200,
"offsetInEndSection": 1372,
"text": "Finally, KN-3 and JTV519, two compounds that stabilize RyR2 in the closed state, prevent the induction of triggered activity and suppress the inducibility of sustained AF. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20080988",
"endSection": "abstract",
"offsetInBeginSection": 1639,
"offsetInEndSection": 1718,
"text": "JTV-519 greatly reduced the frequency of ouabain-induced arrhythmogenic events."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20080988",
"endSection": "abstract",
"offsetInBeginSection": 1914,
"offsetInEndSection": 1995,
"text": "Stabilization of RyR2 by JTV-519 effectively reduces these triggered arrhythmias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17994112",
"endSection": "abstract",
"offsetInBeginSection": 1473,
"offsetInEndSection": 1537,
"text": "These findings may reveal the anti-arrhythmic potential of K201."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17994112",
"endSection": "abstract",
"offsetInBeginSection": 225,
"offsetInEndSection": 340,
"text": "The preferential ryanodine receptor stabilizer (K201) possesses antiarrhythmic effects through calcium regulation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17644079",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 153,
"text": "The drug K201 (JTV-519) increases inotropy and suppresses arrhythmias in failing hearts, but the effects of K201 on normal hearts is unknown. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16825580",
"endSection": "abstract",
"offsetInBeginSection": 1510,
"offsetInEndSection": 1616,
"text": "K201 fails to prevent DADs in RyR2(R4496C+/-) myocytes and ventricular arrhythmias in RyR2(R4496C+/-) mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16825580",
"endSection": "abstract",
"offsetInBeginSection": 1071,
"offsetInEndSection": 1198,
"text": "In vivo administration of K201 failed to prevent induction of polymorphic ventricular tachycardia (VT) in RyR2(R4496C+/-) mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16672364",
"endSection": "abstract",
"offsetInBeginSection": 893,
"offsetInEndSection": 1089,
"text": "The 1,4-benzothiazepine JTV519, which increases the binding affinity of calstabin-2 for RyR2, inhibited the diastolic SR Ca2+ leak, monophasic action potential alternans and triggered arrhythmias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16185151",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 720,
"text": "In arrhythmias, the calstabin2 stabiliser JTV519 did not prevent arrhythmias in calstabin2-/- mice, but reduced the arrhythmias in calstabin2+/- mice, illustrating the antiarrhythmic potential of stabilising calstablin2. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15584870",
"endSection": "abstract",
"offsetInBeginSection": 412,
"offsetInEndSection": 652,
"text": "In three models of arrhythmias, the calstabin2 stabiliser JTV519 did not prevent arrhythmias in calstabin2(-/-) mice, but reduced the arrhythmias in calstabin2(+/-) mice, illustrating the antiarrhythmic potential of stabilising calstabin2. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15073377",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 645,
"text": "A derivative of 1,4-benzothiazepine (JTV519) increased the affinity of calstabin2 for RyR2, which stabilized the closed state of RyR2 and prevented the Ca2+ leak that triggers arrhythmias. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12890053",
"endSection": "abstract",
"offsetInBeginSection": 1480,
"offsetInEndSection": 1732,
"text": "JTV-519 had significant protective effects on atrial fibrillation in the canine sterile pericarditis model, mainly by increasing effective refractory period, suggesting that it may have potential as a novel antiarrhythmic agent for atrial fibrillation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12890053",
"endSection": "abstract",
"offsetInBeginSection": 871,
"offsetInEndSection": 1002,
"text": "JTV-519 significantly decreased the mean number of sustained atrial fibrillation episodes (from 4.2 +/- 2.9 to 0 +/- 0, P < 0.01). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11090108",
"endSection": "abstract",
"offsetInBeginSection": 1652,
"offsetInEndSection": 1851,
"text": "We conclude that JTV-519 can exert antiarrhythmic effects against AF by inhibiting repolarizing K(+) currents. The drug may be useful for the treatment of AF in patients with ischaemic heart disease."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000889"
] |
[
{
"o": "C109183",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A16995906"
},
{
"o": "JTV-519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17004235"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17004235",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7798511"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A16995906",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV 519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16995906"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "C109183",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A17004235"
},
{
"o": "JTV-519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17004235"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17004235",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7798511"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A16995906",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV 519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16995906"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "C109183",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A7798511"
},
{
"o": "JTV-519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17004235"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17004235",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7798511"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A16995906",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV 519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16995906"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "MeSH",
"p": "http://www.w3.org/2004/02/skos/core#note",
"s": "http://linkedlifedata.com/resource/umls/label/A16995906"
},
{
"o": "JTV-519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17004235"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17004235",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7798511"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A16995906",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV 519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16995906"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "MeSH",
"p": "http://www.w3.org/2004/02/skos/core#note",
"s": "http://linkedlifedata.com/resource/umls/label/A17004235"
},
{
"o": "JTV-519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17004235"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17004235",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7798511"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A16995906",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV 519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16995906"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "MeSH",
"p": "http://www.w3.org/2004/02/skos/core#note",
"s": "http://linkedlifedata.com/resource/umls/label/A7798511"
},
{
"o": "JTV-519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17004235"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17004235",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7798511"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A16995906",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV 519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16995906"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "http://linkedlifedata.com/resource/umls/id/C0668089",
"p": "http://www.w3.org/2004/02/skos/core#broader",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "K-201",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A1334561"
},
{
"o": "JTV-519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17004235"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17004235",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7798511"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A16995906",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "JTV 519",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16995906"
},
{
"o": "K201 compound",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A1362694"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7798511",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0754680"
},
{
"o": "http://linkedlifedata.com/resource/umls/id/C0754680",
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] |
52b2f1724003448f5500000b
|
bioasq_yesno
|
yesno
|
Does the 3D structure of the genome remain stable during cell differentiation?
|
['no']
|
[
"no"
] |
['Many studies have suggested a link between the spatial organization of genomes and fundamental biological processes such as genome reprogramming, gene expression, and differentiation. The open chromatin of embryonic stem cells (ESCs) condenses into repressive heterochromatin as cells exit the pluripotent state. The relation between alterations in chromatin structure and changes in gene expression during cell differentiation has served as a paradigm to understand the link between genome organization and function. Insulators are involved in 3D genome organization at multiple spatial scales and are important for dynamic reorganization of chromatin structure during reprogramming and differentiation. Architectural proteins orchestrate higher-order chromatin organization through the establishment of interactions between regulatory elements across multiple spatial scales. The regulation of these proteins, their interaction with DNA, and their co-occurrence in the genome, may be responsible for the plasticity of 3D chromatin architecture that dictates cell and time-specific blueprints of gene expression.', "Chromatin insulators have emerged as one of the central components of the genome organization tool-kit across species. We identify large, megabase-sized local chromatin interaction domains, which we term 'topological domains', as a pervasive structural feature of the genome organization. Many studies have suggested a link between the spatial organization of genomes and fundamental biological processes such as genome reprogramming, gene expression, and differentiation. Thus, p63 and its direct target Brg1 play an essential role in remodelling the higher-order chromatin structure of the EDC and in the specific positioning of this locus within the landscape of the 3D nuclear space, as required for the efficient expression of EDC genes in epidermal progenitor cells during skin development."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22495300",
"http://www.ncbi.nlm.nih.gov/pubmed/26340639",
"http://www.ncbi.nlm.nih.gov/pubmed/25218583",
"http://www.ncbi.nlm.nih.gov/pubmed/24346698",
"http://www.ncbi.nlm.nih.gov/pubmed/24305663",
"http://www.ncbi.nlm.nih.gov/pubmed/25479748",
"http://www.ncbi.nlm.nih.gov/pubmed/24905166",
"http://www.ncbi.nlm.nih.gov/pubmed/23199754",
"http://www.ncbi.nlm.nih.gov/pubmed/25693564"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22495300",
"endSection": "abstract",
"offsetInBeginSection": 940,
"offsetInEndSection": 1109,
"text": "We identify large, megabase-sized local chromatin interaction domains, which we term 'topological domains', as a pervasive structural feature of the genome organization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22495300",
"endSection": "abstract",
"offsetInBeginSection": 1207,
"offsetInEndSection": 1376,
"text": "The domains are stable across different cell types and highly conserved across species, indicating that topological domains are an inherent property of mammalian genomes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26340639",
"endSection": "abstract",
"offsetInBeginSection": 547,
"offsetInEndSection": 733,
"text": "Insulators are involved in 3D genome organization at multiple spatial scales and are important for dynamic reorganization of chromatin structure during reprogramming and differentiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25218583",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "The relation between alterations in chromatin structure and changes in gene expression during cell differentiation has served as a paradigm to understand the link between genome organization and function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25218583",
"endSection": "abstract",
"offsetInBeginSection": 521,
"offsetInEndSection": 929,
"text": "Architectural proteins orchestrate higher-order chromatin organization through the establishment of interactions between regulatory elements across multiple spatial scales. The regulation of these proteins, their interaction with DNA, and their co-occurrence in the genome, may be responsible for the plasticity of 3D chromatin architecture that dictates cell and time-specific blueprints of gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24346698",
"endSection": "abstract",
"offsetInBeginSection": 198,
"offsetInEndSection": 430,
"text": "The role of 3D genome organisation in the control and execution of lineage-specific transcription programmes during the development and differentiation of multipotent stem cells into specialised cell types remains poorly understood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24346698",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Chromatin structural states and their remodelling, including higher-order chromatin folding and three-dimensional (3D) genome organisation, play an important role in the control of gene expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24346698",
"endSection": "abstract",
"offsetInBeginSection": 431,
"offsetInEndSection": 666,
"text": "Here, we show that substantial remodelling of the higher-order chromatin structure of the epidermal differentiation complex (EDC), a keratinocyte lineage-specific gene locus on mouse chromosome 3, occurs during epidermal morphogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24305663",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Many studies have suggested a link between the spatial organization of genomes and fundamental biological processes such as genome reprogramming, gene expression, and differentiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25479748",
"endSection": "abstract",
"offsetInBeginSection": 717,
"offsetInEndSection": 908,
"text": "Moreover, we reveal that formation of such highly condensed, transcriptionally repressed heterochromatin promotes transcriptional activation of differentiation genes and loss of pluripotency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25479748",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "The open chromatin of embryonic stem cells (ESCs) condenses into repressive heterochromatin as cells exit the pluripotent state."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25479748",
"endSection": "abstract",
"offsetInBeginSection": 551,
"offsetInEndSection": 715,
"text": "we find that localized heterochromatin condensation of ribosomal RNA genes initiates establishment of highly condensed chromatin structures outside of the nucleolus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24905166",
"endSection": "abstract",
"offsetInBeginSection": 522,
"offsetInEndSection": 676,
"text": "We focus on the emerging relationship between genome organization and lineage-specific transcriptional regulation, which we argue are inextricably linked."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23199754",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 408,
"text": "Cells face the challenge of storing two meters of DNA in the three-dimensional (3D) space of the nucleus that spans only a few microns. The nuclear organization that is required to overcome this challenge must allow for the accessibility of the gene regulatory machinery to the DNA and, in the case of embryonic stem cells (ESCs), for the transcriptional and epigenetic changes that accompany differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23199754",
"endSection": "abstract",
"offsetInBeginSection": 715,
"offsetInEndSection": 1076,
"text": "In this review we summarize some of the recent findings illuminating the 3D structure of the eukaryotic genome, as well as the relationship between genome topology and function from the level of whole chromosomes to enhancer-promoter loops with a focus on features affecting genome organization in ESCs and changes in nuclear organization during differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25693564",
"endSection": "abstract",
"offsetInBeginSection": 481,
"offsetInEndSection": 742,
"text": "We observe that although self-associating chromatin domains are stable during differentiation, chromatin interactions both within and between domains change in a striking manner, altering 36% of active and inactive chromosomal compartments throughout the genome"
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002454",
"http://amigo.geneontology.org/amigo/term/GO:0030154",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016678"
] |
[] |
56ebfac12ac5ed1459000001
|
bioasq_yesno
|
factoid
|
Inhibition of which transporter is the mechanism of action of drug Canagliflozin?
|
['sodium glucose co-transporter 2']
|
[
"sodium glucose co-transporter 2",
"SGLT2",
"Sodium-glucose transport protein 2",
"Sodium-glucose cotransporter 2",
"Sodium-glucose co-transporter type 2"
] |
Inhibition of sodium glucose co-transporter 2 (SGLT2) is the major mechanism of action of canagliflozin. Canagliflozin is the first SGLT2 inhibitor to be approved in the USA for the treatment of type 2 diabetes and is under regulatory review in the EU. Other SGLT2 inhibitors include dapagliflozin and empagliflozin.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22621689",
"http://www.ncbi.nlm.nih.gov/pubmed/22547464",
"http://www.ncbi.nlm.nih.gov/pubmed/21680987",
"http://www.ncbi.nlm.nih.gov/pubmed/24257692",
"http://www.ncbi.nlm.nih.gov/pubmed/24040872",
"http://www.ncbi.nlm.nih.gov/pubmed/24025022",
"http://www.ncbi.nlm.nih.gov/pubmed/23895803",
"http://www.ncbi.nlm.nih.gov/pubmed/23729000",
"http://www.ncbi.nlm.nih.gov/pubmed/23590413",
"http://www.ncbi.nlm.nih.gov/pubmed/23563279",
"http://www.ncbi.nlm.nih.gov/pubmed/23412078",
"http://www.ncbi.nlm.nih.gov/pubmed/23326927",
"http://www.ncbi.nlm.nih.gov/pubmed/23042029",
"http://www.ncbi.nlm.nih.gov/pubmed/23087012",
"http://www.ncbi.nlm.nih.gov/pubmed/10481836"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24257692",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 436,
"text": "During the past year, two SGLT2 inhibitors, canagliflozin and dapagliflozin, have been approved for the treatment of type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24040872",
"endSection": "abstract",
"offsetInBeginSection": 680,
"offsetInEndSection": 955,
"text": "Currently dapagliflozin, one of the three most advanced SGLT2 inhibitors in the development (along with canagliflozin and empagliflozin), is already in the market in few European countries and canagliflozin has been approved from the Food and Drug Administration (FDA) in US."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24025022",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Sodium glucose co-transporter 2 (SGLT2) inhibition with canagliflozin in type 2 diabetes mellitus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24025022",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 636,
"text": "This report reviews the potentially beneficial effects of SGLT2 inhibitors in type 2 diabetes mellitus, specifically focusing on canagliflozin, the only SGLT2 inhibitor approved for use in the United States."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23895803",
"endSection": "abstract",
"offsetInBeginSection": 109,
"offsetInEndSection": 290,
"text": "The sodium glucose co-transporter 2 inhibitor canagliflozin lowered blood glucose, blood pressure, and body weight, with increased risk of urogenital infections in Phase 2 studies. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23729000",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 266,
"text": "Canagliflozin (Invokana™), an oral selective sodium-glucose co-transporter 2 (SGLT2) inhibitor, is under global development with Mitsubishi Tanabe Pharma and Janssen Pharmaceuticals, a subsidiary of Johnson and Johnson, for the treatment of type 2 diabetes mellitus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23729000",
"endSection": "abstract",
"offsetInBeginSection": 669,
"offsetInEndSection": 780,
"text": "Canagliflozin is the first SGLT2 inhibitor to be approved in the USA and is under regulatory review in the EU. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23590413",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Canagliflozin , an inhibitor of sodium-glucose cotransporter 2, for the treatment of type 2 diabetes mellitus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23590413",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 141,
"text": "Canagliflozin is an orally administered sodium glucose cotransporter 2 inhibitor proposed for the treatment of type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23563279",
"endSection": "abstract",
"offsetInBeginSection": 471,
"offsetInEndSection": 665,
"text": "In this review, we summarize recent animal and human studies on ipragliflozin and other SGLT2 inhibitors including dapagliflozin, canagliflozin, empagliflozin, tofogliflozin, and luseogliflozin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23412078",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 116,
"text": "Canagliflozin, a sodium glucose cotransporter (SGLT) 2 inhibitor, is also a low-potency SGLT1 inhibitor. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23412078",
"endSection": "abstract",
"offsetInBeginSection": 1665,
"offsetInEndSection": 1834,
"text": "Canagliflozin reduces postprandial plasma glucose and insulin by increasing UGE (via renal SGLT2 inhibition) and delaying RaO, likely due to intestinal SGLT1 inhibition."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002352",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0051051",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0032410",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004364",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D045504"
] |
[] |
5335c7f2d6d3ac6a34000051
|
bioasq_factoid
|
yesno
|
Are immune cells affected in Amyotrophic Lateral Sclerosis?
|
['yes']
|
[
"yes"
] |
['In ALS T-cell deficiency increases neuronal loss, while boosting T cell levels reduces it.', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'The intrathymic injection of donor spleen cells into antilymphocyte serum (ALS)-treated mice induces significant prolongation of donor skin grafts. To elucidate possible mechanisms involved in the induction of unresponsiveness in ALS-treated mice after intrathymic injection of donor spleen cells, we have analysed the reactivity of lymphoid cells from unresponsive mice in various ways. Here, we show that in the mutant superoxide dismutase 1 G93A (mSOD1) mouse model of ALS, the levels of natural killer T (NKT) cells increased dramatically, and T-cell distribution was altered both in lymphoid organs and in the spinal cord relative to wild-type mice. Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25904790",
"http://www.ncbi.nlm.nih.gov/pubmed/21829620",
"http://www.ncbi.nlm.nih.gov/pubmed/7551976",
"http://www.ncbi.nlm.nih.gov/pubmed/7595631",
"http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"http://www.ncbi.nlm.nih.gov/pubmed/17852013",
"http://www.ncbi.nlm.nih.gov/pubmed/20406178",
"http://www.ncbi.nlm.nih.gov/pubmed/24995608",
"http://www.ncbi.nlm.nih.gov/pubmed/25199710"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25904790",
"endSection": "abstract",
"offsetInBeginSection": 787,
"offsetInEndSection": 1125,
"text": "Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25904790",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Immunization with a Myelin-Derived Antigen Activates the Brain's Choroid Plexus for Recruitment of Immunoregulatory Cells to the CNS and Attenuates Disease Progression in a Mouse Model of ALS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21829620",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Amyotrophic lateral sclerosis (ALS) is a rapidly progressing fatal neurodegenerative disorder characterized by the selective death of motor neurons (MN) in the spinal cord, and is associated with local neuroinflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21829620",
"endSection": "abstract",
"offsetInBeginSection": 403,
"offsetInEndSection": 486,
"text": "T-cell deficiency increases neuronal loss, while boosting T cell levels reduces it."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17852013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": " Immunological disturbances have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Chemokines are involved in the recruitment of immune cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20406178",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "The immune system has been found to be involved with positive and negative effects in the nervous system of amyotrophic lateral sclerosis (ALS) patients. In general, T cells, B cells, NK cells, mast cells, macrophages, dendritic cells, microglia, antibodies, complement and cytokines participate in limiting damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17852013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "Immunological disturbances have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Chemokines are involved in the recruitment of immune cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20406178",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "The immune system has been found to be involved with positive and negative effects in the nervous system of amyotrophic lateral sclerosis (ALS) patients. In general, T cells, B cells, NK cells, mast cells, macrophages, dendritic cells, microglia, antibodies, complement and cytokines participate in limiting damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24995608",
"endSection": "abstract",
"offsetInBeginSection": 2147,
"offsetInEndSection": 2458,
"text": "We propose the following mechanism for the effect of mesenchymal stem cells (MSCs) administered intrathecally in amyotrophic lateral sclerosis (ALS): MSCs increase infiltration of peripheral immune cells into CNS and skew the infiltrated immune cells toward regulatory T lymphocytes (Treg ) and Th2 lymphocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17852013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": " Immunological disturbances have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Chemokines are involved in the recruitment of immune cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20406178",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "The immune system has been found to be involved with positive and negative effects in the nervous system of amyotrophic lateral sclerosis (ALS) patients. In general, T cells, B cells, NK cells, mast cells, macrophages, dendritic cells, microglia, antibodies, complement and cytokines participate in limiting damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24995608",
"endSection": "abstract",
"offsetInBeginSection": 2147,
"offsetInEndSection": 2458,
"text": "We propose the following mechanism for the effect of mesenchymal stem cells (MSCs) administered intrathecally in amyotrophic lateral sclerosis (ALS): MSCs increase infiltration of peripheral immune cells into CNS and skew the infiltrated immune cells toward regulatory T lymphocytes (Treg ) and Th2 lymphocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25199710",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 271,
"text": "Immune cell infiltration to the brain's territory was considered for decades to reflect a pathological process in which immune cells attack the central nervous system (CNS); such a process is observed in the inflammatory autoimmune disease, multiple sclerosis (MS)."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002477",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000690",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012598",
"http://www.disease-ontology.org/api/metadata/DOID:230"
] |
[] |
56cae51f5795f9a73e000025
|
bioasq_yesno
|
yesno
|
Have the promoter regions of the genes implicated in Rett Syndrome been characterized with CAGE?
|
['yes']
|
[
"yes"
] |
['Yes. Promoter regions of the genes implicated in Rett Syndrome have been characterized using CAGE.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25539566"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25539566",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "CAGE-defined promoter regions of the genes implicated in Rett Syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25539566",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 1212,
"text": "Mutations in three functionally diverse genes cause Rett Syndrome. Although the functions of Forkhead box G1 (FOXG1), Methyl CpG binding protein 2 (MECP2) and Cyclin-dependent kinase-like 5 (CDKL5) have been studied individually, not much is known about their relation to each other with respect to expression levels and regulatory regions. Here we analyzed data from hundreds of mouse and human samples included in the FANTOM5 project, to identify transcript initiation sites, expression levels, expression correlations and regulatory regions of the three genes.RESULTS: Our investigations reveal the predominantly used transcription start sites (TSSs) for each gene including novel transcription start sites for FOXG1. We show that FOXG1 expression is poorly correlated with the expression of MECP2 and CDKL5. We identify promoter shapes for each TSS, the predicted location of enhancers for each gene and the common transcription factors likely to regulate the three genes. Our data imply Polycomb Repressive Complex 2 (PRC2) mediated silencing of Foxg1 in cerebellum.CONCLUSIONS: Our analyses provide a comprehensive picture of the regulatory regions of the three genes involved in Rett Syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25539566",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "CAGE-defined promoter regions of the genes implicated in Rett Syndrome"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25539566",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "CAGE-defined promoter regions of the genes implicated in Rett Syndrome."
}
] | 6
|
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015518",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011401",
"http://www.disease-ontology.org/api/metadata/DOID:1206"
] | null |
589644c478275d0c4a00000d
|
bioasq_yesno
|
factoid
|
Which brain tumors does neuroligin-3 promote?
|
['high-grade gliomas']
|
[
"high-grade gliomas",
"high-grade glioma",
"malignant gliomas",
"malignant glioma",
"grade III gliomas",
"grade IV gliomas",
"anaplastic gliomas",
"glioblastoma",
"glioblastoma multiforme"
] |
['Neuroligin-3 promotes the growth of high-grade gliomas.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28959975"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28959975",
"endSection": "abstract",
"offsetInBeginSection": 605,
"offsetInEndSection": 1576,
"text": "An important mechanism that mediates this neural regulation of brain cancer is activity-dependent cleavage and secretion of the synaptic adhesion molecule neuroligin-3 (NLGN3), which promotes glioma proliferation through the PI3K-mTOR pathway. However, the necessity of NLGN3 for glioma growth, the proteolytic mechanism of NLGN3 secretion, and the further molecular consequences of NLGN3 secretion in glioma cells remain unknown. Here we show that HGG growth depends on microenvironmental NLGN3, identify signalling cascades downstream of NLGN3 binding in glioma, and determine a therapeutically targetable mechanism of secretion. Patient-derived orthotopic xenografts of paediatric GBM, DIPG and adult GBM fail to grow in Nlgn3 knockout mice. NLGN3 stimulates several oncogenic pathways, such as early focal adhesion kinase activation upstream of PI3K-mTOR, and induces transcriptional changes that include upregulation of several synapse-related genes in glioma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28959975",
"endSection": "abstract",
"offsetInBeginSection": 1794,
"offsetInEndSection": 1913,
"text": "This work defines a promising strategy for targeting NLGN3 secretion, which could prove transformative for HGG therapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28959975",
"endSection": "title",
"offsetInBeginSection": -1,
"offsetInEndSection": 81,
"text": "Targeting neuronal activity-regulated neuroligin-3 dependency in high-grade glioma"
}
] | 11
|
BioASQ-training11b
| null | null |
5a9ac4e81d1251d03b000011
|
bioasq_factoid
|
yesno
|
Have studies shown that there is no link between DNA methylation patterns and Post Traumatic Stress Disorder?
|
['no']
|
[
"no"
] |
['Studies do show a correlation of PTSD-related accelerated aging in DNA methylation patterns.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27886370",
"http://www.ncbi.nlm.nih.gov/pubmed/21508515",
"http://www.ncbi.nlm.nih.gov/pubmed/25065861",
"http://www.ncbi.nlm.nih.gov/pubmed/21714072",
"http://www.ncbi.nlm.nih.gov/pubmed/26361058",
"http://www.ncbi.nlm.nih.gov/pubmed/22332656",
"http://www.ncbi.nlm.nih.gov/pubmed/21306736",
"http://www.ncbi.nlm.nih.gov/pubmed/26305478",
"http://www.ncbi.nlm.nih.gov/pubmed/26447678",
"http://www.ncbi.nlm.nih.gov/pubmed/19793403"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26361058",
"endSection": "abstract",
"offsetInBeginSection": 918,
"offsetInEndSection": 1502,
"text": "Using pre-deployment SKA2 methylation levels and childhood trauma exposure, we found that the previously published suicide prediction rule significantly predicted post-deployment PTSD symptoms (AUC=0.66, 95% CI: 0.53-0.79) with an optimal sensitivity of 0.81 and specificity of 0.91. Permutation analysis using random methylation loci supported these findings. Together, these data establish the importance of SKA2 for cortisol stress responsivity and the development of PTSD and provide further evidence that SKA2 is a promising biomarker for stress-related disorders including PTSD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26447678",
"endSection": "abstract",
"offsetInBeginSection": 1126,
"offsetInEndSection": 1307,
"text": " Results provide novel support for PTSD-related accelerated aging in DNAm and extend the evidence base of known DNAm age correlates to the domains of neural integrity and cognition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22332656",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "We investigated serum DNA methylation patterns in genomic repetitive elements, LINE-1 and Alu, for post-traumatic stress disorder (PTSD) cases and controls who were US military service members recently deployed to Afghanistan or Iraq."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26361058",
"endSection": "abstract",
"offsetInBeginSection": 97,
"offsetInEndSection": 321,
"text": "In light of its role in glucocorticoid receptor transactivation, we investigated whether SKA2 DNA methylation influences cortisol stress reactivity and is involved in the development of post-traumatic stress disorder (PTSD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19793403",
"endSection": "abstract",
"offsetInBeginSection": 1398,
"offsetInEndSection": 1579,
"text": "These results suggest that alterations in global methylation pattern are involved in behavioural adaptation to environmental stress and pinpoint Dlgap2 as a possible target in PTSD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21306736",
"endSection": "abstract",
"offsetInBeginSection": 146,
"offsetInEndSection": 286,
"text": "Here we examined whether there was a link between an established rat model of post-traumatic stress disorder (PTSD) and Bdnf DNA methylation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22332656",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 287,
"text": "We investigated serum DNA methylation patterns in genomic repetitive elements, LINE-1 and Alu, for post-traumatic stress disorder (PTSD) cases and controls who were US military service members recently deployed to Afghanistan or Iraq.Cases (n = 75) had a postdeployment diagnosis of PTSD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22332656",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "DNA methylation in repetitive elements and post-traumatic stress disorder: a case-control study of US military service members"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21306736",
"endSection": "abstract",
"offsetInBeginSection": 146,
"offsetInEndSection": 288,
"text": "Here we examined whether there was a link between an established rat model of post-traumatic stress disorder (PTSD) and Bdnf DNA methylation. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22332656",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "DNA methylation in repetitive elements and post-traumatic stress disorder: a case-control study of US military service members."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22332656",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "AIM: We investigated serum DNA methylation patterns in genomic repetitive elements, LINE-1 and Alu, for post-traumatic stress disorder (PTSD) cases and controls who were US military service members recently deployed to Afghanistan or Iraq. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21714072",
"endSection": "abstract",
"offsetInBeginSection": 1221,
"offsetInEndSection": 1398,
"text": "Together, these results suggest that psychosocial stress may alter global and gene-specific DNA methylation patterns potentially associated with peripheral immune dysregulation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19793403",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "DNA methylation in vulnerability to post-traumatic stress in rats: evidence for the role of the post-synaptic density protein Dlgap2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27886370",
"endSection": "abstract",
"offsetInBeginSection": 763,
"offsetInEndSection": 885,
"text": "Subjects with PTSD showed a higher DNA methylation of four CpG sites at the BDNF promoter compared with those without PTSD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26305478",
"endSection": "abstract",
"offsetInBeginSection": 1427,
"offsetInEndSection": 1606,
"text": "Cumulatively, the data suggest that epigenetic variation at SKA2 mediates vulnerability to suicidal behaviors and PTSD through dysregulation of the HPA axis in response to stress."
}
] | 6
|
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D040921",
"http://www.disease-ontology.org/api/metadata/DOID:2055",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013313",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019175"
] | null |
58e2422c6fddd3e83e000011
|
bioasq_yesno
|
yesno
|
Does thyroid hormone affect cardiac remodeling?
|
['yes']
|
[
"yes"
] |
TH affects cardiac remodeling
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23555069",
"http://www.ncbi.nlm.nih.gov/pubmed/23532677",
"http://www.ncbi.nlm.nih.gov/pubmed/22403173",
"http://www.ncbi.nlm.nih.gov/pubmed/22039709",
"http://www.ncbi.nlm.nih.gov/pubmed/20730619",
"http://www.ncbi.nlm.nih.gov/pubmed/20668933",
"http://www.ncbi.nlm.nih.gov/pubmed/19826181",
"http://www.ncbi.nlm.nih.gov/pubmed/18773293",
"http://www.ncbi.nlm.nih.gov/pubmed/18455802",
"http://www.ncbi.nlm.nih.gov/pubmed/17560116",
"http://www.ncbi.nlm.nih.gov/pubmed/17024559",
"http://www.ncbi.nlm.nih.gov/pubmed/21568669",
"http://www.ncbi.nlm.nih.gov/pubmed/23820669",
"http://www.ncbi.nlm.nih.gov/pubmed/18622044",
"http://www.ncbi.nlm.nih.gov/pubmed/19951746",
"http://www.ncbi.nlm.nih.gov/pubmed/18430565",
"http://www.ncbi.nlm.nih.gov/pubmed/20926779",
"http://www.ncbi.nlm.nih.gov/pubmed/16499159",
"http://www.ncbi.nlm.nih.gov/pubmed/17389455",
"http://www.ncbi.nlm.nih.gov/pubmed/21159857",
"http://www.ncbi.nlm.nih.gov/pubmed/18274800",
"http://www.ncbi.nlm.nih.gov/pubmed/20560106",
"http://www.ncbi.nlm.nih.gov/pubmed/22134702"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23555069",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1356,
"text": "The aim of this brief paper is to highlight new developments in understanding the cardioprotective role of thyroid hormone in reverting regulatory networks involved in adverse cardiac remodeling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23532677",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 270,
"text": "Thyroid hormone receptor α1 (TRα1) is shown to be critical for the maturation of cardiomyocytes and for the cellular response to stress. TRα1 is altered during post ischemic cardiac remodeling but the physiological significance of this response is not fully understood. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23532677",
"endSection": "abstract",
"offsetInBeginSection": 1437,
"offsetInEndSection": 1581,
"text": "AMI induces downregulation of thyroid hormone signaling and pharmacological inhibition of TRα1 further depresses post-ischemic cardiac function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22403173",
"endSection": "abstract",
"offsetInBeginSection": 1058,
"offsetInEndSection": 1219,
"text": "These findings reveal crucial roles for Dio3 in heart function and remodeling, which may have pathophysiologic implications for human restrictive cardiomyopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22039709",
"endSection": "abstract",
"offsetInBeginSection": 1309,
"offsetInEndSection": 1661,
"text": "TH administration after AMI prevented tissue hypothyroidism and resulted in decreased beta-MHC expression, increased wall thickening and normalized wallstress, while stretch-induced p38 MAPK activation was increased. We conclude that diabetes exacerbates post-ischemic cardiac remodeling and that tissue hypothyroidism may be involved in this response."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20730619",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Thyroid hormone can favorably remodel the diabetic myocardium after acute myocardial infarction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20730619",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "It has been previously shown that regulators of physiological growth such as thyroid hormone (TH) can favorably remodel the post ischaemic myocardium."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20730619",
"endSection": "abstract",
"offsetInBeginSection": 1768,
"offsetInEndSection": 1965,
"text": "Acute myocardial infarction in diabetic rats results in TH receptor down-regulation with important physiological consequences. TH treatment prevents this response and improves cardiac hemodynamics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20668933",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 567,
"text": "TH affects cardiac remodeling by limiting reperfusion injury, and, at later states, by inducing distinct changes in cardiac chamber geometry in a time-dependent manner."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20668933",
"endSection": "abstract",
"offsetInBeginSection": 568,
"offsetInEndSection": 715,
"text": "Furthermore, administration of TH can convert pathologic to physiologic hypertrophy. These effects are the result of favorable cellular remodeling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19826181",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "Thyroid hormone (TH) is critical in cardiac cell differentiation (regulating contractile proteins and cell geometry) and this effect could be potentially exploited therapeutically in reversing the process of de-differentiation which underlies postischemic cardiac remodeling. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19826181",
"endSection": "abstract",
"offsetInBeginSection": 1182,
"offsetInEndSection": 1549,
"text": "TH treatment partially reverses cardiac dysfunction in rats with old myocardial infarction by favorably changing cardiac chamber geometry and expression of myosin isoforms. Thyroid hormone, unlike current treatments, appears to be a paradigm of therapeutic intervention which aims at restoring cardiac geometry and may prove new effective treatment for heart failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18773293",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 636,
"text": "Changes in thyroid hormone (TH)-TH receptors (TRs) axis occur in the course of post-infarction cardiac remodeling and seem to contribute to cardiac fetal phenotype. TH can \"rebuild\" the post-infarcted heart by preventing the fetal-like pattern of contractile proteins expression, normalizing wall tension, and optimizing cardiac chamber geometry. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18455802",
"endSection": "abstract",
"offsetInBeginSection": 147,
"offsetInEndSection": 342,
"text": "TH, apart from its \"classical\" actions on cardiac contractility and heart rhythm, appears to regulate various intracellular signaling pathways related to stress responses and cardiac remodelling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18455802",
"endSection": "abstract",
"offsetInBeginSection": 720,
"offsetInEndSection": 883,
"text": "More importantly, experimental and clinical studies demonstrate that TH can limit ischaemic injury, attenuate cardiac remodeling and improve cardiac hemodynamics. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17560116",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Thyroid hormone attenuates cardiac remodeling and improves hemodynamics early after acute myocardial infarction in rats."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17560116",
"endSection": "abstract",
"offsetInBeginSection": 1987,
"offsetInEndSection": 2121,
"text": "Thyroid hormone administration early after infarction attenuates cardiac remodeling and significantly improves myocardial performance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17024559",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "It has previously been shown that thyroid hormone can reverse cardiac remodeling in failing hearts by reducing myocardial wall stress due to the unique changes induced in cardiac myocyte shape. "
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013963",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020257"
] |
[] |
52efc041c8da89891000001b
|
bioasq_yesno
|
factoid
|
What disease is small bowel lymphoma commonly associated with
|
[['Celiac disease', 'gluten-associated enteropathy', 'CELIAC SPRU', 'Non tropical spru', 'Gluten Sensitive Enteropath']]
|
[
"Celiac disease",
"gluten-associated enteropathy",
"CELIAC SPRU",
"Non tropical spru",
"Gluten Sensitive Enteropath",
"Celiac sprue",
"Coeliac disease",
"Gluten intolerance"
] |
['Celiac disease']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21532863",
"http://www.ncbi.nlm.nih.gov/pubmed/18212211",
"http://www.ncbi.nlm.nih.gov/pubmed/12002682",
"http://www.ncbi.nlm.nih.gov/pubmed/10912475"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21532863",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Marginal zone B-cell lymphoma of MALT in small intestine associated with amyloidosis: a rare association."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21532863",
"endSection": "abstract",
"offsetInBeginSection": 495,
"offsetInEndSection": 654,
"text": "This is the first case of marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) in the small intestine associated with amyloidosis in Korea"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18212211",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "MR enterography of small-bowel lymphoma: potential for suggestion of histologic subtype and the presence of underlying celiac disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18212211",
"endSection": "abstract",
"offsetInBeginSection": 1571,
"offsetInEndSection": 1839,
"text": "We describe the characteristics of small-bowel lymphoma on MR enterography, identifying a number of key features that may help the interpreting radiologist in suggesting the underlying histologic subtype and whether the presence of underlying celiac disease is likely."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12002682",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "Celiac disease is an autoimmune disorder triggered by ingestion of gluten-containing foods. Epidemiologic studies dating from the 1950s established its association with gastrointestinal malignancies, particularly small bowel lymphoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10912475",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 557,
"text": "An association between untreated coeliac disease and intestinal malignancy is well described so it is possible that patients with undiagnosed coeliac disease constitute a significant reservoir of preventable gastrointestinal malignancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2754219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "An increased incidence of small bowel lymphoma in patients with long-standing celiac sprue is well documented in the literature."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
5509bd6a1180f13250000002
|
bioasq_factoid
|
yesno
|
In clinical trials, the H3 R antagonist CEP-26401 has a positive effect on cognition, yes or no?
|
['yes']
|
[
"yes"
] |
['The H3 R antagonist CEP-26401 had an effect on cognition.', 'CEP-26401 is a novel orally active, brain-penetrant, high-affinity histamine H3 receptor (H3R) antagonist, with potential therapeutic utility in cognition enhancement']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27222271",
"http://www.ncbi.nlm.nih.gov/pubmed/18469850",
"http://www.ncbi.nlm.nih.gov/pubmed/22001260"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27222271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "CEP-26401 is a novel orally active, brain-penetrant, high-affinity histamine H3 receptor (H3R) antagonist, with potential therapeutic utility in cognition enhancement"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22001260",
"endSection": "abstract",
"offsetInBeginSection": 1357,
"offsetInEndSection": 1565,
"text": "hese results demonstrate potent behavioral effects of CEP-26401 in rodent models and suggest that this novel H₃R antagonist may have therapeutic utility in the treatment of cognitive and attentional disorders"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27222271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "CEP-26401 is a novel orally active, brain-penetrant, high-affinity histamine H3 receptor (H3R) antagonist, with potential therapeutic utility in cognition enhancement."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22001260",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "CEP-26401 (irdabisant), a potent and selective histamine H₃ receptor antagonist/inverse agonist with cognition-enhancing and wake-promoting activities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18469850",
"endSection": "abstract",
"offsetInBeginSection": 1208,
"offsetInEndSection": 1451,
"text": "However, although a number of clinical studies examining the efficacy of H3 receptor antagonists for a variety of cognitive disorders are currently underway, no clinical proof of concept for an H3 receptor antagonist has been reported to date."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27222271",
"endSection": "abstract",
"offsetInBeginSection": 1511,
"offsetInEndSection": 1627,
"text": "Further clinical studies are required to establish the potential of low-dose CEP-26401 in cognition enhancement.<br>"
}
] | 11
|
BioASQ-training11b
| null | null |
5c57216e07647bbc4b000018
|
bioasq_yesno
|
yesno
|
Are lamina-associated domains (LADs) associated with transcriptional activation?
|
['no']
|
[
"no"
] |
['Regions of focal DNA hypermethylation and long-range hypomethylation in colorectal cancer coincide with nuclear lamina-associated domains. Such lamina-associated domains (LADs) are thought to help organize chromosomes inside the nucleus and have been associated with gene repression.', 'gene repression', 'The nuclear lamina contributes to the regulation of gene expression and to chromatin organization. Such lamina-associated domains (LADs) are thought to help organize chromosomes inside the nucleus and have been associated with gene repression. Regions of focal DNA hypermethylation and long-range hypomethylation in colorectal cancer coincide with nuclear lamina-associated domains. Extensive changes in DNA methylation are common in cancer and may contribute to oncogenesis through transcriptional silencing of tumor-suppressor genes.', 'Regions of focal DNA hypermethylation and long-range hypomethylation in colorectal cancer coincide with nuclear lamina-associated domains. Extensive changes in DNA methylation are common in cancer and may contribute to oncogenesis through transcriptional silencing of tumor-suppressor genes.', 'No, lamina-associated domains (LADs) are involved in transcriptional silencing and chromatin compaction.', 'Such lamina-associated domains (LADs) are thought to help organize chromosomes inside the nucleus and have been associated with gene repression.', 'Such lamina-associated domains (LADs) are thought to help organize chromosomes inside the nucleus and have been associated with gene repression. The nuclear lamina contributes to the regulation of gene expression and to chromatin organization.', 'Lamina-associated domains (LADs) are thought to help organize chromosomes inside the nucleus and have been associated with gene repression', 'Regions of focal DNA hypermethylation and long-range hypomethylation in colorectal cancer coincide with nuclear lamina-associated domains. Extensive changes in DNA methylation are common in cancer and may contribute to oncogenesis through transcriptional silencing of tumor-suppressor genes. Such lamina-associated domains (LADs) are thought to help organize chromosomes inside the nucleus and have been associated with gene repression. The nuclear lamina contributes to the regulation of gene expression and to chromatin organization.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22120008",
"http://www.ncbi.nlm.nih.gov/pubmed/29517398",
"http://www.ncbi.nlm.nih.gov/pubmed/28525751"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22120008",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Regions of focal DNA hypermethylation and long-range hypomethylation in colorectal cancer coincide with nuclear lamina-associated domains."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22120008",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Extensive changes in DNA methylation are common in cancer and may contribute to oncogenesis through transcriptional silencing of tumor-suppressor genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28525751",
"endSection": "abstract",
"offsetInBeginSection": 107,
"offsetInEndSection": 251,
"text": "Such lamina-associated domains (LADs) are thought to help organize chromosomes inside the nucleus and have been associated with gene repression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29517398",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "The nuclear lamina contributes to the regulation of gene expression and to chromatin organization."
}
] | 11
|
BioASQ-training11b
| null | null |
5cf4dec0a49efeb44c00000c
|
bioasq_yesno
|
factoid
|
What is the average median survival for advanced colorectal cancer patients?
|
['32.4 months', '32 months', '24-30 months']
|
[
"32.4 months",
"32 months",
"24-30 months",
"two years and eight months",
"two years and six months",
"two years",
"two and a half years",
"two years and four months"
] |
['In summary, based on the provided data, the average median overall survival (OS) of advanced colorectal cancer patients has improved over time from approximately 22.6 months between 2004 and 2012 to around 32.4 months for those diagnosed between 2016 and 2019. The weighted average median survival for the entire period is about 28.0 months.', 'According to the abstracts provided, the average median survival for advanced colorectal cancer patients varies depending on the specific study and population. However, based on the information presented, it can be concluded that: * The median overall survival for metastatic colorectal cancer is nearly 2 years (Abstract 1). * Median survival in advanced colorectal cancer patients treated with 5-fluorouracil (5FU) and leucovorin (LV) is between 12 and 18 months, with a specific study reporting a median survival of 18 months (Abstract 3). * The median survival for advanced CRC reported in clinical trials now approaches 2 years (Abstract 4). * In untreated advanced colorectal cancer patients, the median survival was found to be 24 months (range 16-42) (Abstract 5). , Overall, the average median survival for advanced colorectal cancer patients appears to be around 18-24 months.', 'The average median survival for advanced colorectal cancer patients is 20 months.The addition of ramicurumab to second line therapy significantly improved median overall survival.KRAS gene mutation in colorectal cancer patients is closely associated with poor prognosis.Obesity is a risk factor for poor overall survival in patients with colorectal cancer.EGFR, primary tumor site, and multiple metastases of tumor are independent risk factors for poor overall survival in patients with colorectal cancer.Fluorouracil has been the mainstay of chemotherapy for advanced colorectal cancer for over 40 years and is effective in prolonging time to disease progression and survival.', 'Median OS was roughly stable for patients diagnosed between 2004 and 2012 (22.6 months) but since has steadily improved for those diagnosed in 2013 to 2015 (28.8 months), and 2016 to 2019 (32.4 months.', 'The average median survival for advanced colorectal cancer patients is 25 months.', 'The average median survival for advanced colorectal cancer patients has been roughly stable for those diagnosed between 2004 and 2012 at 22.6 months, but has shown a steady improvement for those diagnosed in 2013 to 2015 (28.8 months) and 2016 to 2019 (32.4 months).', 'Median OS was roughly stable for patients diagnosed between 2004 and 2012 (22.6 months) but since has steadily improved for those diagnosed in 2013 to 2015 (28.8 months), and 2016 to 2019 (32.4 months)', '32.4 months\n\nContext: The median OS was 22.6 months for patients diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019.\nQuestion: What is the average median survival for advanced colorectal cancer patients?\nAnswer: 32.4 months\n\nContext: The median OS was 22.6 months for patients diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019.\nQuestion: What is the average median survival for advanced colorectal cancer patients?\nAnswer: 32.4 months\n\nContext: The median OS was 22.6 months for patients diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019.\nQuestion: What is the average median survival for advanced colorectal cancer patients?\nAnswer: 32.4 months\n\nContext:', 'The average median survival for advanced colorectal cancer patients has steadily improved over time, with the median OS being 22.6 months for those diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019.', 'The average median survival for advanced colorectal cancer patients is approximately 20-24 months based on various studies; however, the median overall survival has increased over time due to advancements in treatment strategies.', 'The average median survival for advanced colorectal cancer patients has improved over time. For patients diagnosed between 2004 and 2012, the median OS was 22.6 months, while for those diagnosed in 2013 to 2015, it was 28.8 months, and for those diagnosed in 2016 to 2019, it was 32.4 months.', 'The average median survival time for advanced colorectal cancer patients is approximately 15 months. This is based on the data from several studies that report median survival times ranging from 6 to 25 months. It is important to note that the survival time can vary depending on the stage of the disease, the treatment regimen, and other patient-specific factors.', 'Based on the provided information, the median survival time for patients with advanced or metastatic colorectal cancer ranges from approximately 6 to 25 months, depending on factors such as extent of metastases and treatment received.\n\nWithout treatment, median survival is around 7.5 to 11 months. Systemic chemotherapy modestly improves median survival to about 12 months. More aggressive treatments like regional chemotherapy or combined chemotherapy regimens (e.g. FOLFOX, FOLFIRI) can extend median survival further to 15-17 months or even up to 23-25 months in some cases.\n\nHowever, even with treatment, 5-year survival rates remain low, ranging from under 5% to 31%. Advanced colorectal cancer is rarely curable, although treatments can prolong survival. Median survival is highly variable based on individual patient and cancer characteristics.', "The average median survival for advanced colorectal cancer patients, based on the abstracts provided, appears to be around 7 months. This estimate comes from a review of the natural history of disseminated colorectal cancer, which states that the overall median survival rate of patients with hepatic metastases from colorectal primary cancer is approximately 7 months. However, it's important to note that many patients survive for three years and some even live for more than ten years without any specific treatment. This variability in survival times underscores the complex nature of colorectal cancer and the importance of personalized medical approaches.", 'The median overall survival (OS) for patients diagnosed with advanced colorectal cancer has been improving over the years. For those diagnosed between 2004 and 2012, it was roughly 22.6 months. It improved to 28.8 months for those diagnosed between 2013 and 2015, and further improved to 32.4 months for those diagnosed between 2016 and 2019.', 'The average median survival for advanced colorectal cancer patients is 32.4 months.', "22.6 months for patients diagnosed between 2004 and 2012, 28.8 months for those diagnosed in 2013 to 2015, and 32.4 months for those diagnosed in 2016 to 2019. \n\nPlease go ahead and ask your question. I'll do my best to provide a concise answer. \n\n(Note: Please keep your question related to the context provided.)", "The average median survival for advanced colorectal cancer patients is not explicitly stated in the provided Wikipedia articles. However, the articles mention that the five-year survival rate in the United States was around 65% in 2014, and the individual likelihood of survival depends on factors such as the stage of the cancer, the ability to remove the cancer surgically, and the person's overall health. The articles also discuss various treatment options for colorectal cancer, including surgery, radiation therapy, chemotherapy, and targeted therapy, as well as the importance of early detection and prevention through lifestyle changes and regular screenings.\n\nBased on the provided articles, the median survival time for patients with inoperable liver metastases from colorectal cancer is 7.4 to 11 months. Systemic chemotherapy produces a modest improvement to 12 months, while regional chemotherapy produces a further improvement to 15 to 17 months. The median survival time after diagnosis of metastases is almost comparable with 17 months. The median survival time was 6 months in the entire cohort, 16 months, 7.5 months, 8.5 months for all patients, 11 months for patients with solitary hepatic tumour, and 7.5 months for those with multiple tumours. Combined with regimens such as FOLFOX or FOLFIRI, median survival rates have been increased to an average of 23 months. The 1Y-PFS was 28.5% (median survival time (MST): 7.4 months), 1Y-OS was 76.6% (MST not reached), 3Y-PFS was 5.5% (MST: 7.4 months), and 3Y-OS was 26.4% (MST: 25.2 months).", 'The average median overall survival (OS) of advanced colorectal cancer patients has improved over time: 22.6 months for diagnoses between 2004 and 2012, 28.8 months for those diagnosed between 2013 and 2015, and 32.4 months for those diagnosed between 2016 and 2019. The average median survival across these periods is approximately 28.0 months.', 'The average median survival for advanced colorectal cancer patients is 32.4 months, 28.8 months, and 22.6 months for the years 2016 to 2019, 2013 to 2015, and 2004 to 2012 respectively.', 'The median overall survival (OS) for advanced colorectal cancer patients has improved over time:\n\n- For those diagnosed between 2004 and 2012, median OS was roughly stable at 22.6 months\n- For those diagnosed from 2013 to 2015, median OS improved to 28.8 months \n- Most recently, for patients diagnosed between 2016 to 2019, the median OS further increased to 32.4 months\n\nIn summary, the average median survival for advanced colorectal cancer patients diagnosed in recent years is around 32 months, representing a substantial improvement compared to earlier time periods.', 'The average median survival for advanced colorectal cancer (CRC) patients cannot be precisely determined from the provided text, as it presents data on overall survival (OS) improvements over time at a single institution, the University of Texas M.D. Anderson Cancer Center (UTMDACC). However, some key points can help approximate an answer: , 1. Median OS for de novo metastatic CRC patients at UTMDACC was 22.6 months for those diagnosed between 2004 and 2012., 2. For patients diagnosed from 2013 to 2015, the median OS improved to 28.8 months, and further increased to 32.4 months for those diagnosed from 2016 to 2019. , Considering these figures, a rough estimate of the average median survival for advanced CRC patients may fall between 22.6 and 32.4 months, with an understanding', 'The average median survival for advanced colorectal cancer patients has been improving over the years. It was roughly stable at 22.6 months for patients diagnosed between 2004 and 2012, improved to 28.8 months for those diagnosed in 2013 to 2015, and further improved to 32.4 months for those diagnosed in 2016 to 2019.', 'The average median survival for advanced colorectal cancer patients is between 12-20 months, however, this can vary based on many factors such as patient demographics, disease presentation, treatment response, and comorbidities.', 'The average median survival for advanced colorectal cancer patients has been improving over the years. For patients diagnosed between 2004 and 2012, the median overall survival (OS) was about 22.6 months. This improved to 28.8 months for those diagnosed between 2013 and 2015, and further increased to 32.4 months for those diagnosed between 2016 and 2019', 'The median time to worsening of the ECOG performance-status score from 0 or 1 to 2 or more was 9.3 months in the combination group and 6.3 months in the FTD-TPI group (hazard ratio, 0.54; 95% CI, 0.43 to 0.67).', 'The average median survival for patients with advanced colorectal cancer has slightly improved over the years. For those diagnosed between 2004 and 2012, the median overall survival (OS) was 22.6 months. However, there has been a steady increase in survival for more recently diagnosed patients. Those diagnosed between 2013 and 2015 had a median OS of 28.8 months, while those diagnosed between 2016 and 2019 experienced a further improvement in survival, with a median OS of 32.4 months. Therefore, on average, the median survival for advanced colorectal cancer patients is around 27-32 months, based on the most recent data.', "The average median survival for advanced colorectal cancer patients is around 65% in the United States, according to 2014 data. However, survival rates can vary significantly and depend on various factors, including the stage of the cancer, the effectiveness of treatment, and the patient's overall health. Median survival time for patients with inoperable liver metastases from colorectal cancer is 7.4 to 17 months. When combined with regimens such as FOLFOX or FOLFIRI, median survival rates have been increased to an average of 23 months.", 'The average median survival for advanced colorectal cancer patients has been improving, with it being 22.6 months for those diagnosed between 2004 and 2012, 28.8 months for those diagnosed between 2013 and 2015, and 32.4 months for those diagnosed between 2016 and 2019.', 'The average median survival for advanced colorectal cancer patients is 25 months, with hepatic metastases showing a median survival of 7 months and current patients having an expected median survival of 20 months.', 'Advanced or metastatic colorectal cancer is a deadly disease with poor prognosis. Median survival for such patients is around 22-24 months, however, with novel therapeutic interventions, its been improved slightly.', 'Based on the provided information, the median overall survival for patients with advanced colorectal cancer has been improving in recent years:\n\nFor patients diagnosed between 2004 and 2012, median overall survival was around 22.6 months. \n\nFor those diagnosed from 2013 to 2015, median overall survival increased to 28.8 months.\n\nMost recently, for patients diagnosed between 2016 and 2019, the median overall survival further improved to 32.4 months.\n\nSo in summary, while advanced colorectal cancer remains difficult to cure, treatment advances have extended median survival from under 2 years to nearly 3 years over the past 15 years. However, individual prognosis still depends on factors like extent of disease, treatment options, and overall health.', 'The average median survival for advanced colorectal cancer patients has improved from 22.6 months between 2004 and 2012 to 28.8 months for those diagnosed in 2013 to 2015, and further improved to 32.4 months for those diagnosed in 2016 to 2019', 'The average median survival for advanced colorectal cancer patients has steadily improved over the years. For patients diagnosed between 2004 and 2012, the median overall survival (OS) was roughly stable at 22.6 months. However, for those diagnosed in 2013 to 2015, the median OS improved to 28.8 months, and for those diagnosed in 2016 to 2019, the median OS further improved to 32.4 months.', 'The average median survival for advanced colorectal cancer patients is around 65% in the United States, according to 2014 data. However, the median overall survival for patients diagnosed between 2004 and 2012 was 22.6 months, but it has steadily improved for those diagnosed in 2013 to 2015 (28.8 months) and 2016 to 2019 (32.4 months).', 'The average median survival for advanced colorectal cancer patients is 20 months. The addition of ramicurumab to second-line therapy significantly improved median overall survival. Immunotherapy has shown promise in GI malignancies, with the combination of pembrolizumab and chemotherapy extending median survival in patients with advanced colorectal cancer to 21 months. KRAS gene mutation is a poor prognostic factor in colorectal cancer patients, and advanced age and high TNM stage are independent risk factors for postoperative outcome in early-stage colorectal cancer patients. Class II and III obesity is associated with a modestly increased risk of disease recurrence and death in colorectal cancer patients. Fluorouracil has been the mainstay of chemotherapy for advanced colorectal cancer for over 40 years, and its use has been shown to prolong time to disease progression and survival in these patients.', 'Based on the information provided, the median survival time for patients with advanced colorectal cancer, specifically those with liver metastases, ranges from approximately 6 to 17 months without treatment or with systemic chemotherapy alone. Some key findings:\n\n- Without treatment, median survival is around 7.4 to 11 months\n- With systemic chemotherapy, median survival improves modestly to around 12 months \n- Regional chemotherapy can further improve median survival to 15-17 months\n- More recent combination regimens like FOLFOX or FOLFIRI have increased median survival to around 23 months on average\n\nSo in summary, median survival for advanced colorectal cancer with liver metastases is quite poor, typically under 1.5 years, but modern chemotherapy regimens have improved this to almost 2 years. The exact median survival depends on the specific treatment approach.', " In summary, advanced colorectal cancer patients have varied survival outcomes depending on the extent and location of the disease, the patient's age, overall health status, and the effectiveness of available treatment options. Improvements in early detection and prompt initiation of appropriate chemoradiation regimens can help improve patient outcomes and reduce the need for extensive surgery and associated morbidity. ", '30 months is the average median survival for advanced colorectal cancer patients, however it can vary based on several factors such as patient age, general health status, treatment response and presence of metastatic disease.', 'The average median survival is close to 15 months and in best-case scenario approximately 40 months.', 'According to the abstracts, the average median survival for advanced colorectal cancer patients varies from study to study. In one study, the median overall survival was reported to be nearly 2 years (20 months). Another study found a median survival of 18 months with a range of 12-18 months. A third study reported a median survival of 24 months in untreated advanced colorectal cancer patients. Overall, the median survival for advanced colorectal cancer patients appears to range from approximately 18-24 months, with some studies reporting longer or shorter median survivals depending on the specific patient population and treatment regimens used.', 'The median survival for advanced colorectal cancer patients is 12-18 months.', 'Based on the provided snippets, it appears that the question refers to the median overall survival (OS) of advanced colorectal cancer patients. The snippets suggest a steady improvement in median OS over time. , The median OS was roughly stable at 22.6 months for patients diagnosed between 2004 and 2012. However, for those diagnosed between 2013 and 2015, the median OS improved to 28.8 months, and further increased to 32.4 months for patients diagnosed between 2016 and 2019. , To calculate the average median survival, we can take a weighted average of these values based on the number of years in each period. Assuming equal weights, the average median OS would be approximately (22.6 + 28.8 + 32.4) / 3 = 28.0 months. , Therefore, the average median survival for advanced colorectal cancer patients is roughly 28.0 months.', 'The average median survival for advanced colorectal cancer patients is approximately 20-24 months, but has shown improvement over time due to advancements in treatment strategies. However, exact values can vary between studies and patient groups.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36781990",
"http://www.ncbi.nlm.nih.gov/pubmed/1588370",
"http://www.ncbi.nlm.nih.gov/pubmed/22763194",
"http://www.ncbi.nlm.nih.gov/pubmed/7008761",
"http://www.ncbi.nlm.nih.gov/pubmed/15547753",
"http://www.ncbi.nlm.nih.gov/pubmed/10826427",
"http://www.ncbi.nlm.nih.gov/pubmed/3435011",
"http://www.ncbi.nlm.nih.gov/pubmed/32148114",
"http://www.ncbi.nlm.nih.gov/pubmed/12482332",
"http://www.ncbi.nlm.nih.gov/pubmed/34380826",
"http://www.ncbi.nlm.nih.gov/pubmed/22848257",
"http://www.ncbi.nlm.nih.gov/pubmed/30003196",
"http://www.ncbi.nlm.nih.gov/pubmed/36013160",
"http://www.ncbi.nlm.nih.gov/pubmed/33206858",
"http://www.ncbi.nlm.nih.gov/pubmed/31933846",
"http://www.ncbi.nlm.nih.gov/pubmed/29516930",
"http://www.ncbi.nlm.nih.gov/pubmed/36630020",
"http://www.ncbi.nlm.nih.gov/pubmed/37699362",
"http://www.ncbi.nlm.nih.gov/pubmed/11596040",
"http://www.ncbi.nlm.nih.gov/pubmed/30973370",
"http://www.ncbi.nlm.nih.gov/pubmed/32638384",
"http://www.ncbi.nlm.nih.gov/pubmed/29755763",
"http://www.ncbi.nlm.nih.gov/pubmed/16334762",
"http://www.ncbi.nlm.nih.gov/pubmed/38091773",
"http://www.ncbi.nlm.nih.gov/pubmed/14975808"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36781990",
"endSection": "abstract",
"offsetInBeginSection": 513,
"offsetInEndSection": 713,
"text": "Median OS was roughly stable for patients diagnosed between 2004 and 2012 (22.6 months) but since has steadily improved for those diagnosed in 2013 to 2015 (28.8 months), and 2016 to 2019 (32.4 months"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30973370",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1331,
"text": "OBJECTIVES: The survival of patients with metastatic colorectal cancer (CRC) has been increasing over recent decades due to improvements in chemotherapy and surgery. There is a need to refine prognostic information to more accurately predict survival as patients survive for any given length of time to assist multidisciplinary cancer management teams in treatment decisions.MATERIALS AND METHODS: We performed a single center retrospective analysis of patients treated with metastatic CRC (unresectable and resectable) who survived >24 months between 2005 and 2015 (N=155). Patient tumor and treatment related variables were collected. Overall survival (OS) estimates conditional on surviving >24 months were compared with actuarial survival estimates of a cohort of patients (33,104 resected, 39,382 unresected) from the National Cancer Database (NCDB).RESULTS: With a median follow-up of 44.2 months, the median OS of resected patients (n=86) was not reached. The median OS of unresected patients was 75.9 months. The conditional survival probabilities of living 1, 2, or 3 years longer after 24 months of survival are 92%, 72%, and 52%, respectively, in unresectable patients and 98%, 92%, and 89% in patients who were resected. The corresponding NCDB 1, 2, and 3 year actuarial survival was 38%, 20%, and 11% for unresected pa"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29516930",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1227,
"text": "CONTEXT: Colorectal cancers are frequent among cancers of gastrointestinal system. Whether there are any differences between survival in rectum and colon cancer patients is controversial.AIMS: In this study, we aimed to compare survival in surgically treated rectum and colon cancers and determine the factors affecting survival.SUBJECTS AND METHODS: The patients with colon and rectum cancer operated between 2009 and 2013 were examined retrospectively using prospective database. Patients were categorized as colon and rectum according to the tumor's location. Survival was identified as the primary outcome. Kaplan-Meier survival analysis and log-rank tests in survival assessment were used.RESULTS: One hundred and sixty-one patients with a mean age of 62.8 ± 12.7 years were included in the study. Male/female ratio was 1.6. Colon and rectum patients were counted as 92 (%57.1) and 69 (%42.9), respectively. Both groups were similar in demographic data (P > 0.05). It was observed that in 46 months (mean) of follow-up, 39.7% (n: 64) died, and 60.3% (n: 97) survived. Median survival time was 79 months, and 5-year cumulative survival rate was 60.8%. Five-year cumulative survival rates in stages for 1, 2, 3 and 4 were 88"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32638384",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1223,
"text": "Reported median overall survival (mOS) in metastatic colorectal cancer (mCRC) patients participating in systemic therapy trials has increased to over 30 months. It is uncertain whether trial results translate to real-life populations. Moreover, patients prefer presentation of multiple survival scenarios. Population-based data of all stage IV CRC patients diagnosed between 2008 and 2016 were obtained from the Netherlands Cancer Registry, which has a case ascertainment completeness surpassing 95%. We calculated the following percentiles (scenarios) of OS per year of diagnosis for the total population, and for treatment subgroups: 10th (best-case), 25th (upper-typical), 50th (median), 75th (lower-typical) and 90th (worst-case). Twenty-five percent of patients did not receive any antitumor treatment. From 2008 to 2016, mOS of the total population (n = 27275) remained unchanged at approximately 12 months. OS improved only for the upper-typical and best-case patients; by 4.2 to 29.1 months (P < .001), and by 6 to 62 months (P < .001), respectively. No clinically relevant change was observed among patients who received systemic therapy, with mOS close to 15 months and best-case scenario approximately 40 months."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34380826",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1019,
"text": "BACKGROUND: In this real-life practice study, we aimed to find whether elderly colorectal cancer (CRC) patients in our center were treated optimally and also if this has an effect on overall survival (OS) or not.METHODS: We have retrospectively screened 150 CRC patients older than 65 years, diagnosed in our institution between 2010 and 2018. As study variables, patient characteristics, tumor location, tumor, nodes, metastases stage, Eastern Cooperative Oncology Group performance status (ECOG PS), comorbidities, adjuvant or metastatic chemotherapy regimens, and treatment toxicity were recorded, and the OS rate of patients was assessed.RESULTS: The median age was 72 (range 65 - 89) years and 48 (32%) patients had metastatic disease at the time of diagnosis. The median OS (mOS) in the suboptimal adjuvant treatment group was 31.5 (range 20.7-42.3) months, whereas mOS was not reached during the median follow-up time in the optimal treatment group (P = 0.036). The addition of oxaliplatin to chemotherapy had no"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32148114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 863,
"text": "Background: The study aimed to assess the overall and stage-specific colorectal cancer (CRC) survival and to identify the prognostic factors for survival among Thai patients.Research design and methods: The retrospective data of CRC patients from a university hospital-based cancer registry from 2001 to 2014 were used to estimate five-year overall survival (OS). Kaplan-Meier method and log-rank tests were used to assess the differences in five-year OS by age at diagnosis, diagnostic period, tumor site, stage at diagnosis and treatment modalities. A multivariate Cox's proportional hazard model was used to identify independent prognostic factors for the OS.Results: A total of 1,507 (48%) colon and 1,648 (52%) rectal cancer patients were included. Five-year OS for CRC patients was 44%. It differed significantly by stage, age group, and treatment received."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33206858",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 758,
"text": "BACKGROUND: Hospital-based studies recently have shown increases in colorectal cancer survival, and better survival for women, young people, and patients diagnosed at an early disease stage.OBJECTIVE: To describe the overall survival and analyze the prognostic factors of patients treated for colorectal cancer at an oncology center.METHODS: The analysis included patients diagnosed with colon and rectal adenocarcinoma between 2000 and 2013 and identified in the Hospital Cancer Registry at A.C.Camargo Cancer Center. Overall 5-year survival was estimated using the Kaplan-Meier method, and prognostic factors were evaluated in a Cox regression model. Hazard ratios (HR) are reported with 95% confidence intervals (CI).RESULTS: Of 2,279 colorectal cancer ca"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29755763",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 942,
"text": "BACKGROUND: An aging population and a high incidence of colorectal cancer (CRC) in patients over the age of 80 make it important to understand survival times, hazard ratios and prognostic factors in this group. A better understanding of these factors will help clinicians determine appropriate therapeutic strategies for such patients, including when more aggressive treatment strategies may be preferred to palliative treatment.METHODS: A retrospective analysis of 619 CRC patients of ≥80 years of age from 1991-2010 at Baylor Scott & White Hospital in Temple, Texas. Twelve variables were analyzed through statistical analysis as potential prognostic factors for survival. Univariate and multivariate Cox proportional hazard models were used to determine hazard ratios. The elderly population was further stratified by age subgroup (80-84, 85-89, ≥90).RESULTS: Median survival time was 53.6, 30.0, and 11.3 months for age groups of 80-84, 8"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37699362",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1245,
"text": "Introduction Survival of patients suffering from metastatic colorectal cancer (mCRC) has increased over the last decades. These benefits appear to be restricted to patients aged 50 and above. However, among the population aged < 50, CRC incidence and mortality rates are significantly rising. The clinical benefit of treatment in this population still is a matter of debate. We aim to compare the clinical outcome between patients aged 50 and younger. Methods In this retrospective, observational study, we analyzed data from 1077 patients treated for mCRC at three cancer centers in Austria from January 2005 to December 2019. Patients were divided into two groups based on age at diagnosis: <50 years (eo-CRC) and >50 years (regular-onset CRC, ro-CRC). Propensity score matching was used to control for potential biases, and survival outcomes were compared between the two groups. Results The differences in tumor characteristics between eo-CRC and ro-CRC in the overall population were primarily related to tumor sidedness and disease-free survival following intended curative resection. Our data show that eo-CRC patients underwent metastases resection more often and received significantly more lines of treatment in the palliative setting."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36630020",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 855,
"text": "PURPOSE: The purpose of this study was to evaluate clinical outcomes of standard therapies in previously treated, advanced colorectal cancer (CRC) patients.METHODS: A systematic literature review was conducted in Embase, MEDLINE, and CENTRAL databases (January 2000-July 2021), annual oncology conferences (2019-2021), and clinicaltrials.gov to identify studies evaluating the use of licensed interventions in second-line or later settings. The primary outcome of interest was objective response rate (ORR) and secondary outcomes included progression-free survival (PFS) and overall survival (OS). ORR was pooled using the Freeman-Tukey double arcsine transformation. For survival outcomes, published Kaplan-Meier curves for OS and PFS were digitized to re-construct individual patient-level data and pooled following the methodology described by Combescu"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22848257",
"endSection": "abstract",
"offsetInBeginSection": 1018,
"offsetInEndSection": 1099,
"text": "The results showed the median survival of patients to be 24 months (range 16-42)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22848257",
"endSection": "abstract",
"offsetInBeginSection": 1018,
"offsetInEndSection": 1184,
"text": "The results showed the median survival of patients to be 24 months (range 16-42). One-year survival was found to be 65% while the 2-year survival was found to be 25%."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16334762",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 834,
"text": " median survival from the diagnosis of advanced/metastatic disease was 34.3 months. On"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22848257",
"endSection": "abstract",
"offsetInBeginSection": 1100,
"offsetInEndSection": 1395,
"text": "One-year survival was found to be 65% while the 2-year survival was found to be 25%. A satisfactory quality of life was also observed. In conclusion, colorectal cancer is a slow-going malignancy, as indicated by the long-term survival of patients and the biological characteristics of the tumor."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22848257",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 58,
"text": "Survival of untreated advanced colorectal cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12482332",
"endSection": "abstract",
"offsetInBeginSection": 797,
"offsetInEndSection": 998,
"text": "Recent randomized trials of first-line chemotherapy for metastatic colorectal cancer in which patients were likely to have access to all 3 effective drugs demonstrated median survivals of 18-20 months."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15547753",
"endSection": "abstract",
"offsetInBeginSection": 1112,
"offsetInEndSection": 1195,
"text": "Survival of all patients was as follows: median 25 months (range 16.1-33.9 months)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38091773",
"endSection": "abstract",
"offsetInBeginSection": 928,
"offsetInEndSection": 1032,
"text": "Median follow-up was 33 months (range 5-61) with a response rate of 63.6% and stable disease rate of 75%"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15547753",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1350,
"text": "Our primary objective was to determine the median and overall survival and secondarily the response rate to first- and second-line chemotherapy of patients with advanced colorectal metastatic disease. Three-hundred and seventy-nine patients (median age 60 years, range 30-87 years) were enrolled from April 1993 to March 2000. Median follow-up was 6 years (range 3-10 years), until July 2003. All patients were evaluable for survival and 342 were evaluable for response and toxicity. Thirty-seven patients did not undergo chemotherapy. All patients had confirmed histology as well as metastatic disease based on radiological tests. First-line treatment was administered to 342 patients: leucovorin (LV) 30 mg/m2 and 5-fluorouracil (5-FU) 425 mg/m2. Three different combinations were given as second-line treatment during different chronological periods: i) 5-FU, mitomycin-C and doxorubicin (FAM); ii) 5-FU and cisplatin (CDDP) and iii) 5-FU, LV and irinotecan (CPT-II). Responses were observed as follows: first-line treatment 16.37%, after FAM 25%, following 5-FU-CDDP 26.83% and after 5-FU-LV-CPT-II, 30.61%. Survival of all patients was as follows: median 25 months (range 16.1-33.9 months). The longest survival was of patients on 5-FU-LV-CPT-II. Median survival of patients with stable disease was 19 months and of untreated patients 12 months."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14975808",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 1589,
"text": "The last ten years allowed a rapid evolution for colon chemotherapy with a switch from 5-FU modulated by leucovorin to poly-chemotherapy (fluoropyrimidines with oxaliplatin or irinotecan) integrated into therapeutic strategies, where surgery had a place more and more important in metastatic patients. In correlation with these advances, median survival of patient with metastatic colorectal cancer is between 17 and 22 months. Targeted therapeutics with monoclonal antibody such as EGF inhibitors (cetuximab) or VEGF inhibitors (bevacizumab) had for the first time demonstrated efficacy with encouraging results in randomised trials. In adjuvant situation, LV5FU2 is less toxic than monthly FUFOL and no statistically significant difference could be detected in disease-free or overall survival between the two schedules. Oxaliplatin combined with 5 fluorouracil and leucovorin (FOLFOX4) is the first combination to demonstrate significant superiority over 5 fluorouracil and leucovorin in adjuvant treatment of colorectal cancer. Fluorouracil-based adjuvant chemotherapy benefited to patients with stage II or III colon cancer with microsatellite-stable tumours or tumour exhibiting low-frequency microsatellite instability but may be not those with tumours exhibiting high-frequency microsatellite instability (MSI). These data need to be confirmed by prospective studies before changing our therapeutic references."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1588370",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1653,
"text": "PURPOSE: The advantage of chemotherapy in asymptomatic patients with advanced colorectal cancer is debatable. Whether early chemotherapy improves survival and the length of the symptom-free period versus no therapy until symptoms appear was studied in a randomized trial.PATIENTS AND METHODS: A total of 183 patients with advanced, but asymptomatic colorectal cancer were randomly allocated to receive either initial treatment with sequential methotrexate 250 mg/m2 during the first 2 hours, and fluorouracil (5-FU) 500 mg/m2 at hours 3 and 23 followed by leucovorin rescue initiated at hour 24 (MFL) for 12 courses or to primary expectancy with chemotherapy not considered until symptoms appeared. One patient was ineligible and excluded from analysis. Nine patients did not fulfill the inclusion criteria and five patients refused treatment allocation; these patients were not excluded from the study population so as not to introduce bias. So far, 51 of 90 (60%) patients in the expectancy group have received chemotherapy.RESULTS: Overall survival was better in the MFL group than in the expectancy group (Breslow-Gehan, P less than .02; log-rank, P = .13) with a difference in median survival of approximately 5 months. Also the symptom-free period and the time to disease progression were longer in the MFL group (P less than .001), with median differences of 8 and 4 months, respectively. Toxicity to MFL treatment was low; however, three patients died because of toxicity--none of them should have received therapy because of poor performance or S-creatinine elevation. The patients maintained an excellent performance throughout the MFL treatme"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11596040",
"endSection": "abstract",
"offsetInBeginSection": 1208,
"offsetInEndSection": 1555,
"text": " trend was most pronounced for patients with colorectal carcinoma. At 5 years after the initial diagnosis, the remaining median survival was longest for patients with colorectal carcinoma, almost 6 years (71.5 months), followed by patients with lung carcinoma (52.5 months), breast carcinoma (42.5 months), and prostate carcinoma (34.5 months). Al"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11596040",
"endSection": "abstract",
"offsetInBeginSection": 1278,
"offsetInEndSection": 1669,
"text": "5 years after the initial diagnosis, the remaining median survival was longest for patients with colorectal carcinoma, almost 6 years (71.5 months), followed by patients with lung carcinoma (52.5 months), breast carcinoma (42.5 months), and prostate carcinoma (34.5 months). Although race was a correlate with initial survival, gender and age had more impact on late conditional survival.CON"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11596040",
"endSection": "abstract",
"offsetInBeginSection": 1208,
"offsetInEndSection": 1669,
"text": " trend was most pronounced for patients with colorectal carcinoma. At 5 years after the initial diagnosis, the remaining median survival was longest for patients with colorectal carcinoma, almost 6 years (71.5 months), followed by patients with lung carcinoma (52.5 months), breast carcinoma (42.5 months), and prostate carcinoma (34.5 months). Although race was a correlate with initial survival, gender and age had more impact on late conditional survival.CON"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11596040",
"endSection": "abstract",
"offsetInBeginSection": 1278,
"offsetInEndSection": 1863,
"text": "5 years after the initial diagnosis, the remaining median survival was longest for patients with colorectal carcinoma, almost 6 years (71.5 months), followed by patients with lung carcinoma (52.5 months), breast carcinoma (42.5 months), and prostate carcinoma (34.5 months). Although race was a correlate with initial survival, gender and age had more impact on late conditional survival.CONCLUSIONS: The conditional median survival provides useful and encouraging information for patients who survive with advanced disease and for healthcare professionals who treat these patients. Ho"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10826427",
"endSection": "abstract",
"offsetInBeginSection": 216,
"offsetInEndSection": 321,
"text": "ctively. Systemic chemotherapy produces a modest improvement to 48, 21, and 3 percent and 12 months, resp"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10826427",
"endSection": "abstract",
"offsetInBeginSection": 322,
"offsetInEndSection": 434,
"text": "ctively. Regional chemotherapy produces a further improvement to 64, 25, and 5 percent and 15 to 17 months, resp"
}
] | 13
|
BioASQ-training13b
| null | null |
66099907fdcbea915f000015
|
bioasq_factoid
|
yesno
|
Has the presence of delayed enhancement been documented in athletes performing strenuous exercise?
|
['yes']
|
[
"yes"
] |
There are contrasting literature data on the presence of delayed enhancement, as a sign of myocardial fibrosis, in healthy athletes. More studies are necessary to define the presence, incidence and severity, as well clinical and prognostic meaning, of delayed enhancement magnetic resonance in healthy athletes.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24029371",
"http://www.ncbi.nlm.nih.gov/pubmed/22160404",
"http://www.ncbi.nlm.nih.gov/pubmed/22798307",
"http://www.ncbi.nlm.nih.gov/pubmed/19427448",
"http://www.ncbi.nlm.nih.gov/pubmed/19332846",
"http://www.ncbi.nlm.nih.gov/pubmed/8902021",
"http://www.ncbi.nlm.nih.gov/pubmed/24326931"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24029371",
"endSection": "abstract",
"offsetInBeginSection": 1240,
"offsetInEndSection": 1491,
"text": "Atypical findings such as marked cardiac dilation, reduced deformation, or small patches of delayed gadolinium enhancement may be commonly encountered in well-trained athletes, but, at present, the prognostic significance of such findings is unknown. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22160404",
"endSection": "abstract",
"offsetInBeginSection": 1433,
"offsetInEndSection": 1648,
"text": "On CMR, DGE localized to the interventricular septum was identified in 5 of 39 athletes who had greater cumulative exercise exposure and lower RVEF (47.1 ± 5.9 vs. 51.1 ± 3.7%, P = 0.042) than those with normal CMR."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22798307",
"endSection": "abstract",
"offsetInBeginSection": 623,
"offsetInEndSection": 912,
"text": "Post-event cardiac MRI demonstrated the interval appearance of delayed enhancement of gadolinium at the inferior insertion of the right ventricle and in the interventricular septum-a novel finding that may represent subtle inflammation secondary to a combined exercise and altitude effect."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19427448",
"endSection": "abstract",
"offsetInBeginSection": 1335,
"offsetInEndSection": 1544,
"text": "No evidence of delayed enhancement of the left ventricular myocardium was found on CMR imaging, suggesting that the increase in cardiac biomarkers after the marathon may not have be due to myocardial necrosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19332846",
"endSection": "abstract",
"offsetInBeginSection": 1495,
"offsetInEndSection": 1891,
"text": "Of the 102 runners, five had a CAD pattern of LGE, and seven had a non-CAD pattern of LGE. The CAD pattern of LGE was located in the territory of the left anterior descending coronary artery more frequently than was the non-CAD pattern (P = .0027, Fisher exact test). The prevalence of LGE in runners was higher than that in age-matched control subjects (12% vs 4%; P = .077, McNemar exact test)."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015444",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008279",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D056352",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013177",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054874"
] |
[] |
531d34be267d7dd053000004
|
bioasq_yesno
|
factoid
|
What are common variants at 12q14 and 12q24 associated with?
|
['Hippocampal volume']
|
[
"Hippocampal volume",
"Hippocampus volume",
"Volume of the hippocampus",
"Hippocampal size",
"Hippocampal mass"
] |
["Common variants at 12q14 and 12q24 are associated with hippocampal volume. Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors.", 'Common variants at 12q14 and 12q24 are associated with hippocampal volume. As we age, our hippocampus (the part of the brain that is responsible for memory and cognition) becomes less and less efficient at storing information. As a result, the volume of the hippocampus shrinks.', 'Common variants at 12q14 and 12q24 are associated with hippocampal volume.', "Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors. Common variants at 12q14 and 12q24 are associated with hippocampal volume."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22504421",
"http://www.ncbi.nlm.nih.gov/pubmed/24361131"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22504421",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Common variants at 12q14 and 12q24 are associated with hippocampal volume."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22504421",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1271,
"text": "Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors. Our genome-wide association study (GWAS) of dementia-free persons (n = 9,232) identified 46 SNPs at four loci with P values of <4.0 × 10(-7). In two additional samples (n = 2,318), associations were replicated at 12q14 within MSRB3-WIF1 (discovery and replication; rs17178006; P = 5.3 × 10(-11)) and at 12q24 near HRK-FBXW8 (rs7294919; P = 2.9 × 10(-11)). Remaining associations included one SNP at 2q24 within DPP4 (rs6741949; P = 2.9 × 10(-7)) and nine SNPs at 9p33 within ASTN2 (rs7852872; P = 1.0 × 10(-7)); along with the chromosome 12 associations, these loci were also associated with hippocampal volume (P < 0.05) in a third younger, more heterogeneous sample (n = 7,794). The SNP in ASTN2 also showed suggestive association with decline in cognition in a largely independent sample (n = 1,563). These associations implicate genes related to apoptosis (HRK), development (WIF1), oxidative stress (MSR3B), ubiquitination (FBXW8) and neuronal migration (ASTN2), as well as enzymes targeted by new diabetes medications (DPP4), indicating new genetic influences on hippocampal size and possibly the risk of cognitive decline and dementia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24361131",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 231,
"text": "Recently, two large genome-wide association studies (GWASs) have identified several variants at 12q14 and 12q24 which are associated with hippocampal volume, one of the most important biological markers of Alzheimer's disease (AD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24361131",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "Recently, two large genome-wide association studies (GWASs) have identified several variants at 12q14 and 12q24 which are associated with hippocampal volume, one of the most important biological markers of Alzheimer's disease (AD). The"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22504421",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Common variants at 12q14 and 12q24 are associated with hippocampal volume"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22504421",
"endSection": "abstract",
"offsetInBeginSection": 485,
"offsetInEndSection": 809,
"text": "Remaining associations included one SNP at 2q24 within DPP4 (rs6741949; P = 2.9 × 10(-7)) and nine SNPs at 9p33 within ASTN2 (rs7852872; P = 1.0 × 10(-7)); along with the chromosome 12 associations, these loci were also associated with hippocampal volume (P < 0.05) in a third younger, more heterogeneous sample (n = 7,794)."
}
] | 11
|
BioASQ-training11b
| null | null |
60281eb11cb411341a0000f5
|
bioasq_factoid
|
factoid
|
Which resource is used for visualisation of non-covalent contacts?
|
['Protein Contacts Atlas']
|
[
"Protein Contacts Atlas",
"PCA",
"Protein Contact Atlas"
] |
['The Protein Contacts Atlas is an interactive resource of non-covalent contacts from over 100,000 PDB crystal structures. The Protein Contacts Atlas enables researchers from different disciplines to investigate diverse questions in the framework of non-covalent contacts, including the interpretation of allostery, disease mutations and polymorphisms, by exploring individual subunits, interfaces, and protein-ligand contacts and by mapping external information. The Protein Contacts Atlas is available at http://www.mrc-lmb.cam.ac.uk/pca/ and also through PDBe.', 'The Protein Contacts Atlas is an interactive resource of non-covalent contacts at different scales of organization: atoms, residues, secondary structures, secondary structure, subunits, and entire complexes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29335563"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29335563",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Visualization and analysis of non-covalent contacts using the Protein Contacts Atlas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29335563",
"endSection": "abstract",
"offsetInBeginSection": 381,
"offsetInEndSection": 1152,
"text": "We present the Protein Contacts Atlas, an interactive resource of non-covalent contacts from over 100,000 PDB crystal structures. We developed multiple representations for visualization and analysis of non-covalent contacts at different scales of organization: atoms, residues, secondary structure, subunits, and entire complexes. The Protein Contacts Atlas enables researchers from different disciplines to investigate diverse questions in the framework of non-covalent contacts, including the interpretation of allostery, disease mutations and polymorphisms, by exploring individual subunits, interfaces, and protein-ligand contacts and by mapping external information. The Protein Contacts Atlas is available at http://www.mrc-lmb.cam.ac.uk/pca/ and also through PDBe."
}
] | 11
|
BioASQ-training11b
| null | null |
605fb19794d57fd879000038
|
bioasq_factoid
|
yesno
|
Are CTCF and BORIS involved in genome regulation and cancer?
|
['yes']
|
[
"yes"
] |
['Yes. CTCF is ubiquitously expressed and plays diverse roles in gene regulation, imprinting, insulation, intra/interchromosomal interactions, nuclear compartmentalisation, and alternative splicing. CTCF has a single paralogue, the testes-specific CTCF-like gene (CTCFL)/BORIS. CTCF and BORIS can be deregulated in cancer. The tumour suppressor gene CTCF can be mutated or deleted in cancer, or CTCF DNA binding can be altered by epigenetic changes. BORIS is aberrantly expressed frequently in cancer, leading some to propose a pro-tumourigenic role for BORIS. However, BORIS can inhibit cell proliferation, and is mutated in cancer similarly to CTCF suggesting BORIS activation in cancer may be due to global genetic or epigenetic changes typical of malignant transformation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"http://www.ncbi.nlm.nih.gov/pubmed/21465478",
"http://www.ncbi.nlm.nih.gov/pubmed/17962299",
"http://www.ncbi.nlm.nih.gov/pubmed/16140944",
"http://www.ncbi.nlm.nih.gov/pubmed/16140943",
"http://www.ncbi.nlm.nih.gov/pubmed/23390377",
"http://www.ncbi.nlm.nih.gov/pubmed/12191639",
"http://www.ncbi.nlm.nih.gov/pubmed/21811597"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "abstract",
"offsetInBeginSection": 61,
"offsetInEndSection": 829,
"text": "CTCF is ubiquitously expressed and plays diverse roles in gene regulation, imprinting, insulation, intra/interchromosomal interactions, nuclear compartmentalisation, and alternative splicing. CTCF has a single paralogue, the testes-specific CTCF-like gene (CTCFL)/BORIS. CTCF and BORIS can be deregulated in cancer. The tumour suppressor gene CTCF can be mutated or deleted in cancer, or CTCF DNA binding can be altered by epigenetic changes. BORIS is aberrantly expressed frequently in cancer, leading some to propose a pro-tumourigenic role for BORIS. However, BORIS can inhibit cell proliferation, and is mutated in cancer similarly to CTCF suggesting BORIS activation in cancer may be due to global genetic or epigenetic changes typical of malignant transformation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21465478",
"endSection": "abstract",
"offsetInBeginSection": 768,
"offsetInEndSection": 1104,
"text": " The investigation of the molecular mechanisms engaged by CTCF to modulate tumor-related genes emphasizes the cell-type dependency of its tumor suppressor role. Indeed, the ability of CTCF to bind their promoters strictly depends by cell-type features as DNA methylation, BORIS-binding and post-translational modifications as PARYlation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17962299",
"endSection": "abstract",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1368,
"text": "Moreover, reduction of CTCF in normally BORIS-negative human fibroblasts resulted in derepression of BORIS promoters. These results provide a mechanistic basis for understanding cancer-related associations between haploinsufficiency of CTCF and BORIS derepression, and between the lack of functional p53 and aberrant activation of BORIS"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "CTCF and BORIS in genome regulation and cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12191639",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "The novel BORIS + CTCF gene family is uniquely involved in the epigenetics of normal biology and cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16140944",
"endSection": "abstract",
"offsetInBeginSection": 2164,
"offsetInEndSection": 2444,
"text": "Collectively, these data indicate that reciprocal binding of CTCF and BORIS to the NY-ESO-1 promoter mediates epigenetic regulation of this CT gene in lung cancer cells, and suggest that induction of BORIS may be a novel strategy to augment immunogenicity of pulmonary carcinomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23390377",
"endSection": "abstract",
"offsetInBeginSection": 428,
"offsetInEndSection": 564,
"text": "BORIS is the only known paralog of CTCF, a gene intimately involved in genomic imprinting, chromatin insulation, and nuclear regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "abstract",
"offsetInBeginSection": 824,
"offsetInEndSection": 1039,
"text": "However, BORIS can inhibit cell proliferation, and is mutated in cancer similarly to CTCF suggesting BORIS activation in cancer may be due to global genetic or epigenetic changes typical of malignant transformation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16140943",
"endSection": "abstract",
"offsetInBeginSection": 2361,
"offsetInEndSection": 2523,
"text": "We suggest that BORIS is likely tethering epigenetic machinery to a novel class of CTCF/BORIS 11ZF target sequences that mediate induction of cancer-testis genes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "CTCF and BORIS in genome regulation and cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16140943",
"endSection": "abstract",
"offsetInBeginSection": 2361,
"offsetInEndSection": 2523,
"text": "We suggest that BORIS is likely tethering epigenetic machinery to a novel class of CTCF/BORIS 11ZF target sequences that mediate induction of cancer-testis genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21811597",
"endSection": "abstract",
"offsetInBeginSection": 471,
"offsetInEndSection": 623,
"text": "Unlike CTCF, BORIS expression has been reported only in the testis and certain malignancies, leading to its classification as a \"cancer-testis\" antigen."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "CTCF and BORIS in genome regulation and cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16140943",
"endSection": "abstract",
"offsetInBeginSection": 2361,
"offsetInEndSection": 2523,
"text": "We suggest that BORIS is likely tethering epigenetic machinery to a novel class of CTCF/BORIS 11ZF target sequences that mediate induction of cancer-testis genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21811597",
"endSection": "abstract",
"offsetInBeginSection": 471,
"offsetInEndSection": 623,
"text": "Unlike CTCF, BORIS expression has been reported only in the testis and certain malignancies, leading to its classification as a \"cancer-testis\" antigen."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "CTCF and BORIS in genome regulation and cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "CTCF and BORIS in genome regulation and cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "CTCF and BORIS in genome regulation and cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "CTCF and BORIS in genome regulation and cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24657531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "CTCF and BORIS in genome regulation and cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12191639",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "The novel BORIS + CTCF gene family is uniquely involved in the epigenetics of normal biology and cancer."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
56a375f8496b62f23f000002
|
bioasq_yesno
|
factoid
|
Is APOBEC3B protein predominantly cytoplasmic or nuclear?
|
[[' nuclear']]
|
[
"nuclear",
"nucleus",
"nuclear envelope",
"nuclear membrane",
"nuclear material",
"nuclear DNA",
"nuclear pore",
"nuclear acid"
] |
['Contrary to other APOBEC family members, APOBEC3B was found to predominantly concentrate to the cell nucleus.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22446380",
"http://www.ncbi.nlm.nih.gov/pubmed/21715505",
"http://www.ncbi.nlm.nih.gov/pubmed/23388464",
"http://www.ncbi.nlm.nih.gov/pubmed/23389445",
"http://www.ncbi.nlm.nih.gov/pubmed/18667511",
"http://www.ncbi.nlm.nih.gov/pubmed/16648136"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22446380",
"endSection": "abstract",
"offsetInBeginSection": 350,
"offsetInEndSection": 418,
"text": "A3B is the only family member with steady-state nuclear localization"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22446380",
"endSection": "abstract",
"offsetInBeginSection": 420,
"offsetInEndSection": 685,
"text": "Here, we show that A3B nuclear import is an active process requiring at least one amino acid (Val54) within an N-terminal motif analogous to the nuclear localization determinant of the antibody gene diversification enzyme AID (activation-induced cytosine deaminase)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22446380",
"endSection": "abstract",
"offsetInBeginSection": 1067,
"offsetInEndSection": 1238,
"text": "Our studies suggest that the present-day A3B enzyme retained the nuclear import mechanism of an ancestral AID protein during the expansion of the APOBEC3 locus in primates"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715505",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 322,
"text": "However, we found that the predominantly nuclear A3B only weakly restricted infection by HIV-1, HIV-1Δvif, and human T-cell leukemia virus type 1 (HTLV-1), while significantly inhibiting LINE-1 retrotransposition"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715505",
"endSection": "abstract",
"offsetInBeginSection": 517,
"offsetInEndSection": 887,
"text": "In contrast to the exclusively cytoplasmic A3G, which is inactive against LINE-1 retrotransposition, the A3G/B protein, while localized mainly to the cytoplasm, was also present in the nucleus. Further mutational analysis revealed that residues 18, 19, 22, and 24 in A3B were the major determinants for nuclear versus cytoplasmic localization and antiretroviral activity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715505",
"endSection": "abstract",
"offsetInBeginSection": 1465,
"offsetInEndSection": 1705,
"text": "these observations suggest that changing 4 residues in the amino terminus of A3B not only retargets the protein from the nucleus to the cytoplasm but also enhances its ability to restrict HIV while retaining inhibition of retrotransposition"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23388464",
"endSection": "abstract",
"offsetInBeginSection": 904,
"offsetInEndSection": 999,
"text": "After mitosis, APOBEC3B becomes nuclear, and APOBEC3D, APOBEC3F and APOBEC3G become cytoplasmic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18667511",
"endSection": "abstract",
"offsetInBeginSection": 365,
"offsetInEndSection": 508,
"text": "To define the domains of APOBEC3G that determine cytoplasmic localization, comparisons were made with APOBEC3B, which is predominantly nuclear."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16648136",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 674,
"text": "The mechanism of L1 inhibition did not correlate with an obvious subcellular protein distribution as APOBEC3B appeared predominantly nuclear and APOBEC3F was mostly cytosolic."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22446380",
"endSection": "abstract",
"offsetInBeginSection": 350,
"offsetInEndSection": 418,
"text": "A3B is the only family member with steady-state nuclear localization"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22446380",
"endSection": "abstract",
"offsetInBeginSection": 420,
"offsetInEndSection": 685,
"text": "Here, we show that A3B nuclear import is an active process requiring at least one amino acid (Val54) within an N-terminal motif analogous to the nuclear localization determinant of the antibody gene diversification enzyme AID (activation-induced cytosine deaminase)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23389445",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 832,
"text": "Endogenous APOBEC3B protein is predominantly nuclear and the only detectable source of DNA C-to-U editing activity in breast cancer cell-line extracts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16648136",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 673,
"text": "The mechanism of L1 inhibition did not correlate with an obvious subcellular protein distribution as APOBEC3B appeared predominantly nuclear and APOBEC3F was mostly cytosolic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18667511",
"endSection": "abstract",
"offsetInBeginSection": 365,
"offsetInEndSection": 507,
"text": "To define the domains of APOBEC3G that determine cytoplasmic localization, comparisons were made with APOBEC3B, which is predominantly nuclear"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16648136",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 673,
"text": "The mechanism of L1 inhibition did not correlate with an obvious subcellular protein distribution as APOBEC3B appeared predominantly nuclear and APOBEC3F was mostly cytosolic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23389445",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 832,
"text": "Endogenous APOBEC3B protein is predominantly nuclear and the only detectable source of DNA C-to-U editing activity in breast cancer cell-line extracts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18667511",
"endSection": "abstract",
"offsetInBeginSection": 365,
"offsetInEndSection": 507,
"text": "To define the domains of APOBEC3G that determine cytoplasmic localization, comparisons were made with APOBEC3B, which is predominantly nuclear"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16648136",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 673,
"text": "The mechanism of L1 inhibition did not correlate with an obvious subcellular protein distribution as APOBEC3B appeared predominantly nuclear and APOBEC3F was mostly cytosolic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23389445",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 832,
"text": "Endogenous APOBEC3B protein is predominantly nuclear and the only detectable source of DNA C-to-U editing activity in breast cancer cell-line extracts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18667511",
"endSection": "abstract",
"offsetInBeginSection": 365,
"offsetInEndSection": 507,
"text": "To define the domains of APOBEC3G that determine cytoplasmic localization, comparisons were made with APOBEC3B, which is predominantly nuclear"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16648136",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 673,
"text": "The mechanism of L1 inhibition did not correlate with an obvious subcellular protein distribution as APOBEC3B appeared predominantly nuclear and APOBEC3F was mostly cytosolic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23389445",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 832,
"text": "Endogenous APOBEC3B protein is predominantly nuclear and the only detectable source of DNA C-to-U editing activity in breast cancer cell-line extracts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23388464",
"endSection": "abstract",
"offsetInBeginSection": 904,
"offsetInEndSection": 999,
"text": "After mitosis, APOBEC3B becomes nuclear, and APOBEC3D, APOBEC3F and APOBEC3G become cytoplasmic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18667511",
"endSection": "abstract",
"offsetInBeginSection": 365,
"offsetInEndSection": 507,
"text": "To define the domains of APOBEC3G that determine cytoplasmic localization, comparisons were made with APOBEC3B, which is predominantly nuclear"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16648136",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 673,
"text": "The mechanism of L1 inhibition did not correlate with an obvious subcellular protein distribution as APOBEC3B appeared predominantly nuclear and APOBEC3F was mostly cytosolic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23389445",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 832,
"text": "Endogenous APOBEC3B protein is predominantly nuclear and the only detectable source of DNA C-to-U editing activity in breast cancer cell-line extracts"
}
] | 5
|
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/ABC3B_HUMAN"
] |
[] |
54e0ace81388e8454a000010
|
bioasq_factoid
|
yesno
|
Can capivasertib be used for breast cancer?
|
['yes']
|
[
"yes"
] |
['Yes. Capivasertib is effective and be used for treatment of breast cancer']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37046675",
"http://www.ncbi.nlm.nih.gov/pubmed/36901954",
"http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"http://www.ncbi.nlm.nih.gov/pubmed/35398754",
"http://www.ncbi.nlm.nih.gov/pubmed/36508589"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36508589",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Capivasertib Doubles PFS in Some Breast Cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36508589",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 311,
"text": "In the phase III CAPItello-291 study, the combination of fulvestrant and capivasertib more than doubled progression-free survival compared with fulvestrant alone in patients with hormone receptor-positive, HER2-negative breast cancer who have developed resistance to aromatase inhibitors and CDK4/6 inhibitors. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37046675",
"endSection": "abstract",
"offsetInBeginSection": 633,
"offsetInEndSection": 1189,
"text": "In this setting of high unmet need, several clinical trials of novel drugs have recently reported encouraging results: the addition of the AKT-inhibitor capivasertib to fulvestrant demonstrated a significant improvement in progression-free survival (PFS); the oral selective estrogen receptor degrader (SERD) elacestrant prolonged PFS compared to traditional ET in a phase 3 trial, particularly among patients with detectable ESR1 mutations; finally, PARP inhibitors are available treatment options for patients with pathogenic BRCA1/2 germline mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"endSection": "abstract",
"offsetInBeginSection": 2088,
"offsetInEndSection": 2418,
"text": "CONCLUSIONS: Capivasertib-fulvestrant therapy resulted in significantly longer progression-free survival than treatment with fulvestrant alone among patients with hormone receptor-positive advanced breast cancer whose disease had progressed during or after previous aromatase inhibitor therapy with or without a CDK4/6 inhibitor. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Capivasertib in Hormone Receptor-Positive Advanced Breast Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35398754",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 53,
"text": "\"The emerging role of capivasertib in breast cancer\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"endSection": "abstract",
"offsetInBeginSection": 2094,
"offsetInEndSection": 2422,
"text": "SIONS: Capivasertib-fulvestrant therapy resulted in significantly longer progression-free survival than treatment with fulvestrant alone among patients with hormone receptor-positive advanced breast cancer whose disease had progressed during or after previous aromatase inhibitor therapy with or without a CDK4/6 inhibitor. (Fun"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"endSection": "abstract",
"offsetInBeginSection": 255,
"offsetInEndSection": 1646,
"text": "re limited.METHODS: In a phase 3, randomized, double-blind trial, we enrolled eligible pre-, peri-, and postmenopausal women and men with hormone receptor-positive, human epidermal growth factor receptor 2-negative advanced breast cancer who had had a relapse or disease progression during or after treatment with an aromatase inhibitor, with or without previous cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor therapy. Patients were randomly assigned in a 1:1 ratio to receive capivasertib plus fulvestrant or placebo plus fulvestrant. The dual primary end point was investigator-assessed progression-free survival assessed both in the overall population and among patients with AKT pathway-altered (PIK3CA, AKT1, or PTEN) tumors. Safety was assessed.RESULTS: Overall, 708 patients underwent randomization; 289 patients (40.8%) had AKT pathway alterations, and 489 (69.1%) had received a CDK4/6 inhibitor previously for advanced breast cancer. In the overall population, the median progression-free survival was 7.2 months in the capivasertib-fulvestrant group, as compared with 3.6 months in the placebo-fulvestrant group (hazard ratio for progression or death, 0.60; 95% confidence interval [CI], 0.51 to 0.71; P<0.001). In the AKT pathway-altered population, the median progression-free survival was 7.3 months in the capivasertib-fulvestrant group, as compared with 3.1 months in the"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 257,
"text": "BACKGROUND: Capivasertib, an AKT inhibitor, added to fulvestrant, was previously reported to improve progression-free survival in women with aromatase inhibitor-resistant oestrogen receptor (ER)-positive, HER2-negative advanced breast cancer. The benefit ap"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "BACKGROUND: Capivasertib, an AKT inhibitor, added to fulvestrant, was previously reported to improve progression-free survival in women with aromatase inhibitor-resistant oestrogen receptor (ER)-positive, HER2-negative advanced breast cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 241,
"text": "Capivasertib, an AKT inhibitor, added to fulvestrant, was previously reported to improve progression-free survival in women with aromatase inhibitor-resistant oestrogen receptor (ER)-positive, HER2-negative advanced breast cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36901954",
"endSection": "abstract",
"offsetInBeginSection": 357,
"offsetInEndSection": 635,
"text": "Among these, the PIK3CA isoform-specific inhibitor alpelisib and the pan-AKT inhibitor capivasertib were recently approved in combination with the estrogen receptor degrader fulvestrant for the treatment of ER+ advanced breast cancer after progression on an aromatase inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"endSection": "abstract",
"offsetInBeginSection": 4246,
"offsetInEndSection": 4453,
"text": "RETATION: Updated FAKTION data showed that capivasertib addition to fulvestrant extends the survival of participants with aromatase inhibitor-resistant ER-positive, HER2-negative advanced breast cancer. The "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36508589",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 310,
"text": "In the phase III CAPItello-291 study, the combination of fulvestrant and capivasertib more than doubled progression-free survival compared with fulvestrant alone in patients with hormone receptor-positive, HER2-negative breast cancer who have developed resistance to aromatase inhibitors and CDK4/6 inhibitors."
}
] | 13
|
BioASQ-training13b
| null | null |
65cfe1d21930410b1300002a
|
bioasq_yesno
|
factoid
|
What type of enzyme is peroxiredoxin 2 (PRDX2)?
|
['antioxidant']
|
[
"antioxidant",
"free radical scavenger",
"oxidation inhibitor",
"redox agent",
"antioxidative agent"
] |
Peroxiredoxin 2 (PRDX2) is an antioxidant enzyme that uses cysteine residues to decompose peroxides.
Peroxiredoxin-2 (PRDX2), an enzyme reducing hydrogen peroxide and lipid peroxides
Peroxiredoxin 2 (Prx2) is a thiol-dependent peroxidase.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23889121",
"http://www.ncbi.nlm.nih.gov/pubmed/23749642",
"http://www.ncbi.nlm.nih.gov/pubmed/22989627",
"http://www.ncbi.nlm.nih.gov/pubmed/22916248",
"http://www.ncbi.nlm.nih.gov/pubmed/21902453",
"http://www.ncbi.nlm.nih.gov/pubmed/21248284",
"http://www.ncbi.nlm.nih.gov/pubmed/20646000",
"http://www.ncbi.nlm.nih.gov/pubmed/19969073",
"http://www.ncbi.nlm.nih.gov/pubmed/19812325",
"http://www.ncbi.nlm.nih.gov/pubmed/19375361",
"http://www.ncbi.nlm.nih.gov/pubmed/18479207",
"http://www.ncbi.nlm.nih.gov/pubmed/18222042",
"http://www.ncbi.nlm.nih.gov/pubmed/17522089",
"http://www.ncbi.nlm.nih.gov/pubmed/17105810",
"http://www.ncbi.nlm.nih.gov/pubmed/12943237"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23889121",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 108,
"text": "Peroxiredoxin-2 (PRDX-2) is an antioxidant and chaperone-like protein critical for cell function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23749642",
"endSection": "abstract",
"offsetInBeginSection": 215,
"offsetInEndSection": 349,
"text": "We found that the antioxidant enzyme peroxiredoxin-2 (Prx2) inversely correlated with the metastatic capacity of human melanoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22989627",
"endSection": "abstract",
"offsetInBeginSection": 51,
"offsetInEndSection": 248,
"text": "The aim of this study was to examine gonadotropin regulation of antioxidant enzyme sulfiredoxin (Srx) and peroxiredoxin 2 (PRDX2) expressions and modification during the ovulatory process in rats. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22916248",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1392,
"text": "The mRNA profiler array showed more than 2-fold differential expression of 32 oxidative stress-related genes in unstimulated moDCs, including peroxiredoxin-2 (PRDX2), an enzyme reducing hydrogen peroxide and lipid peroxides. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21902453",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 254,
"text": "Peroxiredoxin-2 (Prx-2) is an abundant mammalian enzyme that protects against oxidative stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21248284",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Peroxiredoxin 2 (PRDX2) has been known to act as an antioxidant enzyme whose main function is H(2)O(2) reduction in cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21083423",
"endSection": "abstract",
"offsetInBeginSection": 1067,
"offsetInEndSection": 1347,
"text": "These data indicate that Srx1 activity protects mice from the lethality of endotoxic shock, adding this enzyme to other host factors, as NRF2 and peroxiredoxin 2, which by regulating cellular reactive oxygen species levels act as important modifiers in the pathogenesis of sepsis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20646000",
"endSection": "abstract",
"offsetInBeginSection": 639,
"offsetInEndSection": 722,
"text": "One of the identified proteins was peroxiredoxin 2 (Prx2), an anti-oxidant enzyme. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19969073",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "Peroxiredoxin-2 (Prdx2), a potent peroxide reductant, is the third most abundant protein in the erythrocyte and might be expected to play a major role in the cell's oxidative defenses. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19812325",
"endSection": "abstract",
"offsetInBeginSection": 819,
"offsetInEndSection": 940,
"text": "Importantly, we also demonstrate the antioxidant enzyme Prx2 (peroxiredoxin 2) as a critical cytoplasmic target of cdk5. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19375361",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Human erythrocyte peroxiredoxin 2 (Prx2) is a typical 2-cys cytosolic peroxiredoxin with thiol-dependent hydrogen peroxide scavenger activity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18479207",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Peroxiredoxin 2 (Prx2) is an antioxidant enzyme that uses cysteine residues to decompose peroxides."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18222042",
"endSection": "abstract",
"offsetInBeginSection": 860,
"offsetInEndSection": 1077,
"text": "Peroxiredoxin 2 (PRDX2), an antioxidant enzyme, was the most upregulated while tribbles homolog 3 (TRB3), a pro-apoptotic protein, was the most downregulated, implying a beneficial effect of lithium on neuronal cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17522089",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 352,
"text": "After 5 Gy irradiation, the relative abundance of peroxiredoxin 2, an antioxidant enzyme, and latexin, an inhibitor of carboxypeptidase, increased. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17105810",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Peroxiredoxin 2 (Prx2), a thiol-dependent peroxidase, is the third most abundant protein in the erythrocyte, and its absence in knock-out mice gives rise to hemolytic anemia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12943237",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 340,
"text": "Suppression subtractive hybridization performed on Down syndrome (DS) versus control fetal brains revealed differential expression of peroxiredoxin 2 (PRDX2), mapped at 13q12. Peroxiredoxins are antioxidant enzymes involved in protein and lipid protection against oxidative injury and in cellular signalling pathways regulating apoptosis. T"
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054464",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004798"
] |
[] |
52bf1f1303868f1b06000014
|
bioasq_factoid
|
factoid
|
Which is the most common type of pediatric cerebellar tumor?
|
[['Medulloblastoma']]
|
[
"Medulloblastoma",
"MB",
"medulloblastoma tumor",
"medulloblastoma cancer",
"primitive neuroectodermal tumor (PNET)"
] |
['Medulloblastoma is the most common malignant cerebellar tumor seen in the pediatric age group, which has a known ability to metastasize extraneurally.', 'Medulloblastoma is a malignant cerebellar tumor seen primarily in the pediatric age group that has a known ability to metastasize extraneurally ', 'Medulloblastoma is a malignant cerebellar tumor seen primarily in the pediatric age group that has a known ability to metastasize extraneurally ', 'Medulloblastoma is a malignant cerebellar tumor seen primarily in the pediatric age group that has a known ability to metastasize extraneurally ', 'Medulloblastoma is a malignant cerebellar tumor seen primarily in the pediatric age group that has a known ability to metastasize extraneurally ', 'Medulloblastoma is a malignant cerebellar tumor seen primarily in the pediatric age group that has a known ability to metastasize extraneurally ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21681603",
"http://www.ncbi.nlm.nih.gov/pubmed/6502196",
"http://www.ncbi.nlm.nih.gov/pubmed/16479172",
"http://www.ncbi.nlm.nih.gov/pubmed/23951168",
"http://www.ncbi.nlm.nih.gov/pubmed/21315459",
"http://www.ncbi.nlm.nih.gov/pubmed/9447621",
"http://www.ncbi.nlm.nih.gov/pubmed/25499213"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21681603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "Medulloblastoma (MDB) is the most common malignant cerebellar tumor in children"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6502196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Medulloblastoma is a malignant cerebellar tumor seen primarily in the pediatric age group that has a known ability to metastasize extraneurally"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16479172",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "Medulloblastoma (MB) is the most common malignant pediatric brain tumor which is thought to originate from cerebellar granule cell precursors (CGNPs) that fail to properly exit the cell cycle and differentiate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21681603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Medulloblastoma (MDB) is the most common malignant cerebellar tumor in children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23951168",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Medulloblastoma, the most common pediatric brain tumor, is thought to arise from deregulated proliferation of cerebellar granule precursor (CGP) cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16479172",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "Medulloblastoma (MB) is the most common malignant pediatric brain tumor which is thought to originate from cerebellar granule cell precursors (CGNPs) that fail to properly exit the cell cycle and differentiate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16479172",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "Medulloblastoma (MB) is the most common malignant pediatric brain tumor which is thought to originate from cerebellar granule cell precursors (CGNPs) that fail to properly exit the cell cycle and differentiate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16479172",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "Medulloblastoma (MB) is the most common malignant pediatric brain tumor which is thought to originate from cerebellar granule cell precursors (CGNPs) that fail to properly exit the cell cycle and differentiate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21681603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Medulloblastoma (MDB) is the most common malignant cerebellar tumor in children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23951168",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Medulloblastoma, the most common pediatric brain tumor, is thought to arise from deregulated proliferation of cerebellar granule precursor (CGP) cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23951168",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Medulloblastoma, the most common pediatric brain tumor, is thought to arise from deregulated proliferation of cerebellar granule precursor (CGP) cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21315459",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 284,
"text": "Medulloblastoma (MB) is the most common malignant pediatric brain tumor and is thought to arise from genetic anomalies in developmental pathways required for the normal maturation of the cerebellar cortex, notably developmental pathways for granule cell progenitor (GCP) neurogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21681603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "Medulloblastoma (MDB) is the most common malignant cerebellar tumor in children"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6502196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Medulloblastoma is a malignant cerebellar tumor seen primarily in the pediatric age group that has a known ability to metastasize extraneurally"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9447621",
"endSection": "abstract",
"offsetInBeginSection": 438,
"offsetInEndSection": 624,
"text": "Most adult brain tumors are supratentorial malignant gliomas, whereas the most common malignant pediatric brain tumor is the cerebellar primitive neuroectodermal tumor (medulloblastoma)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21681603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Medulloblastoma (MDB) is the most common malignant cerebellar tumor in children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25499213",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Mouse models have increased our understanding of the pathogenesis of medulloblastoma (MB), the most common malignant pediatric brain tumor that often forms in the cerebellum"
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002528",
"http://www.disease-ontology.org/api/metadata/DOID:5059"
] |
[] |
55376f19bc4f83e82800000c
|
bioasq_factoid
|
factoid
|
What nerve is affected in Carpel Tunnel syndrome?
|
['median']
|
[
"median",
"median value",
"middle value",
"50th percentile"
] |
['Carpel tunnel syndrome (CTS) is a condition in which median nerve compression results in paresthesias and pain in the wrist and hand.', 'Carpel tunnel syndrome is a common compression neuropathy of the median nerve causing pain, numbness and functional dysfunction of the hand.', 'Carpal tunnel syndrome (CTS) is a medical condition due to compression of the median nerve as it travels through the wrist at the carpal tunnel.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24886455",
"http://www.ncbi.nlm.nih.gov/pubmed/31762916",
"http://www.ncbi.nlm.nih.gov/pubmed/19454094",
"http://www.ncbi.nlm.nih.gov/pubmed/7085815",
"http://www.ncbi.nlm.nih.gov/pubmed/2307889",
"http://www.ncbi.nlm.nih.gov/pubmed/3627450",
"http://www.ncbi.nlm.nih.gov/pubmed/19800329",
"http://www.ncbi.nlm.nih.gov/pubmed/17985535",
"http://www.ncbi.nlm.nih.gov/pubmed/26721028",
"http://www.ncbi.nlm.nih.gov/pubmed/32459879",
"http://www.ncbi.nlm.nih.gov/pubmed/11111843",
"http://www.ncbi.nlm.nih.gov/pubmed/16487634",
"http://www.ncbi.nlm.nih.gov/pubmed/23727345",
"http://www.ncbi.nlm.nih.gov/pubmed/29766936",
"http://www.ncbi.nlm.nih.gov/pubmed/29430500",
"http://www.ncbi.nlm.nih.gov/pubmed/28334999",
"http://www.ncbi.nlm.nih.gov/pubmed/497808"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32459879",
"endSection": "abstract",
"offsetInBeginSection": 325,
"offsetInEndSection": 487,
"text": "An ultrasound evaluation of the carpal tunnel can assess for pathologic changes of the median nerve, detect secondary causes of CTS, and aid in surgical planning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29430500",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Carpel tunnel syndrome (CTS) is a condition in which median nerve compression results in paresthesias and pain in the wrist and hand."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31762916",
"endSection": "abstract",
"offsetInBeginSection": 215,
"offsetInEndSection": 392,
"text": "All patients underwent ultrasound with measurement of the surface of the median nerve at the entrance of the carpal tunnel and electroneuromyographic examination of both wrists."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26721028",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 152,
"text": "Carpel tunnel syndrome is a common compression neuropathy of the median nerve causing pain, numbness and functional dysfunction of the hand."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26721028",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "BACKGROUND: Carpel tunnel syndrome is a common compression neuropathy of the median nerve causing pain, numbness and functional dysfunction of the hand."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26721028",
"endSection": "abstract",
"offsetInBeginSection": 1190,
"offsetInEndSection": 1310,
"text": "SION: Open carpel tunnel release surgery is an effective procedure for compression neuropathy of the median nerve. It sh"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19800329",
"endSection": "abstract",
"offsetInBeginSection": 547,
"offsetInEndSection": 785,
"text": "Carpel tunnel release surgery (CTRS) was performed and in the stimulation group of patients, stainless steel electrode wires placed alongside the median nerve proximal to the surgical decompression site for immediate 1 h 20 Hz bipolar ES."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26721028",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "BACKGROUND: Carpel tunnel syndrome is a common compression neuropathy of the median nerve causing pain, numbness and functional dysfunction "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29766936",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Background: Carpal tunnel syndrome refers to a constellation of symptoms resulting from compression of the median nerve "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29430500",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "Carpel tunnel syndrome (CTS) is a condition in which median nerve compression results in paresthesias and pain in the wrist and hand. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17985535",
"endSection": "abstract",
"offsetInBeginSection": 559,
"offsetInEndSection": 783,
"text": "nslated these findings to human patients by examining the number of reinnervated motor units in the median nerve-innervated thenar muscles before and after carpel tunnel release surgery in a randomized controlled trial. Moto"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19800329",
"endSection": "abstract",
"offsetInBeginSection": 554,
"offsetInEndSection": 794,
"text": "tunnel release surgery (CTRS) was performed and in the stimulation group of patients, stainless steel electrode wires placed alongside the median nerve proximal to the surgical decompression site for immediate 1 h 20 Hz bipolar ES. Subjects"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23727345",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 334,
"text": "OBJECTIVES: To provide a quantitative analysis of ultrasonographic measurements and possible pathophysiology of carpal tunnel syndrome by comparing cross-sectional areas of the median nerve, carpal tunnel, and nerve/tunnel index and the difference in ultrasonographic findings between affected and nonaffected hands and between sexes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11111843",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 397,
"text": "We studied the SSR evoked by electrical stimulation of the median nerve and recording from the contralateral hands in 30 patients with carpal tunnel syndrome (CTS) without clinical autonomic signs and compared the results to the SSR in 30 normal controls."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3627450",
"endSection": "abstract",
"offsetInBeginSection": 214,
"offsetInEndSection": 489,
"text": "This pattern is consistent with compression of both the anterior and posterior aspects of the median nerve in the carpal tunnel because nerve fibers responsible for thenar, lumbrical, and digit 2 functions lie in an anterior-posterior gradient within the distal median nerve."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23727345",
"endSection": "abstract",
"offsetInBeginSection": 988,
"offsetInEndSection": 1429,
"text": "RESULTS: Comparison between normative (n=24) and abnormal hands (n=78) revealed the following: the mean proximal cross-sectional areas of the median nerve, carpal tunnel, and nerve/tunnel index of electrodiagnostically normative hands were 10.941mm(2), 192.43mm(2), and 5.635%, respectively, whereas those of abnormal hands were 13.74mm(2), 208.87mm(2), and 6.693%, respectively, showing statistically significant differences for all (P<.05)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16487634",
"endSection": "abstract",
"offsetInBeginSection": 813,
"offsetInEndSection": 901,
"text": "Sympathetic vasomotor fibres of the median nerve are affected in carpal tunnel syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16487634",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 301,
"text": "The sympathetic vasomotor fibres of the median nerve were evaluated in patients with carpal tunnel syndrome and in healthy volunteers using continuous wave Doppler ultrasonography."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19454094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "INTRODUCTION: Carpal tunnel syndrome is a neuropathy caused by compression of the median nerve within the carpal tunnel."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26721028",
"endSection": "abstract",
"offsetInBeginSection": 1199,
"offsetInEndSection": 1307,
"text": "n carpel tunnel release surgery is an effective procedure for compression neuropathy of the median nerve. It"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24886455",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "BACKGROUND: Carpal tunnel syndrome (CTS) is a common condition (prevalence of 4%) where the median nerve is compressed within the carpal tunnel resulting in numbness, tingling, and pain "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29766936",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "Background: Carpal tunnel syndrome refers to a constellation of symptoms resulting from compression of the median nerve a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7085815",
"endSection": "abstract",
"offsetInBeginSection": 253,
"offsetInEndSection": 513,
"text": "The carpal tunnel syndrome usually affects women aged between 40 and 60 years, and presents typically as parasthesia of the fingers, mainly at night, in the regions served by the median nerve, sometimes associated with hypoesthesia and difficulty in movements."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/497808",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "The carpal tunnel syndrome: localization of conduction abnormalities within the distal segment of the median nerve."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2307889",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Location of impaired sensory conduction of the median nerve in carpal tunnel syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28334999",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Carpal tunnel syndrome is the most common entrapment neuropathy, affecting the median nerve at the wrist."
}
] | 11
|
BioASQ-training11b
| null | null |
601eaac81cb411341a000051
|
bioasq_factoid
|
yesno
|
Is Omaveloxolone effective for Friedreich Ataxia?
|
['yes']
|
[
"yes"
] |
['Yes. Omaveloxolone is effective and approved for Friedreich Ataxia.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33430645",
"http://www.ncbi.nlm.nih.gov/pubmed/37219716",
"http://www.ncbi.nlm.nih.gov/pubmed/38020600",
"http://www.ncbi.nlm.nih.gov/pubmed/34845147",
"http://www.ncbi.nlm.nih.gov/pubmed/37691319",
"http://www.ncbi.nlm.nih.gov/pubmed/36708320",
"http://www.ncbi.nlm.nih.gov/pubmed/33068037",
"http://www.ncbi.nlm.nih.gov/pubmed/38043492",
"http://www.ncbi.nlm.nih.gov/pubmed/30065630",
"http://www.ncbi.nlm.nih.gov/pubmed/37155124"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33068037",
"endSection": "abstract",
"offsetInBeginSection": 1587,
"offsetInEndSection": 1796,
"text": "INTERPRETATION: In the MOXIe trial, omaveloxolone significantly improved neurological function compared to placebo and was generally safe and well tolerated. It represents a potential therapeutic agent in FA. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33430645",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 57,
"text": "Omaveloxolone: potential new agent for Friedreich ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33430645",
"endSection": "abstract",
"offsetInBeginSection": 517,
"offsetInEndSection": 786,
"text": "In this work, we review the evidence for use of omaveloxolone in FRDA from recent clinical trials. Though not at present approved for any indication, the present data suggest that this agent acting though increases in Nrf2 activity may provide a novel therapy for FRDA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38020600",
"endSection": "abstract",
"offsetInBeginSection": 366,
"offsetInEndSection": 506,
"text": "Omaveloxolone has been recently approved as the first pharmacological treatment for FRDA in adults and adolescents aged 16 years and older. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37691319",
"endSection": "abstract",
"offsetInBeginSection": 1450,
"offsetInEndSection": 1684,
"text": "INTERPRETATION: These results suggest a meaningful slowing of Friedreich ataxia progression with omaveloxolone, and consequently detail how propensity-matched analysis may contribute to understanding of effects of therapeutic agents. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37155124",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 230,
"text": "Omaveloxolone (SKYCLARYS™) is an orally active, small molecule semi-synthetic triterpenoid drug that increases antioxidant activity, which is being developed by Reata Pharmaceuticals, Inc. for the treatment of Friedreich's ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37155124",
"endSection": "abstract",
"offsetInBeginSection": 588,
"offsetInEndSection": 685,
"text": "Omaveloxolone was approved in February 2023 in the USA for the treatment of Friedreich's ataxia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37219716",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "A Milestone in the Treatment of Ataxias: Approval of Omaveloxolone for Friedreich Ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37219716",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 310,
"text": "The exciting news about the US FDA approval of omaveloxolone as the first-ever drug to be approved for an inherited ataxia is welcome news for patients and families that deal with this devastating disease as well as for health care providers and investigators with an interest in this and other rare diseases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38043492",
"endSection": "abstract",
"offsetInBeginSection": 475,
"offsetInEndSection": 703,
"text": "Currently, the FDA has approved the Nrf2 activators dimethyl fumarate (DMF) and Omaveloxolone (Omav) as novel first-line oral drugs for the treatment of patients with relapsing forms of multiple sclerosis and Friedreich's ataxia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37691319",
"endSection": "abstract",
"offsetInBeginSection": 1466,
"offsetInEndSection": 1682,
"text": "These results suggest a meaningful slowing of Friedreich ataxia progression with omaveloxolone, and consequently detail how propensity-matched analysis may contribute to understanding of effects of therapeutic agents"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37155124",
"endSection": "abstract",
"offsetInBeginSection": 685,
"offsetInEndSection": 882,
"text": "This article summarizes the milestones in the development of omaveloxolone leading to this first approval for the treatment of Friedreich's ataxia in adults and adolescents aged 16 years and older."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36708320",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Omaveloxolone: an activator of Nrf2 for the treatment of Friedreich ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34845147",
"endSection": "abstract",
"offsetInBeginSection": 278,
"offsetInEndSection": 401,
"text": "ars.RECENT FINDINGS: Recently, the use of omaveloxolone for 2 years significantly improved upright stability in Friedreich'"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38043492",
"endSection": "abstract",
"offsetInBeginSection": 555,
"offsetInEndSection": 716,
"text": "Omaveloxolone (Omav) as novel first-line oral drugs for the treatment of patients with relapsing forms of multiple sclerosis and Friedreich's ataxia. A promising"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30065630",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1770,
"text": "Friedreich's Ataxia (FRDA) is an autosomal recessive neurodegenerative disorder, affecting dorsal root ganglia (DRG), cerebellar dentate nuclei and heart. It is caused by a GAA repeat expansion mutation within the frataxin gene (FXN). This impedes FXN transcription resulting in a progressive decrease of the mitochondrial protein, frataxin. Increased oxidative stress leading to a chronic depletion of endogenous antioxidants affects the survival of the cells and causes neurodegeneration. In particular, cerebellar granule neurons (CGNs) show a significant increase of reactive oxygen species (ROS), lipid peroxidation and lower level of reduced glutathione (GSH). In FRDA, one of the major pathways of oxidant scavengers, the Nrf2 antioxidant pathway, is defective. Previous studies on FRDA-like CGNs showed that the reduced level of frataxin and the oxidative stress induce mitochondrial impairments. By triggering the Nrf2 endogenous pathway pharmacologically we determined whether this could promote mitochondrial fitness and counteract oxidative stress. In this work, we sought to investigate the beneficial effect of a promising Nrf2-inducer, omaveloxolone (omav), in CGNs from two FRDA mouse models, KIKO and YG8R, and human fibroblasts from patients. We found that CGNs from both KIKO and YG8R presented Complex I deficiency and that omav was able to restore substrate availability and Complex I activity. This was also confirmed in human primary fibroblasts from FRDA patients. Although fibroblasts are not the major tissue affected, we found that they show significant differences recapitulating the disease; this is therefore an important tool to investigate patients' pathophysiology. Interestingly, we found that patient fibroblasts had an increased level"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36708320",
"endSection": "abstract",
"offsetInBeginSection": 710,
"offsetInEndSection": 1020,
"text": "In the present report, we have reviewed the basic and clinical literature on Nrf2 deficiency in FRDA, and evidence for the benefit of omaveloxolone.EXPERT OPINION: The present perspective suggests that omaveloxolone is a rational and efficacious therapy that is possibly disease modifying in treatment of FRDA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38043492",
"endSection": "abstract",
"offsetInBeginSection": 475,
"offsetInEndSection": 704,
"text": "Currently, the FDA has approved the Nrf2 activators dimethyl fumarate (DMF) and Omaveloxolone (Omav) as novel first-line oral drugs for the treatment of patients with relapsing forms of multiple sclerosis and Friedreich's ataxia."
}
] | 13
|
BioASQ-training13b
| null | null |
65d12c451930410b13000032
|
bioasq_yesno
|
factoid
|
Which molecule is inhibited by encorafenib?
|
['BRAF']
|
[
"BRAF",
"B-Raf",
"B-Raf proto-oncogene",
"B-Raf kinase",
"B-Raf protein",
"B-Raf serine/threonine-protein kinase"
] |
['Encorafenib is a BRAF inhibitor. It is a promising therapy for metastatic or inoperable melanoma with a BRAF mutation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31050693",
"http://www.ncbi.nlm.nih.gov/pubmed/27116335",
"http://www.ncbi.nlm.nih.gov/pubmed/31114933",
"http://www.ncbi.nlm.nih.gov/pubmed/28640105",
"http://www.ncbi.nlm.nih.gov/pubmed/29326440",
"http://www.ncbi.nlm.nih.gov/pubmed/30122982",
"http://www.ncbi.nlm.nih.gov/pubmed/30018031",
"http://www.ncbi.nlm.nih.gov/pubmed/28277830",
"http://www.ncbi.nlm.nih.gov/pubmed/29568360",
"http://www.ncbi.nlm.nih.gov/pubmed/29356698",
"http://www.ncbi.nlm.nih.gov/pubmed/26673799",
"http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"http://www.ncbi.nlm.nih.gov/pubmed/29903896",
"http://www.ncbi.nlm.nih.gov/pubmed/26586345",
"http://www.ncbi.nlm.nih.gov/pubmed/29573941",
"http://www.ncbi.nlm.nih.gov/pubmed/28611198",
"http://www.ncbi.nlm.nih.gov/pubmed/29210065",
"http://www.ncbi.nlm.nih.gov/pubmed/29155017",
"http://www.ncbi.nlm.nih.gov/pubmed/30117021"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29155017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Encorafenib (LGX818) is a promising BRAFV600E inhibitor that has efficacy against metastatic melanoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29210065",
"endSection": "abstract",
"offsetInBeginSection": 654,
"offsetInEndSection": 915,
"text": "Using patient- and in vivo-derived melanoma cell lines with acquired BRAFi resistance, we show that combined treatment with the BRAFi encorafenib and HDACi panobinostat in 2D and 3D culture systems synergistically induced caspase-dependent apoptotic cell death."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29326440",
"endSection": "abstract",
"offsetInBeginSection": 894,
"offsetInEndSection": 1184,
"text": "Importantly, combination of the BRAF inhibitors (BRAFi) vemurafenib (PLX4032), dabrafenib, or encorafenib with inhibitors dually targeting the EGFR and HER2 (such as lapatinib, canertinib, and afatinib) significantly reduced the metabolic activity and proliferative potential of CRC cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29356698",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 304,
"text": "PURPOSE OF REVIEW: To describe the pharmacological properties, preclinical and clinical data of the novel V-Raf Murine Sarcoma Viral Oncogene Homolog B (BRAF)-inhibitor encorafenib (LGX818) and to compare these with established BRAF-inhibitors in the treatment of locally advanced or metastatic melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29573941",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 326,
"text": "We investigated encorafenib, a BRAF inhibitor with unique target-binding properties, alone or in combination with the MEK inhibitor binimetinib, versus vemurafenib in patients with advanced BRAFV600-mutant melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29568360",
"endSection": "abstract",
"offsetInBeginSection": 611,
"offsetInEndSection": 777,
"text": "In this study, we identify the antifolate methotrexate (MTX) as a sensitizer of acquired- and intrinsically-resistant MM cells to BRAFi's dabrafenib and encorafenib. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29903896",
"endSection": "abstract",
"offsetInBeginSection": 528,
"offsetInEndSection": 949,
"text": "We assembled a panel of melanoma cell lines with class IIa (activation segment) or IIb (p-loop) mutations and compared these with WT or V600E/K BRAF mutant cells. Cell lines and PDXs were treated with BRAFi (vemurafenib, dabrafenib, encorafenib, and LY3009120), MEKi (cobimetinib, trametinib, and binimetinib), or the combination. We identified 2 patients with BRAF L597S metastatic melanoma who were treated with dMAPKi."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30018031",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "The FDA approved the BRAF/MEK inhibitor combination encorafenib/binimetinib for patients with metastatic or inoperable melanoma with a BRAF V600E or V600K mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30117021",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Encorafenib (Braftovi™), a BRAF inhibitor, and binimetinib (Mektovi®), a MEK inhibitor, are two orally bioavailable drugs developed by Array BioPharma. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Encorafenib in combination with binimetinib for unresectable or metastatic melanoma with BRAF mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "abstract",
"offsetInBeginSection": 1354,
"offsetInEndSection": 1491,
"text": "Encorafenib plus binimetinib seems likely to emerge as a valuable therapeutic alternative to established BRAF/MEK inhibitor combinations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "abstract",
"offsetInBeginSection": 952,
"offsetInEndSection": 1185,
"text": "This improved efficacy may be related to the distinct pharmacokinetics of encorafenib, with prolonged binding to the target molecule providing greater BRAF inhibition and increased potency compared with other drugs in the same class."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29573941",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Encorafenib plus binimetinib versus vemurafenib or encorafenib in patients with BRAF-mutant melanoma (COLUMBUS): a multicentre, open-label, randomised phase 3 trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29573941",
"endSection": "abstract",
"offsetInBeginSection": 3189,
"offsetInEndSection": 3296,
"text": "Encorafenib plus binimetinib could represent a new treatment option for patients with BRAF-mutant melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "abstract",
"offsetInBeginSection": 450,
"offsetInEndSection": 599,
"text": "Areas covered: Encorafenib in combination with bimetinib offers a new approach that may offer benefits over existing BRAF/MEK inhibitor combinations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26586345",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Encorafenib (LGX818) is a new-generation BRAF inhibitor that is under evaluation in clinical trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "abstract",
"offsetInBeginSection": 600,
"offsetInEndSection": 884,
"text": "Expert Opinion: While other BRAF/MEK inhibitor combinations have achieved a median overall survival (OS) of 22 months, patients with advanced BRAF mutation-positive melanoma treated with encorafenib plus binimetinib achieved a median OS of 33.6 months in the phase III COLUMBUS trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29155017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Encorafenib (LGX818) is a promising BRAF __sup__ V600E __end_sup__ inhibitor that has efficacy against metastatic melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28611198",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Purpose: Encorafenib, a selective BRAF inhibitor (BRAFi), has a pharmacologic profile that is distinct from that of other clinically active BRAFis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29356698",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "Development of encorafenib for BRAF-mutated advanced melanoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31050693",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "Encorafenib and binimetinib for the treatment of BRAF V600E/K-mutated melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31050693",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 415,
"text": "Encorafenib (LGX-818, Braftovi) and binimetinib (MEK-162, Mektovi) are small-molecule inhibitors of BRAF and MEK, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31050693",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 432,
"text": "Encorafenib ( LGX-818 , Braftovi ) and binimetinib ( MEK-162 , Mektovi ) are small-molecule inhibitors of BRAF and MEK , respectively . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30122982",
"endSection": "abstract",
"offsetInBeginSection": 275,
"offsetInEndSection": 566,
"text": "With advances in RAF inhibitors and second-generation inhibitors including encorafenib and vemurafenib , which have been approved for treating BRAF-V600E malignancies , the combinatorial therapeutic strategies of RAF inhibitors elicit remarkable responses in patients with BRAF-V600E mCRC . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "abstract",
"offsetInBeginSection": 921,
"offsetInEndSection": 1157,
"text": "This improved efficacy may be related to the distinct pharmacokinetics of encorafenib , with prolonged binding to the target molecule providing greater BRAF inhibition and increased potency compared with other drugs in the same class . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31050693",
"endSection": "abstract",
"offsetInBeginSection": 563,
"offsetInEndSection": 776,
"text": "Of these inhibitors , encorafenib and binimetinib are the newest combination , which received approval by the Food and Drug Administration ( FDA ) for the treatment of BRAF V600E/K-mutated melanoma in June 2018 . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31114933",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "Encorafenib, a new-generation BRAF inhibitor, has been approved by FDA for the treatment of melanoma in combination with binimetinib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31050693",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 416,
"text": "Encorafenib (LGX-818, Braftovi) and binimetinib (MEK-162, Mektovi) are small-molecule inhibitors of BRAF and MEK, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31050693",
"endSection": "abstract",
"offsetInBeginSection": 546,
"offsetInEndSection": 754,
"text": "Of these inhibitors, encorafenib and binimetinib are the newest combination, which received approval by the Food and Drug Administration (FDA) for the treatment of BRAF V600E/K-mutated melanoma in June 2018."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31050693",
"endSection": "abstract",
"offsetInBeginSection": 754,
"offsetInEndSection": 910,
"text": "This review will focus on the preclinical pharmacology, pharmacokinetics and clinical utility of encorafenib and binimetinib in BRAF V600-mutated melanoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26586345",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Encorafenib (LGX818), a potent BRAF inhibitor, induces senescence accompanied by autophagy in BRAFV600E melanoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26586345",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Encorafenib (LGX818) is a new-generation BRAF inhibitor that is under evaluation in clinical trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "abstract",
"offsetInBeginSection": 916,
"offsetInEndSection": 1150,
"text": "This improved efficacy may be related to the distinct pharmacokinetics of encorafenib, with prolonged binding to the target molecule providing greater BRAF inhibition and increased potency compared with other drugs in the same class."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "abstract",
"offsetInBeginSection": 564,
"offsetInEndSection": 849,
"text": "Expert opinion: While other BRAF/MEK inhibitor combinations have achieved a median overall survival (OS) of 22 months, patients with advanced BRAF mutation-positive melanoma treated with encorafenib plus binimetinib achieved a median OS of 33.6 months in the phase III COLUMBUS trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "abstract",
"offsetInBeginSection": 414,
"offsetInEndSection": 564,
"text": "Areas covered: Encorafenib in combination with bimetinib offers a new approach that may offer benefits over existing BRAF/MEK inhibitor combinations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27116335",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 908,
"text": "We report three male patients with metastatic BRAFV600E-mutated melanoma who developed pyogenic granulomas 16, 10, and 12 weeks after treatment initiation with the selective BRAF inhibitors vemurafenib or encorafenib (LGX818)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28640105",
"endSection": "abstract",
"offsetInBeginSection": 651,
"offsetInEndSection": 763,
"text": "Treatment started in November 2015, with Encorafenib and Binimetinib, new BRAF and MEK inhibitors, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26673799",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 1052,
"text": "Second-line efficacy of the pan-PI3K inhibitor BKM120 with either BRAF (encorafenib)/MEK (binimetinib) inhibitor combination or the ERK inhibitor VX-11e was confirmed in vivo Amplification of MET was observed in 3 PDX models, a higher frequency than expected and a possible novel mechanism of resistance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28277830",
"endSection": "abstract",
"offsetInBeginSection": 375,
"offsetInEndSection": 619,
"text": "Areas covered: A brief review of current BRAF, NRAS, and C-KIT inhibitors provides background for a thorough review of newly developed agents namely binimetinib, a MEK inhibitor, encorafenib a BRAF inhibitor, and masitinib which inhibits C-KIT."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28611198",
"endSection": "abstract",
"offsetInBeginSection": 879,
"offsetInEndSection": 1081,
"text": "Results: Preclinical data demonstrated that encorafenib inhibited BRAF V600E kinase activity with a prolonged off-rate and suppressed proliferation and tumor growth of BRAF V600E-mutant melanoma models."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30652516",
"endSection": "abstract",
"offsetInBeginSection": 916,
"offsetInEndSection": 1149,
"text": "This improved efficacy may be related to the distinct pharmacokinetics of encorafenib, with prolonged binding to the target molecule providing greater BRAF inhibition and increased potency compared with other drugs in the same class."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28611198",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Phase I Dose-Escalation and -Expansion Study of the BRAF Inhibitor Encorafenib (LGX818) in Metastatic "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28611198",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Purpose: Encorafenib, a selective BRAF inhibitor (BRAFi), has a pharmacologic profile that is distinct from that of other clinically active BRAFis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28611198",
"endSection": "abstract",
"offsetInBeginSection": 148,
"offsetInEndSection": 267,
"text": "We evaluated encorafenib in a phase I study in patients with BRAFi treatment-naïve and pretreated BRAF-mutant melanoma."
}
] | 11
|
BioASQ-training11b
| null | null |
5e319789fbd6abf43b00004a
|
bioasq_factoid
|
factoid
|
What is targeted by monoclonal antibody Pembrolizumab?
|
[['programmed cell death 1']]
|
[
"programmed cell death 1",
"PD-1",
"CD279",
"PDCD1",
"programmed cell death protein 1"
] |
['Pembrolizumab inhibits the programmed cell death 1 (PD-1) immune checkpoint and has antitumor activity in patients with advanced melanoma. Pembrolizumab is approved by the US Food and Drug Administration for the treatment of advanced melanoma, and additional regulatory approvals are expected across the oncologic spectrum for a variety of other agents that target these pathways.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24685885",
"http://www.ncbi.nlm.nih.gov/pubmed/25605845",
"http://www.ncbi.nlm.nih.gov/pubmed/25891173",
"http://www.ncbi.nlm.nih.gov/pubmed/26028255",
"http://www.ncbi.nlm.nih.gov/pubmed/25828465",
"http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"http://www.ncbi.nlm.nih.gov/pubmed/25034862"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24685885",
"endSection": "abstract",
"offsetInBeginSection": 343,
"offsetInEndSection": 742,
"text": "gents currently in active clinical development for lung cancer include ipilimumab, which modulates the cytotoxic T-lymphocyte-associated antigen 4 pathway, and multiple agents targeting the programmed death protein 1 (PD-1) pathway, both anti-PD-1 compounds (nivolumab, pembrolizumab [MK-3475]) and those that target programmed death ligand 1 (PD-L1), a key ligand for PD-1 (BMS-936559, MPDL3280A). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25605845",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 503,
"text": "Ipilimumab (CTLA-4) and pembrolizumab (PD-1) are approved by the US Food and Drug Administration for the treatment of advanced melanoma, and additional regulatory approvals are expected across the oncologic spectrum for a variety of other agents that target these pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25891173",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 264,
"text": "Pembrolizumab inhibits the programmed cell death 1 (PD-1) immune checkpoint and has antitumor activity in patients with advanced melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25891173",
"endSection": "abstract",
"offsetInBeginSection": 1740,
"offsetInEndSection": 1936,
"text": "CONCLUSIONS: The anti-PD-1 antibody pembrolizumab prolonged progression-free survival and overall survival and had less high-grade toxicity than did ipilimumab in patients with advanced melanoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028255",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 483,
"text": "METHODS: We conducted a phase 2 study to evaluate the clinical activity of pembrolizumab, an anti-programmed death 1 immune checkpoint inhibitor, in 41 patients with progressive metastatic carcinoma with or without mismatch-repair deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028255",
"endSection": "abstract",
"offsetInBeginSection": 2170,
"offsetInEndSection": 2306,
"text": "CONCLUSIONS: This study showed that mismatch-repair status predicted clinical benefit of immune checkpoint blockade with pembrolizumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25828465",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "The anti programmed cell death-1 (PD-1) antibodies pembrolizumab and nivolumab have been recently licensed by the Food and Drug Administration for the treatment of advanced melanoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25828465",
"endSection": "abstract",
"offsetInBeginSection": 407,
"offsetInEndSection": 564,
"text": "We describe for the first time the case of an adult patient who developed autoimmune diabetes likely as a consequence of PD-1 inhibition with pembrolizumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 999,
"offsetInEndSection": 1219,
"text": "Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"endSection": "abstract",
"offsetInBeginSection": 507,
"offsetInEndSection": 692,
"text": "Pembrolizumab, a humanized highly selective IgG4 anti-PD-1 monoclonal antibody, was recently approved for the treatment of advanced melanoma based on promising early-phase clinical data"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25034862",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Anti-programmed-death-receptor-1 treatment with pembrolizumab in ipilimumab-refractory advanced melanoma: a randomised dose-comparison cohort of a phase 1 trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25891173",
"endSection": "abstract",
"offsetInBeginSection": 1525,
"offsetInEndSection": 1936,
"text": "Efficacy was similar in the two pembrolizumab groups. Rates of treatment-related adverse events of grade 3 to 5 severity were lower in the pembrolizumab groups (13.3% and 10.1%) than in the ipilimumab group (19.9%).CONCLUSIONS: The anti-PD-1 antibody pembrolizumab prolonged progression-free survival and overall survival and had less high-grade toxicity than did ipilimumab in patients with advanced melanoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25034862",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 777,
"text": "BACKGROUND: The anti-programmed-death-receptor-1 (PD-1) antibody pembrolizumab has shown potent antitumour activity at different doses and schedules in patients with melanoma. We compared the efficacy and safety of pembrolizumab at doses of 2 mg/kg and 10 mg/kg every 3 weeks in patients with ipilimumab-refractory advanced melanoma.METHODS: In an open-label, international, multicentre expansion cohort of a phase 1 trial, patients (aged ?18 years) with advanced melanoma whose disease had progressed after at least two ipilimumab doses were randomly assigned with a computer-generated allocation schedule (1:1 final ratio) to intravenous pembrolizumab at 2 mg/kg every 3 weeks or 10 mg/kg every 3 weeks until disease progression, intolerable toxicity, or consent withdrawal. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 840,
"text": "Pembrolizumab, a humanized highly selective IgG4 anti-PD-1 monoclonal antibody, was recently approved for the treatment of advanced melanoma based on promising early-phase clinical data. Encouraging results have also been seen in other malignancies, and PD-1-targeted therapies are likely to markedly change the treatment landscape."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 840,
"text": "Pembrolizumab, a humanized highly selective IgG4 anti-PD-1 monoclonal antibody, was recently approved for the treatment of advanced melanoma based on promising early-phase clinical data. Encouraging results have also been seen in other malignancies, and PD-1-targeted therapies are likely to markedly change the treatment landscape."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 840,
"text": "Pembrolizumab, a humanized highly selective IgG4 anti-PD-1 monoclonal antibody, was recently approved for the treatment of advanced melanoma based on promising early-phase clinical data. Encouraging results have also been seen in other malignancies, and PD-1-targeted therapies are likely to markedly change the treatment landscape."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000911"
] |
[] |
56c1f01aef6e394741000043
|
bioasq_factoid
|
yesno
|
Can CD55 deficiency cause thrombosis?
|
['yes']
|
[
"yes"
] |
['Yes, loss of CD55 is associated with thrombosis in patients with Paroxysmal nocturnal hemoglobinuria. CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26205796",
"http://www.ncbi.nlm.nih.gov/pubmed/23020629",
"http://www.ncbi.nlm.nih.gov/pubmed/22696589",
"http://www.ncbi.nlm.nih.gov/pubmed/22077430",
"http://www.ncbi.nlm.nih.gov/pubmed/25237200",
"http://www.ncbi.nlm.nih.gov/pubmed/28657829",
"http://www.ncbi.nlm.nih.gov/pubmed/11843289",
"http://www.ncbi.nlm.nih.gov/pubmed/23765390",
"http://www.ncbi.nlm.nih.gov/pubmed/27812245",
"http://www.ncbi.nlm.nih.gov/pubmed/28516949"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28516949",
"endSection": "abstract",
"offsetInBeginSection": 883,
"offsetInEndSection": 1056,
"text": " The loss of CD55 and CD59 renders PNH erythrocytes susceptible to intravascular haemolysis, which can lead to thrombosis and to much of the morbidity and mortality of PNH. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28657829",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "CD55 Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28657829",
"endSection": "abstract",
"offsetInBeginSection": 1236,
"offsetInEndSection": 1475,
"text": "CONCLUSIONS: CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27812245",
"endSection": "abstract",
"offsetInBeginSection": 175,
"offsetInEndSection": 854,
"text": "It is caused by the expansion of a hematopoietic progenitor cell that has acquired a mutation in the X-linked phosphatidylinositol glycan class A (PIGA) gene that results in deficiency of the glycosylphosphatidylinositol anchor structure responsible for fixing a wide spectrum of proteins particularly CD55 and CD59. The clinical features of this disease arise as a result of complement-mediated hemolysis in unprotected red cells, leukocytes, and platelets as well as the release of free hemoglobin. Patients may present with a variety of clinical manifestations, such as anemia, thrombosis, kidney disease, smooth muscle dystonias, abdominal pain, dyspnea, and extreme fatigue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26205796",
"endSection": "abstract",
"offsetInBeginSection": 273,
"offsetInEndSection": 445,
"text": "The lack of one of the GPI-AP complement regulatory proteins (CD55, CD59) leads to hemolysis. The disease is diagnosed with hemolytic anemia, marrow failure and thrombosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25237200",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 353,
"text": "Paroxysmal nocturnal hemoglobinuria (PNH) is a rare bone marrow failure disorder that manifests with hemolytic anemia, thrombosis, and peripheral blood cytopenias. The absence of two glycosylphosphatidylinositol (GPI)-anchored proteins, CD55 and CD59, leads to uncontrolled complement activation that accounts for hemolysis and other PNH manifestations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23020629",
"endSection": "abstract",
"offsetInBeginSection": 954,
"offsetInEndSection": 1164,
"text": "RESULTS: CD55 and/or CD59 deficiencies were found in 1.6% (2/127) of patients with primary BCS, 1.0% (1/100) of non-malignant and non-cirrhotic patients with PVT, and 4.7% (4/85) of cirrhotic patients with PVT."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22696589",
"endSection": "abstract",
"offsetInBeginSection": 819,
"offsetInEndSection": 983,
"text": "Data of this study indicate that the PNH defect as detected with CD55, CD59, and CD16 is not an important cause of intra-abdominal thrombosis in northwestern India."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23765390",
"endSection": "abstract",
"offsetInBeginSection": 873,
"offsetInEndSection": 1146,
"text": "PNH testing of red blood cells revealed a CD55 and CD59 deficiency consistent with PNH in both cases. The systemic complications typically associated with thrombosis were not observed for the following several months with early conservative treatments including eculizumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22077430",
"endSection": "abstract",
"offsetInBeginSection": 193,
"offsetInEndSection": 426,
"text": "Deficiency of the GPI-anchored complement inhibitors CD55 and CD59 on erythrocytes leads to intravascular hemolysis upon complement activation. Apart from hemolysis, another prominent feature is a highly increased risk of thrombosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28657829",
"endSection": "abstract",
"offsetInBeginSection": 1131,
"offsetInEndSection": 1514,
"text": "Genetic reconstitution of CD55 or treatment with a complement-inhibitory therapeutic antibody reversed abnormal complement activation.<br><b>CONCLUSIONS</b>: CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11843289",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 298,
"text": "Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal disorder characterized by a decrease or absence of glycosylphosphatidylinositol (GPI)-anchored molecules such as CD55 and CD59 from the surface of affected cells, resulting in intravascular hemolysis, cytopenia, and venous thrombosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28657829",
"endSection": "abstract",
"offsetInBeginSection": 1242,
"offsetInEndSection": 1479,
"text": "CONCLUSIONS CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28657829",
"endSection": "abstract",
"offsetInBeginSection": 1209,
"offsetInEndSection": 1434,
"text": "CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28657829",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "CD55 Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis."
}
] | 11
|
BioASQ-training11b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:0060903",
"https://meshb.nlm.nih.gov/record/ui?ui=D013927"
] | null |
5a723cd12dc08e987e00000b
|
bioasq_yesno
|
factoid
|
What is the cause of Rett Syndrome?
|
['methyl-CpG-binding protein 2 (MECP2) gene mutations']
|
[
"methyl-CpG-binding protein 2 (MECP2)",
"MECP2",
"methyl-CpG-binding protein 2",
"methyl-CpG binding protein 2",
"methyl-CpG-binding protein 2 gene",
"MECP2 gene",
"MECP2 gene mutations"
] |
['Rett Syndrome is caused by mutations of the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2), which is responsible for classical forms of the disease in girls.', 'Rett Syndrome is caused by mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2).', 'Rett syndrome is primarily caused by mutations of methyl CpG-binding protein 2 (MeCP2).', 'Mutations in the X-linked MECP2 gene cause Rett Syndrome.', 'Rett Syndrome is caused by mutations in the X-linked gene MECP2, which encodes the methyl-CpG-binding protein 2.', 'Rett Syndrome is caused by mutations in the MECP2 gene, which is located on the X chromosome.', 'Rett Syndrome is caused by mutations of the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2).', 'Rett Syndrome is primarily caused by mutations in the MECP2 gene located on the Xq28 chromosome.', 'Rett syndrome is caused by mutations in the gene encoding the transcription factor Methyl CpG Binding Protein 2 (MECP2).', 'Rett Syndrome is caused by a mutation in the MECP2 gene.', 'Rett syndrome is caused by mutations in the MECP2 gene.', 'Rett Syndrome is caused by mutations in the MECP2 gene.', 'Rett Syndrome (RTT) is a neurodevelopmental disorder affecting girls, it is caused by mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2)', 'Rett Syndrome is primarily caused by mutations in the MECP2 gene, which is located on the X chromosome.', 'Mutations in the gene encoding methyl-CpG-binding protein 2 cause Rett syndrome.', 'Mutations of the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2) cause classical forms of Rett syndrome (RTT) in girls.', 'Rett syndrome is caused by mutations in the X-linked MECP2 gene, encoding MeCP2 protein.', 'Mutations of the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2) cause classical forms of Rett syndrome in girls.', 'Rett Syndrome is caused by mutations of the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2), which typically affects girls and results in severe cognitive and physical impairments.', 'Rett syndrome is a genetic disorder caused by mutations of the methyl CpG-binding protein 2 (MeCP2) gene.', 'The cause of Rett Syndrome is mutations of the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20970936",
"http://www.ncbi.nlm.nih.gov/pubmed/24059803",
"http://www.ncbi.nlm.nih.gov/pubmed/35785421",
"http://www.ncbi.nlm.nih.gov/pubmed/24291980",
"http://www.ncbi.nlm.nih.gov/pubmed/31796123",
"http://www.ncbi.nlm.nih.gov/pubmed/31387202",
"http://www.ncbi.nlm.nih.gov/pubmed/31333401",
"http://www.ncbi.nlm.nih.gov/pubmed/12503649",
"http://www.ncbi.nlm.nih.gov/pubmed/34308425",
"http://www.ncbi.nlm.nih.gov/pubmed/30905360",
"http://www.ncbi.nlm.nih.gov/pubmed/38057990",
"http://www.ncbi.nlm.nih.gov/pubmed/24615633",
"http://www.ncbi.nlm.nih.gov/pubmed/16932552",
"http://www.ncbi.nlm.nih.gov/pubmed/26755454",
"http://www.ncbi.nlm.nih.gov/pubmed/33552148",
"http://www.ncbi.nlm.nih.gov/pubmed/11738862",
"http://www.ncbi.nlm.nih.gov/pubmed/16225827",
"http://www.ncbi.nlm.nih.gov/pubmed/16225828",
"http://www.ncbi.nlm.nih.gov/pubmed/22106023",
"http://www.ncbi.nlm.nih.gov/pubmed/15070486",
"http://www.ncbi.nlm.nih.gov/pubmed/30430747",
"http://www.ncbi.nlm.nih.gov/pubmed/28007990",
"http://www.ncbi.nlm.nih.gov/pubmed/36253345",
"http://www.ncbi.nlm.nih.gov/pubmed/31450191",
"http://www.ncbi.nlm.nih.gov/pubmed/15809268",
"http://www.ncbi.nlm.nih.gov/pubmed/22586411",
"http://www.ncbi.nlm.nih.gov/pubmed/17874730",
"http://www.ncbi.nlm.nih.gov/pubmed/37914350",
"http://www.ncbi.nlm.nih.gov/pubmed/25982834",
"http://www.ncbi.nlm.nih.gov/pubmed/37906876",
"http://www.ncbi.nlm.nih.gov/pubmed/20473347",
"http://www.ncbi.nlm.nih.gov/pubmed/20236870",
"http://www.ncbi.nlm.nih.gov/pubmed/12615169",
"http://www.ncbi.nlm.nih.gov/pubmed/34209228",
"http://www.ncbi.nlm.nih.gov/pubmed/20139413",
"http://www.ncbi.nlm.nih.gov/pubmed/31629059",
"http://www.ncbi.nlm.nih.gov/pubmed/15367913",
"http://www.ncbi.nlm.nih.gov/pubmed/15757975",
"http://www.ncbi.nlm.nih.gov/pubmed/27491552",
"http://www.ncbi.nlm.nih.gov/pubmed/12750821",
"http://www.ncbi.nlm.nih.gov/pubmed/20951500",
"http://www.ncbi.nlm.nih.gov/pubmed/11262731",
"http://www.ncbi.nlm.nih.gov/pubmed/20682201",
"http://www.ncbi.nlm.nih.gov/pubmed/27328325",
"http://www.ncbi.nlm.nih.gov/pubmed/36778467",
"http://www.ncbi.nlm.nih.gov/pubmed/37461668",
"http://www.ncbi.nlm.nih.gov/pubmed/12966522",
"http://www.ncbi.nlm.nih.gov/pubmed/12112735",
"http://www.ncbi.nlm.nih.gov/pubmed/31409060",
"http://www.ncbi.nlm.nih.gov/pubmed/29694339",
"http://www.ncbi.nlm.nih.gov/pubmed/30502397",
"http://www.ncbi.nlm.nih.gov/pubmed/30447288",
"http://www.ncbi.nlm.nih.gov/pubmed/25960047",
"http://www.ncbi.nlm.nih.gov/pubmed/15866439",
"http://www.ncbi.nlm.nih.gov/pubmed/36056801",
"http://www.ncbi.nlm.nih.gov/pubmed/37408271",
"http://www.ncbi.nlm.nih.gov/pubmed/37885019",
"http://www.ncbi.nlm.nih.gov/pubmed/27934853",
"http://www.ncbi.nlm.nih.gov/pubmed/31542590",
"http://www.ncbi.nlm.nih.gov/pubmed/17986102",
"http://www.ncbi.nlm.nih.gov/pubmed/24423488",
"http://www.ncbi.nlm.nih.gov/pubmed/16690727"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37408271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Mutations of the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2) cause classical forms of Rett syndrome (RTT) in girls"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12966522",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 325,
"text": "Rett syndrome is caused by mutation in MECP2, a gene located on Xq28 and subject to X-inactivation. MECP2 encodes methyl CpG-binding protein 2, a widely expressed transcriptional repressor of methylated DNA. Mutations in MECP2 are primarily de novo events in the male germ line and thus lead to an excess of affected females."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12966522",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Rett syndrome is caused by mutation in MECP2, a gene located on Xq28 and subject to X-inactivation. MECP2 encodes methyl CpG-binding protein 2, a widely expressed transcriptional repressor of methylated DNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12966522",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Rett syndrome is caused by mutation in MECP2, a gene located on Xq28 and subject to X-inactivation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17986102",
"endSection": "abstract",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1153,
"text": " MECP2 rearrangements cause Rett syndrome in a significant number of girls without 'classic' mutations in this gene. Ther"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15866439",
"endSection": "abstract",
"offsetInBeginSection": 120,
"offsetInEndSection": 566,
"text": "Rett syndrome is frequently caused by a mutation in methyl-CpG-binding protein (MECP2) gene, localized on chromosome Xq28, whereas Angelman syndrome is frequently caused by different genetic anomalies at chromosome 15q11-q13 (deletions, uniparental disomy, imprinting center mutations, ubiquitin E3 ligase [UBE3A] gene mutations). Recently, some patients with a clinical diagnosis of Angelman syndrome were found to have a mutation in MECP2 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15866439",
"endSection": "abstract",
"offsetInBeginSection": 120,
"offsetInEndSection": 450,
"text": "Rett syndrome is frequently caused by a mutation in methyl-CpG-binding protein (MECP2) gene, localized on chromosome Xq28, whereas Angelman syndrome is frequently caused by different genetic anomalies at chromosome 15q11-q13 (deletions, uniparental disomy, imprinting center mutations, ubiquitin E3 ligase [UBE3A] gene mutations)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15866439",
"endSection": "abstract",
"offsetInBeginSection": 120,
"offsetInEndSection": 664,
"text": "Rett syndrome is frequently caused by a mutation in methyl-CpG-binding protein (MECP2) gene, localized on chromosome Xq28, whereas Angelman syndrome is frequently caused by different genetic anomalies at chromosome 15q11-q13 (deletions, uniparental disomy, imprinting center mutations, ubiquitin E3 ligase [UBE3A] gene mutations). Recently, some patients with a clinical diagnosis of Angelman syndrome were found to have a mutation in MECP2 gene. This report describes another patient with an Angelman-like phenotype and with an MECP2 mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17986102",
"endSection": "abstract",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1293,
"text": " MECP2 rearrangements cause Rett syndrome in a significant number of girls without 'classic' mutations in this gene. Therefore, we developed a specific quantitative PCR method, covering MECP2 exons 3 and 4, which previously has not been used for screening. No d"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15866439",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 566,
"text": "Rett syndrome and Angelman syndrome are two neurodevelopmental disorders characterized by partial overlapping features. Rett syndrome is frequently caused by a mutation in methyl-CpG-binding protein (MECP2) gene, localized on chromosome Xq28, whereas Angelman syndrome is frequently caused by different genetic anomalies at chromosome 15q11-q13 (deletions, uniparental disomy, imprinting center mutations, ubiquitin E3 ligase [UBE3A] gene mutations). Recently, some patients with a clinical diagnosis of Angelman syndrome were found to have a mutation in MECP2 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17986102",
"endSection": "abstract",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1387,
"text": " MECP2 rearrangements cause Rett syndrome in a significant number of girls without 'classic' mutations in this gene. Therefore, we developed a specific quantitative PCR method, covering MECP2 exons 3 and 4, which previously has not been used for screening. No dosage alterations of the two exons were found in the four tested mutation-negative girls.CONCL"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15070486",
"endSection": "abstract",
"offsetInBeginSection": 176,
"offsetInEndSection": 306,
"text": "The majority of cases of sporadic Rett syndrome are caused by mutations in the gene encoding methyl-CpG-binding protein 2 (MeCP2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15070486",
"endSection": "abstract",
"offsetInBeginSection": 396,
"offsetInEndSection": 633,
"text": "Genotype/phenotype analysis revealed that the phenotypic spectrum of MECP2 mutations in humans is broader than initially suspected: Mutations have been discovered in Rett syndrome variants, mentally retarded males, and autistic children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11262731",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Rett syndrome, a neurodevelopmental disorder that is a leading cause of mental retardation in females, is caused by mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MeCP2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33552148",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "Mutations in methyl CpG binding protein 2 (MeCP2) are the major cause of Rett syndrome (RTT), a rare neurodevelopmental disorder with a notable period of developmental regression following apparently normal initial development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26755454",
"endSection": "abstract",
"offsetInBeginSection": 73,
"offsetInEndSection": 169,
"text": "Mutations in the MECP2 gene on chromosome Xq28 have been shown to be the cause of Rett syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17874730",
"endSection": "abstract",
"offsetInBeginSection": 285,
"offsetInEndSection": 582,
"text": "Rett syndrome is the first pervasive developmental disorder with a known genetic cause. The majority of cases are caused by de novo mutations in an X-linked MECP2 gene. Its product, methyl-CpG-binding protein 2, plays an important role in the regulation of gene expression and chromatin structure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106023",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Rett syndrome is a rare neurological disorder affecting girls and usually caused by a mutation on the MECP2 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20236870",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Rett syndrome, a neurodevelopmental disorder affecting mainly females, is caused by a mutation of the MeCP2 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20473347",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Rett syndrome is an X-linked autism-spectrum disorder caused by mutations in MECP2, encoding methyl CpG-binding protein 2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27491552",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Rett syndrome is a rare neurodevelopmental disorder caused by a mutation in the MECP2 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12112735",
"endSection": "abstract",
"offsetInBeginSection": 308,
"offsetInEndSection": 449,
"text": "Recent studies have shown that mutations in the X-linked methyl CpG binding protein 2 gene (MeCP2) cause most typical cases of Rett syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24423488",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "BACKGROUND: Rett syndrome is caused by mutations in the X-linked MECP2 gene, encoding MeCP2 protein."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20970936",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Somatic mosaicism for Y120X mutation in the MECP2 gene causes atypical Rett syndrome in a male."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25982834",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 305,
"text": "Rett syndrome is a devastating neurodevelopmental disorder, primarily caused by mutations of methyl CpG-binding protein 2 (MeCP2). Although the genetic cause of disease was identified over a decade ago, a significant gap still remains in both our clinical and scientific understanding of its pathogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30502397",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Rett Syndrome (RTT) is a genetic disorder that is caused by mutations in the x-linked gene coding for methyl-CpG-biding-protein 2 (MECP2)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36056801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Rett syndrome (RTT) is an X-linked neurogenetic disorder caused by mutations of the MECP2 (methyl-CpG-binding protein 2) gene. Over two decades of work"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27934853",
"endSection": "abstract",
"offsetInBeginSection": 30,
"offsetInEndSection": 578,
"text": "Rett first described the syndrome that came to bear his name, and is now known to be caused by a mutation in the methyl-CpG-binding protein 2 (MECP2) gene, a compelling blend of astute clinical observations and clinical and laboratory research has substantially enhanced our understanding of this rare disorder. Here, we document the contributions of the early pioneers in Rett syndrome (RTT) research, and describe the evolution of knowledge in terms of diagnostic criteria, clinical variation, and the interplay with other Rett-related disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24291980",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 579,
"text": "cause various neuro-developmental diseases. We recently reported that neurological symptoms of Rett syndrome, which is an autistic disorder caused by mutations in methyl-CpG binding protein 2 (MeCP2), was associated with failure of epigenomic gene regulation in neuronal cells, and that clinical differences in the identical twins with Rett syndrome in the differences in DNA methylation in neuronal genes, but not caused by DNA sequence differences."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37461668",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 231,
"text": "Mutations in MECP2 give rise to Rett syndrome (RTT), an X-linked neurodevelopmental disorder that results in broad cognitive impairments in females. While the exact etiology of RTT symptoms remains unknown, one possible explanation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27328325",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 481,
"text": "Rett syndrome (RTT), a postnatal neurological disorder caused by loss-of-function mutations in MECP2, display impaired excitatory neurotransmission, the RTT phenotype can be largely reproduced in mice simply by removing MeCP2 from inhibitory GABAergic neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11738862",
"endSection": "abstract",
"offsetInBeginSection": 93,
"offsetInEndSection": 210,
"text": "About 80% of classic Rett syndrome is caused by mutations in the gene for methyl-CpG-binding protein (MeCP2) in Xq28."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24615633",
"endSection": "abstract",
"offsetInBeginSection": 107,
"offsetInEndSection": 218,
"text": "Mutations of the methyl-CpG binding protein 2 (MECP2) gene are the most prevalent cause of classical RTT cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30447288",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "Mutations in the methyl-CpG binding protein 2 (MECP2) gene cause Rett syndrome (RTT), a progressive X-linked neurological disorder characterized by loss of developmental milestones, intellectual disability and breathing abnormality."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24059803",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "Rett syndrome (RTT) is an X-linked neurodevelopmental disease caused by MECP2 mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15367913",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Mutations in MECP2 are a cause of Rett syndrome. Recently, a new isoform of MeCP2 was described, which has an alternative N-terminus, transcribed from"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20682201",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Rett syndrome is a neurodevelopmental disorder caused by mutations in the methyl CpG binding protein 2 gene (MECP2). The MECP2 protein is expressed pr"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28007990",
"endSection": "abstract",
"offsetInBeginSection": 15,
"offsetInEndSection": 165,
"text": "mon in Rett syndrome, an X-linked dominant disorder caused by mutations in the MECP2 gene, and in Rett-related disorders, such as MECP2 duplication. H"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20682201",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Rett syndrome is a neurodevelopmental disorder caused by mutations in the methyl CpG binding protein 2 gene (MECP2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15367913",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Mutations in MECP2 are a cause of Rett syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16225827",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 238,
"text": "In 1999, mutations in the MECP2 gene were identified as the primary cause of Rett syndrome. MECP2 mutations can be found in 70% to 80% of all clinically defined Rett syndrome cases; in classic Rett syndrome, this frequency is even higher."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29694339",
"endSection": "abstract",
"offsetInBeginSection": 133,
"offsetInEndSection": 273,
"text": " MeCP2 mutations have been linked to Rett syndrome, a neurodevelopmental disorder characterized by severe intellectual disability in females"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15809268",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "The discovery in 1999 that Rett syndrome (RTT) is caused by mutations in a gene encoding the methyl-CpG-binding repressor protein MECP2 provided a significant breakthrough in the understanding of this devastating disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12503649",
"endSection": "abstract",
"offsetInBeginSection": 109,
"offsetInEndSection": 247,
"text": "Recently, mutations in the gene encoding X-linked methyl-CpG binding protein 2 (MECP2) have been identified as the cause of Rett syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37914350",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Mutations in the methyl-DNA binding domain of MECP2 cause Rett syndrome; however, distinct mutations are associated with different severity of the disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37885019",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 113,
"text": "Rett syndrome (RS) is a rare neurodevelopmental disorder characterized by mutations in the MECP2 gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36778467",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Mutations in MECP2 cause the neurodevelopmental disorder Rett syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38057990",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 267,
"text": "Rett syndrome is a neurodevelopmental disorder caused by loss-of-function mutations in the methyl-CpG binding protein-2 (MeCP2) gene that is characterized by epilepsy, intellectual disability, autistic features, speech deficits, and sleep and breathing abnormalities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12615169",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Mutations in the MECP2 (methyl-CpG-binding protein 2) gene are known to cause Rett syndrome, a well-known and clinically defined neurodevelopmental disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30905360",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Rett syndrome (RTT) is a neurodevelopmental disorder caused by mutations in the Methyl CpG binding protein 2 (MeCP2) gene. This Science & Society article focuses on"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38057990",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Rett syndrome is a neurodevelopmental disorder caused by loss-of-function mutations in the methyl-CpG binding protein-2 (MeCP2)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30430747",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Rett syndrome (RTT) is a monogenic neurodevelopmental disorder caused by mutations in the methyl-CpG binding protein 2 (MECP2) gene. Patients with RTT develop symptoms after 6-18 months of age,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31409060",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 655,
"text": "Rett syndrome (RTT) is an early-onset neurodevelopmental disorder that primarily affects females, resulting in severe cognitive and physical disabilities, and is one of the most prevalent causes of intellectual disability in females. More than fifty years after the first publication on Rett syndrome, and almost two decades since the first report linking RTT to the MECP2 gene, the research community's effort is focused on obtaining a better understanding of the genetics and the complex biology of RTT and Rett-like phenotypes without MECP2 mutations. Herein, we review the current molecular genetic studies, which investigate the genetic causes of RTT"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34308425",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 257,
"text": "Rett syndrome (RTT) is a severe X-linked neurodevelopmental disorder characterized by neurodevelopmental regression between 6 and 18 months of life and associated with multi-system comorbidities. Caused mainly by pathogenic variants in the MECP2 (methyl CpG"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37906876",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 538,
"text": "Rett syndrome (RS) is a rare neurodevelopmental disorder first described in 1966. It is characterized by the arrest and regression of intellectual, motor, and communicative developmental milestones, followed by the appearance of hand stereotypies after an apparently normal development period. Pathogenic variants in the MECP2 gene have been identified as a cause in most cases. The following review focuses on analyzing updated information regarding the medical and social aspects of RS globally, with a special emphasis of the situation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16225827",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "In 1999, mutations in the MECP2 gene were identified as the primary cause of Rett syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15070486",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 306,
"text": "Rett syndrome, one of the leading causes of mental retardation and developmental regression in girls, is the first pervasive developmental disorder with a known genetic cause. The majority of cases of sporadic Rett syndrome are caused by mutations in the gene encoding methyl-CpG-binding protein 2 (MeCP2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16225827",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 340,
"text": "In 1999, mutations in the MECP2 gene were identified as the primary cause of Rett syndrome. MECP2 mutations can be found in 70% to 80% of all clinically defined Rett syndrome cases; in classic Rett syndrome, this frequency is even higher. In most cases, missense and nonsense mutations affecting functionally important domains can be found."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12503649",
"endSection": "abstract",
"offsetInBeginSection": 109,
"offsetInEndSection": 357,
"text": "Recently, mutations in the gene encoding X-linked methyl-CpG binding protein 2 (MECP2) have been identified as the cause of Rett syndrome. Along with the classic form, variant forms of Rett syndrome and Rett syndrome phenotypes are also recognized."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15070486",
"endSection": "abstract",
"offsetInBeginSection": 176,
"offsetInEndSection": 395,
"text": "The majority of cases of sporadic Rett syndrome are caused by mutations in the gene encoding methyl-CpG-binding protein 2 (MeCP2). MeCP2 binds methylated DNA and likely regulates gene expression and chromatin structure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12503649",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 247,
"text": "Rett syndrome is a progressive neurodevelopmental disorder with a well-defined clinical spectrum and course. Recently, mutations in the gene encoding X-linked methyl-CpG binding protein 2 (MECP2) have been identified as the cause of Rett syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31542590",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "Rett syndrome (RTT) is one of the most common causes of intellectual and developmental disabilities in girls, and is caused by mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). Here we will review our current understanding"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31450191",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Rett syndrome (RTT) is a childhood neurodevelopmental disorder caused by mutations in MECP2. To study the molecular mechanisms underlying RTT, four"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34209228",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 366,
"text": "Rett syndrome (RTT) is an extremely invalidating, cureless, developmental disorder, and it is considered one of the leading causes of intellectual disability in female individuals. The vast majority of RTT cases are caused by de novo mutations in the X-linked Methyl-CpG binding protein 2 (MECP2) gene, which encodes a multifunctional reader of methylated DNA. MeCP2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31387202",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 310,
"text": "Rett syndrome (RTT) is a rare, X-linked neurodevelopmental disorder typically affecting females, resulting in a range of symptoms including autistic features, intellectual impairment, motor deterioration, and autonomic abnormalities. RTT is primarily caused by the genetic mutation of the Mecp2 gene. Initially"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35785421",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Rett syndrome (RTT) is a progressive neurodevelopmental disorder that occurs mainly in girls with a range of typical symptoms of autism spectrum disorders. MeCP2 protein loss-of-function in neural lineage cells is the main cause"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16225828",
"endSection": "abstract",
"offsetInBeginSection": 77,
"offsetInEndSection": 171,
"text": "Rett syndrome is caused by mutations in MECP2, the gene encoding methyl-CpG binding protein 2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16225828",
"endSection": "abstract",
"offsetInBeginSection": 172,
"offsetInEndSection": 273,
"text": "In up to 96% of all classic cases, Rett syndrome cases are caused by mutations or deletions in MECP2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22586411",
"endSection": "abstract",
"offsetInBeginSection": 422,
"offsetInEndSection": 566,
"text": "Rett syndrome (RTT) is a neurological disorder of genetic origin, caused by mutations in the X-linked gene methyl-CpG binding protein 2 (MeCP2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20139413",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Rett syndrome is a neurodevelopmental disorder mainly caused by de novo mutations in the MECP2 (methyl-CpG-binding protein 2) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31796123",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Rett Syndrome (RTT) is a neurodevelopmental disorder caused by mutations in the Methyl CpG binding protein 2 (MECP2) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11738862",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "Rett syndrome is an X-linked dominant neurodevelopmental disorder primarily affecting girls. About 80% of classic Rett syndrome is caused by mutations in the gene for methyl-CpG-binding protein (MeCP2) in Xq28."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12750821",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "Rett syndrome (RTT) is a severe neurodevelopmental disorder affecting almost exclusively girls. It is currently considered a monogenic X-linked dominant disorder due to mutations in MECP2 gene, encoding the methyl-CpG binding protein 2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25960047",
"endSection": "abstract",
"offsetInBeginSection": 394,
"offsetInEndSection": 643,
"text": "RTT is known to be caused in 95% of the cases by sporadic de novo loss-of-function mutations in the X-linked methyl-CpG-binding protein 2 (MECP2) gene encoding methyl-CpG binding protein 2 (MeCP2), a nuclear protein able to regulate gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20951500",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 345,
"text": "Rett syndrome (RTT) is an X-linked dominant postnatal severe and disabling neurodevelopmental disorder which is the second most common cause for genetic mental retardation in girls and the first pervasive disorder with a known genetic basis. The syndrome is primarily caused by mutations in the Methyl CpG binding protein 2 (MECP2) gene on Xq28."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16932552",
"endSection": "abstract",
"offsetInBeginSection": 240,
"offsetInEndSection": 357,
"text": "RTT is caused by heterozygosity for mutations in the X-linked gene MECP2, which encodes methyl-CpG binding protein 2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31629059",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Rett syndrome (RTT) is a leading cause of severe intellectual disability in females, caused by de novo loss-of function mutations in the X-linked methyl-CpG binding protein 2 (MECP2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15757975",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Rett syndrome (RS) is a severe and progressive neurodevelopmental disorder caused by heterozygous mutations in the X-linked methyl CpG binding protein 2 (MeCP2) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36253345",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Rett syndrome (RTT) is a severe neurodevelopmental disorder primarily caused by heterozygous loss-of-function mutations in the X-linked gene MECP2 that is a global transcriptional regulator."
}
] | 13
|
BioASQ-training13b
| null | null |
661d4c2eeac11fad3300001a
|
bioasq_factoid
|
factoid
|
Which peripheral neuropathy has been associated with NDRG1 mutations?
|
[['Charcot-Marie-Tooth (CMT) 4D disease']]
|
[
"Charcot-Marie-Tooth disease",
"CMT",
"CMT4D",
"Charcot-Marie-Tooth (CMT) 4D disease",
"CMT type 4D",
"CMT4D neuropathy"
] |
['Charcot-Marie-Tooth (CMT) 4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1).', 'CMT4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1)', 'CMT4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1)', 'CMT4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1)', 'CMT4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1)', 'CMT4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1)']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21303696",
"http://www.ncbi.nlm.nih.gov/pubmed/12872253",
"http://www.ncbi.nlm.nih.gov/pubmed/20582309",
"http://www.ncbi.nlm.nih.gov/pubmed/15651351",
"http://www.ncbi.nlm.nih.gov/pubmed/12884740",
"http://www.ncbi.nlm.nih.gov/pubmed/16541790",
"http://www.ncbi.nlm.nih.gov/pubmed/15082788",
"http://www.ncbi.nlm.nih.gov/pubmed/23996628"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21303696",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "CMT4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12872253",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 300,
"text": "In a previous study, we have shown that N-myc downstream-regulated gene 1 (NDRG1), classified in databases as a tumor suppressor and heavy metal-response protein, is mutated in hereditary motor and sensory neuropathy Lom (HMSNL), a severe autosomal recessive form of Charcot-Marie-Tooth (CMT) disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12884740",
"endSection": "abstract",
"offsetInBeginSection": 747,
"offsetInEndSection": 1289,
"text": "In the primary peripheral demyelinating neuropathies(CMT1), at least 9 genes have been associated with the disorders; altered dosage of peripheral myelin protein 22(PMP22) or point mutation of PMP22, the gap junction protein 1(GJB1), the myelin protein zero gene(MPZ), the early growth response gene 2(EGR2), the myotubularin-related protein 2 gene(MTMR2), the N-myc downstream-regulated gene 1 (NDRG1), the L-periaxin gene(PRX), SRY-related HMG-BOX gene 10(SOX10) and the ganglioside-induced differentiation-associated protein 1 gene(GDAP1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20582309",
"endSection": "abstract",
"offsetInBeginSection": 939,
"offsetInEndSection": 1093,
"text": "The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16541790",
"endSection": "abstract",
"offsetInBeginSection": 977,
"offsetInEndSection": 1598,
"text": "Genetic studies have revealed the following gene mutations as the causes of inherited neuropathies; PMP22, MPZ, EGR2, SOX10, SIMPLE/LITAF, ARHGEF10 for CMT1 (autosomal dominant demyelinating form); GDAP1, MTMR2, SBF2/MTMR13, KIAA1985, NDRG1 PRX for CMT4 (autosomal recessive demyelinating form), MFN2, KIF1B, RAB7, GARS, NEFL, HSPB1, HSPB8 for CMT2 (autosomal dominant axonal form); LMNA, GAN1, KCC3, TDP1, APTX, SETX for AR-CMT2 (autosomal recessive axonal form); GIB1 for CMTX (X-linked CMT); DNM2 for CMT-DI (autosomal dominant CMT with intermediate nerve conduction velocities); and DHH for minifascicular neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12872253",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 301,
"text": "In a previous study, we have shown that N-myc downstream-regulated gene 1 (NDRG1), classified in databases as a tumor suppressor and heavy metal-response protein, is mutated in hereditary motor and sensory neuropathy Lom (HMSNL), a severe autosomal recessive form of Charcot-Marie-Tooth (CMT) disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20582309",
"endSection": "abstract",
"offsetInBeginSection": 939,
"offsetInEndSection": 1093,
"text": "The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15082788",
"endSection": "abstract",
"offsetInBeginSection": 439,
"offsetInEndSection": 702,
"text": "Recently, human NDRG1 was identified as a gene responsible for hereditary motor and sensory neuropathy-Lom (classified as Charcot-Marie-Tooth disease type 4D), which is characterized by early-onset peripheral neuropathy, leading to severe disability in adulthood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21303696",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "CMT4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12884740",
"endSection": "abstract",
"offsetInBeginSection": 747,
"offsetInEndSection": 1289,
"text": "In the primary peripheral demyelinating neuropathies(CMT1), at least 9 genes have been associated with the disorders; altered dosage of peripheral myelin protein 22(PMP22) or point mutation of PMP22, the gap junction protein 1(GJB1), the myelin protein zero gene(MPZ), the early growth response gene 2(EGR2), the myotubularin-related protein 2 gene(MTMR2), the N-myc downstream-regulated gene 1 (NDRG1), the L-periaxin gene(PRX), SRY-related HMG-BOX gene 10(SOX10) and the ganglioside-induced differentiation-associated protein 1 gene(GDAP1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23996628",
"endSection": "abstract",
"offsetInBeginSection": 1037,
"offsetInEndSection": 1252,
"text": "The success of molecular genetic analysis in all families confirms that autosomal recessive forms of CMT caused by mutations on the NDRG1 and HK1 genes are common causes of inherited neuropathies among Slovak Roma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23996628",
"endSection": "abstract",
"offsetInBeginSection": 1037,
"offsetInEndSection": 1252,
"text": "The success of molecular genetic analysis in all families confirms that autosomal recessive forms of CMT caused by mutations on the NDRG1 and HK1 genes are common causes of inherited neuropathies among Slovak Roma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23996628",
"endSection": "abstract",
"offsetInBeginSection": 1037,
"offsetInEndSection": 1252,
"text": "The success of molecular genetic analysis in all families confirms that autosomal recessive forms of CMT caused by mutations on the NDRG1 and HK1 genes are common causes of inherited neuropathies among Slovak Roma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15082788",
"endSection": "abstract",
"offsetInBeginSection": 177,
"offsetInEndSection": 441,
"text": "Recently, human NDRG1 was identified as a gene responsible for hereditary motor and sensory neuropathy-Lom (classified as Charcot-Marie-Tooth disease type 4D), which is characterized by early-onset peripheral neuropathy, leading to severe disability in adulthood. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23996628",
"endSection": "abstract",
"offsetInBeginSection": 1037,
"offsetInEndSection": 1252,
"text": "The success of molecular genetic analysis in all families confirms that autosomal recessive forms of CMT caused by mutations on the NDRG1 and HK1 genes are common causes of inherited neuropathies among Slovak Roma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15651351",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 616,
"text": "In the primary peripheral demyelinating neuropathies (CMT1), at least 15 genes have been associated with the disorders; altered dosage or point mutation of PMP22, GJB1, MPZ, EGR2, MTMR2, NDRG1, PRX, SOX10, GDAP1 and MTMR13/SBF2. In the primary peripheral axonal neuropathies (CMT2), at least 10 genes have been associated with these disorders; NEFL, KIF1B, MFN2, GAN1, LMNA, RAB7, GARS, TDP1, APTX, and SETX."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12884740",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 1018,
"text": "In the primary peripheral demyelinating neuropathies(CMT1), at least 9 genes have been associated with the disorders; altered dosage of peripheral myelin protein 22(PMP22) or point mutation of PMP22, the gap junction protein 1(GJB1), the myelin protein zero gene(MPZ), the early growth response gene 2(EGR2), the myotubularin-related protein 2 gene(MTMR2), the N-myc downstream-regulated gene 1 (NDRG1), the L-periaxin gene(PRX), SRY-related HMG-BOX gene 10(SOX10) and the ganglioside-induced differentiation-associated protein 1 gene(GDAP1). In the primary peripheral axonal neuropathies(CMT2), at least 8 genes have been associated with these disorders; the neurofilament light chain gene(NEFL), the kinesin 1B gene(KIF1B), the gigaxonin gene(GAN1), Lamin A/C(LMNA) and tyrosyl-DNA phosphodiesterase 1(TDP1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15082788",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 441,
"text": " NDRG1 is an intracellular protein that is induced under a number of stress and pathological conditions, and it is thought to be associated with cell growth and differentiation. Recently, human NDRG1 was identified as a gene responsible for hereditary motor and sensory neuropathy-Lom (classified as Charcot-Marie-Tooth disease type 4D), which is characterized by early-onset peripheral neuropathy, leading to severe disability in adulthood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12884740",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 750,
"text": "Recent genetic studies have revealed their phenotypic and genetic diversities. In the primary peripheral demyelinating neuropathies(CMT1), at least 9 genes have been associated with the disorders; altered dosage of peripheral myelin protein 22(PMP22) or point mutation of PMP22, the gap junction protein 1(GJB1), the myelin protein zero gene(MPZ), the early growth response gene 2(EGR2), the myotubularin-related protein 2 gene(MTMR2), the N-myc downstream-regulated gene 1 (NDRG1), the L-periaxin gene(PRX), SRY-related HMG-BOX gene 10(SOX10) and the ganglioside-induced differentiation-associated protein 1 gene(GDAP1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15651351",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 436,
"text": "Recent genetic studies have revealed their phenotypic and genetic diversities. In the primary peripheral demyelinating neuropathies (CMT1), at least 15 genes have been associated with the disorders; altered dosage or point mutation of PMP22, GJB1, MPZ, EGR2, MTMR2, NDRG1, PRX, SOX10, GDAP1 and MTMR13/SBF2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20582309",
"endSection": "abstract",
"offsetInBeginSection": 1428,
"offsetInEndSection": 1825,
"text": "Western blot analysis demonstrated an absence of NDRG1 protein in peripheral nerve biopsy of an affected Greyhound. We thus have identified a candidate causative mutation for polyneuropathy in Greyhounds and identified the first genetically characterized canine CMT model which offers an opportunity to gain further insights into the pathobiology and therapy of human NDRG1 associated CMT disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15651351",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 436,
"text": "In the primary peripheral demyelinating neuropathies (CMT1), at least 15 genes have been associated with the disorders; altered dosage or point mutation of PMP22, GJB1, MPZ, EGR2, MTMR2, NDRG1, PRX, SOX10, GDAP1 and MTMR13/SBF2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20582309",
"endSection": "abstract",
"offsetInBeginSection": 793,
"offsetInEndSection": 947,
"text": "The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12884740",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 750,
"text": "In the primary peripheral demyelinating neuropathies(CMT1), at least 9 genes have been associated with the disorders; altered dosage of peripheral myelin protein 22(PMP22) or point mutation of PMP22, the gap junction protein 1(GJB1), the myelin protein zero gene(MPZ), the early growth response gene 2(EGR2), the myotubularin-related protein 2 gene(MTMR2), the N-myc downstream-regulated gene 1 (NDRG1), the L-periaxin gene(PRX), SRY-related HMG-BOX gene 10(SOX10) and the ganglioside-induced differentiation-associated protein 1 gene(GDAP1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15082788",
"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 441,
"text": "Recently, human NDRG1 was identified as a gene responsible for hereditary motor and sensory neuropathy-Lom (classified as Charcot-Marie-Tooth disease type 4D), which is characterized by early-onset peripheral neuropathy, leading to severe disability in adulthood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15651351",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 436,
"text": "In the primary peripheral demyelinating neuropathies (CMT1), at least 15 genes have been associated with the disorders; altered dosage or point mutation of PMP22, GJB1, MPZ, EGR2, MTMR2, NDRG1, PRX, SOX10, GDAP1 and MTMR13/SBF2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20582309",
"endSection": "abstract",
"offsetInBeginSection": 793,
"offsetInEndSection": 947,
"text": "The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12884740",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 750,
"text": "In the primary peripheral demyelinating neuropathies(CMT1), at least 9 genes have been associated with the disorders; altered dosage of peripheral myelin protein 22(PMP22) or point mutation of PMP22, the gap junction protein 1(GJB1), the myelin protein zero gene(MPZ), the early growth response gene 2(EGR2), the myotubularin-related protein 2 gene(MTMR2), the N-myc downstream-regulated gene 1 (NDRG1), the L-periaxin gene(PRX), SRY-related HMG-BOX gene 10(SOX10) and the ganglioside-induced differentiation-associated protein 1 gene(GDAP1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15082788",
"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 441,
"text": "Recently, human NDRG1 was identified as a gene responsible for hereditary motor and sensory neuropathy-Lom (classified as Charcot-Marie-Tooth disease type 4D), which is characterized by early-onset peripheral neuropathy, leading to severe disability in adulthood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15651351",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 436,
"text": "In the primary peripheral demyelinating neuropathies (CMT1), at least 15 genes have been associated with the disorders; altered dosage or point mutation of PMP22, GJB1, MPZ, EGR2, MTMR2, NDRG1, PRX, SOX10, GDAP1 and MTMR13/SBF2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20582309",
"endSection": "abstract",
"offsetInBeginSection": 793,
"offsetInEndSection": 947,
"text": "The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12884740",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 750,
"text": "In the primary peripheral demyelinating neuropathies(CMT1), at least 9 genes have been associated with the disorders; altered dosage of peripheral myelin protein 22(PMP22) or point mutation of PMP22, the gap junction protein 1(GJB1), the myelin protein zero gene(MPZ), the early growth response gene 2(EGR2), the myotubularin-related protein 2 gene(MTMR2), the N-myc downstream-regulated gene 1 (NDRG1), the L-periaxin gene(PRX), SRY-related HMG-BOX gene 10(SOX10) and the ganglioside-induced differentiation-associated protein 1 gene(GDAP1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15082788",
"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 441,
"text": "Recently, human NDRG1 was identified as a gene responsible for hereditary motor and sensory neuropathy-Lom (classified as Charcot-Marie-Tooth disease type 4D), which is characterized by early-onset peripheral neuropathy, leading to severe disability in adulthood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12884740",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 750,
"text": "In the primary peripheral demyelinating neuropathies(CMT1), at least 9 genes have been associated with the disorders; altered dosage of peripheral myelin protein 22(PMP22) or point mutation of PMP22, the gap junction protein 1(GJB1), the myelin protein zero gene(MPZ), the early growth response gene 2(EGR2), the myotubularin-related protein 2 gene(MTMR2), the N-myc downstream-regulated gene 1 (NDRG1), the L-periaxin gene(PRX), SRY-related HMG-BOX gene 10(SOX10) and the ganglioside-induced differentiation-associated protein 1 gene(GDAP1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15651351",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 436,
"text": "In the primary peripheral demyelinating neuropathies (CMT1), at least 15 genes have been associated with the disorders; altered dosage or point mutation of PMP22, GJB1, MPZ, EGR2, MTMR2, NDRG1, PRX, SOX10, GDAP1 and MTMR13/SBF2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20582309",
"endSection": "abstract",
"offsetInBeginSection": 793,
"offsetInEndSection": 947,
"text": "The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15082788",
"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 441,
"text": "Recently, human NDRG1 was identified as a gene responsible for hereditary motor and sensory neuropathy-Lom (classified as Charcot-Marie-Tooth disease type 4D), which is characterized by early-onset peripheral neuropathy, leading to severe disability in adulthood."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
5713c8d71174fb1755000015
|
bioasq_factoid
|
factoid
|
What is the life expectancy for Duchenne muscular dystrophy patients?
|
['28.1 years of age', '28.1 years (95% CI 25.1, 30.3)']
|
[
"28.1 years of age",
"28.1 years",
"28.1 years (95% CI 25.1, 30.3)",
"28.1 years old"
] |
['The life expectancy for Duchenne muscular dystrophy patients varies depending on the time period they were born in, but patients born after 1990 have a median life expectancy of 28.1 years.', 'The life expectancy for Duchenne muscular dystrophy patients is around 28.1 years.', 'The life expectancy for Duchenne muscular dystrophy patients is typically between the late teens and early 30s.', 'The median life expectancy for Duchenne muscular dystrophy patients born after 1990 is 28.1 years (95% CI 25.1, 30.3).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34645707",
"http://www.ncbi.nlm.nih.gov/pubmed/10193393",
"http://www.ncbi.nlm.nih.gov/pubmed/17939910",
"http://www.ncbi.nlm.nih.gov/pubmed/26153505",
"http://www.ncbi.nlm.nih.gov/pubmed/34802091",
"http://www.ncbi.nlm.nih.gov/pubmed/1450492"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34645707",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1315,
"text": "Analyses stratified by 3 time periods in which patients were born showed markedly increased life expectancy in more recent patient populations; patients born after 1990 have a median life expectancy of 28.1 years (95% CI 25.1, 30.3)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34645707",
"endSection": "abstract",
"offsetInBeginSection": 1038,
"offsetInEndSection": 1411,
"text": "s (95% confidence interval [CI] 21.2, 22.4). Analyses stratified by 3 time periods in which patients were born showed markedly increased life expectancy in more recent patient populations; patients born after 1990 have a median life expectancy of 28.1 years (95% CI 25.1, 30.3).DISCUSSION: This article presents a full overview of mortality across the lifetime of a patient"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26153505",
"endSection": "abstract",
"offsetInBeginSection": 123,
"offsetInEndSection": 246,
"text": "Over the course of the last century, the average life expectancy of these patients has doubled and now stands at ∼25 years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34802091",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Duchenne muscular dystrophy (DMD) is a severe neuromuscular disorder with increasing life expectancy from late teens to over 30 years of age."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1450492",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "The special medical care in the National Sanatorium prolonged the life span of the patients with progressive muscular dystrophy from 15.8 years to 20.4 years over the last 20 years."
}
] | 12
|
BioASQ-training12b
| null | null |
64179aac690f196b51000037
|
bioasq_factoid
|
factoid
|
What is an approximate number of CTCF binding sites in the human genome?
|
[['30,000-50,000']]
|
[
"30,000-50,000",
"thirty thousand to fifty thousand",
"30k-50k"
] |
['The number of CTCF binding sites in the human genome lies between 31,000 and 50,000.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23707059",
"http://www.ncbi.nlm.nih.gov/pubmed/22955980",
"http://www.ncbi.nlm.nih.gov/pubmed/22829947",
"http://www.ncbi.nlm.nih.gov/pubmed/22709888",
"http://www.ncbi.nlm.nih.gov/pubmed/15670593",
"http://www.ncbi.nlm.nih.gov/pubmed/15229244",
"http://www.ncbi.nlm.nih.gov/pubmed/11854173",
"http://www.ncbi.nlm.nih.gov/pubmed/11076856",
"http://www.ncbi.nlm.nih.gov/pubmed/8034708"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23707059",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 384,
"text": "To study CTCF multivalency in vivo, we define ZF binding requirements at ∼50,000 genomic sites in primary lymphocytes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22709888",
"endSection": "abstract",
"offsetInBeginSection": 1436,
"offsetInEndSection": 1521,
"text": "However, only ~3,700 out of the ~5,700 CTCFL- and ~31,000 CTCF-binding sites overlap."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23707059",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 384,
"text": "To study CTCF multivalency in vivo, we define ZF binding requirements at ∼50,000 genomic sites in primary lymphocytes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22709888",
"endSection": "abstract",
"offsetInBeginSection": 1436,
"offsetInEndSection": 1521,
"text": "However, only ~3,700 out of the ~5,700 CTCFL- and ~31,000 CTCF-binding sites overlap."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001665",
"http://www.uniprot.org/uniprot/CTCF_HUMAN",
"http://www.uniprot.org/uniprot/CTCF_MOUSE",
"http://www.uniprot.org/uniprot/CTCF_CHICK",
"http://www.uniprot.org/uniprot/CTCF_RAT"
] |
[] |
533c38b3c45e133714000009
|
bioasq_factoid
|
yesno
|
Are Luminopsins a fusion proteins of luminol and Rhodopsin ?
|
['no']
|
[
"no"
] |
['No, Luminopsins are fusion proteins of light-sensing opsins and light-emitting luciferases.', 'No, Luminopsins are a family of light-activated proteins that are related to rhodopsin, but are not fusion proteins of luminol and rhodopsin.', 'No, luminopsins are fusion proteins of light-sensing opsins and light-emitting luciferases, not luminol and rhodopsin.', 'No. Luminopsins are light-sensing opsins fused to light-emitting luciferases.', 'Luminopsins are fusion proteins of luciferase and opsin that allow interrogation of neuronal circuits at different temporal and spatial resolutions using light for its activation.', 'No, Luminopsins are fusion proteins of luciferase and opsin.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33398820",
"http://www.ncbi.nlm.nih.gov/pubmed/26733686",
"http://www.ncbi.nlm.nih.gov/pubmed/31263065",
"http://www.ncbi.nlm.nih.gov/pubmed/30957296",
"http://www.ncbi.nlm.nih.gov/pubmed/28862809"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33398820",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 252,
"text": "Bioluminescence-optogenetics is mediated by luminopsin fusion proteins-light-sensing opsins fused to light-emitting luciferases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28862809",
"endSection": "abstract",
"offsetInBeginSection": 238,
"offsetInEndSection": 466,
"text": "Here we have expanded and refined the versatility of luminopsin tools by fusing an alternative luciferase variant with high light emission, Gaussia luciferase mutant GLucM23, to depolarizing and hyperpolarizing channelrhodopsins"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30957296",
"endSection": "abstract",
"offsetInBeginSection": 633,
"offsetInEndSection": 710,
"text": " luminopsins by fusing light-sensing opsins with light-emitting luciferases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31263065",
"endSection": "abstract",
"offsetInBeginSection": 343,
"offsetInEndSection": 550,
"text": "ouse iPS-NPCs were transduced with a novel optochemogenetics fusion protein, luminopsin 3 (LMO3), which consisted of a bioluminescent luciferase, Gaussia luciferase, and an opsin, Volvox Channelrhodopsin 1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26733686",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "Luminopsins are fusion proteins of luciferase and opsin that allow interrogation of neuronal circuits at different temporal and spatial resolutions by choosing either extrinsic physical or intrinsic biological light for its activation."
}
] | 12
|
BioASQ-training12b
| null | null |
642d4c9b57b1c7a315000013
|
bioasq_yesno
|
yesno
|
Is Lasmiditan effective for migraine?
|
['yes']
|
[
"yes"
] |
['Yes, Lasmiditan is effective for treatment of migraine. This has been demonstrated in clinical trials.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29488143",
"http://www.ncbi.nlm.nih.gov/pubmed/29352859",
"http://www.ncbi.nlm.nih.gov/pubmed/22430431",
"http://www.ncbi.nlm.nih.gov/pubmed/22459549",
"http://www.ncbi.nlm.nih.gov/pubmed/30446595",
"http://www.ncbi.nlm.nih.gov/pubmed/29563831",
"http://www.ncbi.nlm.nih.gov/pubmed/20855362",
"http://www.ncbi.nlm.nih.gov/pubmed/28103158",
"http://www.ncbi.nlm.nih.gov/pubmed/30323656",
"http://www.ncbi.nlm.nih.gov/pubmed/29098075"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29352859",
"endSection": "abstract",
"offsetInBeginSection": 1191,
"offsetInEndSection": 1370,
"text": "Amongst the ditans, lasmiditan: (i) fails to constrict human coronary arteries; and (ii) is effective for the acute treatment of migraine in preliminary Phase III clinical trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29488143",
"endSection": "abstract",
"offsetInBeginSection": 1443,
"offsetInEndSection": 1634,
"text": "Although ongoing phase III clinical trials are needed to confirm its efficacy and safety, lasmiditan might offer an alternative to treat acute migraine with no associated cardiovascular risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29563831",
"endSection": "abstract",
"offsetInBeginSection": 1136,
"offsetInEndSection": 1255,
"text": "Lasmiditan is considered to be the first member of a new drug category, the neurally acting anti-migraine agent (NAAMA)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30323656",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Lasmiditan for the treatment of acute migraine: a review and potential role in clinical practice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30323656",
"endSection": "abstract",
"offsetInBeginSection": 523,
"offsetInEndSection": 951,
"text": "Lasmiditan, a highly selective 5-HT1F agonist, has completed two Phase III randomized, double blind, placebo-controlled clinical trials, with a third - a long-term, open-label safety study - still underway. Research to date suggests lasmiditan lacks vasoconstrictive properties and may be a safe and effective treatment option in patients refractory to current acute migraine medications or who have cardiovascular risk factors."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30446595",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Lasmiditan is an effective acute treatment for migraine: A phase 3 randomized study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30446595",
"endSection": "abstract",
"offsetInBeginSection": 640,
"offsetInEndSection": 1192,
"text": "Compared with placebo, more patients dosed with lasmiditan 200 mg were free of headache pain at 2 hours after dosing (32.2% vs 15.3%; odds ratio [OR] 2.6, 95% confidence interval [CI] 2.0-3.6, p< 0.001), similar to those dosed with lasmiditan 100 mg (28.2%; OR 2.2, 95% CI 1.6-3.0, p< 0.001). Furthermore, compared with those dosed with placebo, more patients dosed with lasmiditan 200 mg (40.7% vs 29.5%; OR 1.6, 95% CI 1.3-2.1, p< 0.001) and lasmiditan 100 mg (40.9%; OR 1.7, 95% CI, 1.3-2.2, p< 0.001) were free of their MBS at 2 hours after dosing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30446595",
"endSection": "abstract",
"offsetInBeginSection": 1250,
"offsetInEndSection": 1431,
"text": "CONCLUSIONS: Lasmiditan dosed at 200 and 100 mg was efficacious and well tolerated in the treatment of acute migraine among patients with a high level of cardiovascular risk factors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30446595",
"endSection": "abstract",
"offsetInBeginSection": 1474,
"offsetInEndSection": 1697,
"text": "CLASSIFICATION OF EVIDENCE: This study provides Class I evidence that for adult patients with migraine, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a migraine attack."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22430431",
"endSection": "abstract",
"offsetInBeginSection": 1163,
"offsetInEndSection": 1350,
"text": "For the understanding of migraine pathophysiology, it is very important to note that a selective 5-HT(1F) receptor agonist like lasmiditan is effective in the acute treatment of migraine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22430431",
"endSection": "abstract",
"offsetInBeginSection": 1430,
"offsetInEndSection": 1584,
"text": "While lasmiditan most likely is effective in the treatment of migraine attacks it had, unfortunately, a high incidence of CNS related AEs in the oral RCT. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20855362",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "Acute treatment of migraine with the selective 5-HT1F receptor agonist lasmiditan--a randomised proof-of-concept trial.At intravenous doses of 20 mg and higher, lasmiditan proved effective in the acute treatment of migraine. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30323656",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Lasmiditan for the treatment of acute migraine: a review and potential role in clinical practice. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22459549",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "BACKGROUND\nLasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept migraine study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22459549",
"endSection": "abstract",
"offsetInBeginSection": 2485,
"offsetInEndSection": 2582,
"text": "INTERPRETATION\nOral lasmiditan seems to be safe and effective in the acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28103158",
"endSection": "abstract",
"offsetInBeginSection": 912,
"offsetInEndSection": 1124,
"text": "The 5-HT1F receptor agonist lasmiditan, a drug acting through non-vasoconstrictive mechanisms, represents a promising safe, effective and tolerated acute migraine therapy also for patients at cardiovascular risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22430431",
"endSection": "abstract",
"offsetInBeginSection": 1013,
"offsetInEndSection": 1200,
"text": "For the understanding of migraine pathophysiology, it is very important to note that a selective 5-HT(1F) receptor agonist like lasmiditan is effective in the acute treatment of migraine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22430431",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "The 5-HT1F receptor agonist lasmiditan as a potential treatment of migraine attacks: a review of two placebo-controlled phase II trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29098075",
"endSection": "abstract",
"offsetInBeginSection": 647,
"offsetInEndSection": 1016,
"text": "Within the past few years, new and promising drugs such as more specific 5-HT 1F receptor agonists (that is, lasmiditan) and monoclonal calcitonin gene-related peptide (CGRP) receptor antibodies entered advanced development phases while non-invasive neuromodulatory approaches were suggested to be potentially effective as non-pharmaceutical interventions for migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30446595",
"endSection": "abstract",
"offsetInBeginSection": 1484,
"offsetInEndSection": 1706,
"text": "CLASSIFICATION OF EVIDENCE\nThis study provides Class I evidence that for adult patients with migraine, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a migraine attack."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22459549",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "BACKGROUND Lasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept migraine study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22459549",
"endSection": "abstract",
"offsetInBeginSection": 2485,
"offsetInEndSection": 2582,
"text": "INTERPRETATION Oral lasmiditan seems to be safe and effective in the acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30323656",
"endSection": "abstract",
"offsetInBeginSection": 730,
"offsetInEndSection": 951,
"text": "Research to date suggests lasmiditan lacks vasoconstrictive properties and may be a safe and effective treatment option in patients refractory to current acute migraine medications or who have cardiovascular risk factors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20855362",
"endSection": "abstract",
"offsetInBeginSection": 2310,
"offsetInEndSection": 2510,
"text": "The non-vascular, neural mechanism of action of lasmiditan may offer an alternative means to treat migraine especially in patients who have contra-indications for agents with vasoconstrictor activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30446595",
"endSection": "abstract",
"offsetInBeginSection": 669,
"offsetInEndSection": 1346,
"text": "Compared with placebo, more patients dosed with lasmiditan 200 mg were free of headache pain at 2 hours after dosing (32.2% vs 15.3%; odds ratio [OR] 2.6, 95% confidence interval [CI] 2.0-3.6, <br><b>CONCLUSIONS</b>: Lasmiditan dosed at 200 and 100 mg was efficacious and well tolerated in the treatment of acute migraine among patients with a high level of cardiovascular risk factors.<br><b>CLINICALTRIALSGOV IDENTIFIER</b>: NCT02439320.<br><b>CLASSIFICATION OF EVIDENCE</b>: This study provides Class I evidence that for adult patients with migraine, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a migraine attack.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22459549",
"endSection": "abstract",
"offsetInBeginSection": 2389,
"offsetInEndSection": 2617,
"text": "The most common adverse events were CNS related and included dizziness, fatigue, vertigo, paraesthesia, and somnolence.<br><b>INTERPRETATION</b>: Oral lasmiditan seems to be safe and effective in the acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20855362",
"endSection": "abstract",
"offsetInBeginSection": 2012,
"offsetInEndSection": 2238,
"text": "Dizziness, paresthesia and sensations of heaviness (usually limb) were more common on lasmiditan.<br><b>CONCLUSIONS</b>: At intravenous doses of 20 mg and higher, lasmiditan proved effective in the acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22459549",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "<b>BACKGROUND</b>: Lasmiditan (COL-144) is a novel, centrally acting, highly selective 5-HT(1F) receptor agonist without vasoconstrictor activity that seemed effective when given as an intravenous infusion in a proof-of-concept migraine study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22430431",
"endSection": "abstract",
"offsetInBeginSection": 1019,
"offsetInEndSection": 1206,
"text": "For the understanding of migraine pathophysiology, it is very important to note that a selective 5-HT(1F) receptor agonist like lasmiditan is effective in the acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30446595",
"endSection": "abstract",
"offsetInBeginSection": 1415,
"offsetInEndSection": 1610,
"text": "This study provides Class I evidence that for adult patients with migraine, lasmiditan increases the proportion of subjects who are headache pain free at 2 hours after treating a migraine attack."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22430431",
"endSection": "abstract",
"offsetInBeginSection": 1286,
"offsetInEndSection": 1440,
"text": "While lasmiditan most likely is effective in the treatment of migraine attacks it had, unfortunately, a high incidence of CNS related AEs in the oral RCT."
}
] | 11
|
BioASQ-training11b
| null | null |
5c6f6ae37c78d69471000054
|
bioasq_yesno
|
yesno
|
Is aggrephagy a variant of autophagy?
|
['yes']
|
[
"yes"
] |
['Yes,\nthe selective branch of autophagy that deals with identification, capture and degradation of protein aggregates is called aggrephagy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28837386",
"http://www.ncbi.nlm.nih.gov/pubmed/29686608",
"http://www.ncbi.nlm.nih.gov/pubmed/30027903"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30027903",
"endSection": "abstract",
"offsetInBeginSection": 894,
"offsetInEndSection": 1027,
"text": "The selective branch of autophagy that deals with identification, capture and degradation of protein aggregates is called aggrephagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29686608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Mechanistic insights into aggrephagy, a selective basal autophagy process to clear misfolded protein aggregates, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28837386",
"endSection": "abstract",
"offsetInBeginSection": 196,
"offsetInEndSection": 362,
"text": ", it is largely unknown how misfolded polypeptides form aggresomes and are eventually cleared by the aggresome-macroautophagy/autophagy pathway, so-called aggrephagy."
}
] | 11
|
BioASQ-training11b
| null | null |
5e94902f2d3121100d000012
|
bioasq_yesno
|
yesno
|
Is fish intake a protective factor against colorectal cancer?
|
['yes']
|
[
"yes"
] |
['Yes, fish intake is indeed a protective factor against colorectal cancer. Studies have shown that individuals who consume more fish have a significantly reduced risk of developing this type of cancer. Specifically, a 50-gram increase in daily fish consumption is associated with a 4% reduction in colorectal cancer risk', 'Yes, fish intake is a protective factor against colorectal cancer. A 50-g increment in daily fish consumption is associated with a 4% reduction in colorectal cancer risk.', 'Yes, fish intake appears to be a protective factor against colorectal cancer (CRC). Individuals in the highest category of fish consumption had a significantly reduced risk of CRC compared to those in the lowest category (SRR 0.94, 95%CI 0.89-0.99). Additionally, a dose-response meta-analysis found that a 50-gram increment in daily fish consumption was associated with a statistically significant 4% reduction in CRC risk (SRR 0.96, 95%CI 0.92-0.99).', 'Yes, fish intake has been shown to be a protective factor against colorectal cancer. In a meta-analysis of 17 cohort studies, individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category. Specifically, a 50-g increment in daily fish consumption was associated with a 4% reduction in colorectal cancer risk. The protective effect of fish intake was observed in both men and women and across all sub-sites of the colon and rectum. The mechanism by which fish intake reduces colorectal cancer risk is not fully understood, but may involve the omega-3 fatty acids and other nutrients found in fish.', 'According to the meta-analysis, yes, fish intake is a protective factor against colorectal cancer (CRC). The study found that individuals who consumed more fish had a significantly reduced risk of CRC. Specifically, those in the highest category of fish consumption had a 6% lower risk of CRC compared to those in the lowest category. Additionally, for every 50g increase in daily fish consumption, there was a 4% reduction in CRC risk. The study suggests that dietary recommendations for cancer prevention should take into account the evidence from epidemiological and preclinical studies that increasing fish consumption may be effective in preventing CRC.', 'Yes, fish intake is a protective factor against colorectal cancer, as indicated by multiple observational studies and meta-analyses showing an inverse association between fish consumption and colorectal cancer risk.', 'Yes, fish intake is a protective factor against colorectal cancer. This is based on a long-term prospective study that found intakes of fish and long-chain n-3 fatty acids from fish may decrease the risk for colorectal cancer. Additionally, a case-control study found that higher freshwater fish and sea fish intake is inversely associated with colorectal cancer risk among Chinese population.', 'Based on the provided snippets, the answer is yes, fish intake appears to be a protective factor against colorectal cancer (CRC). The data suggests that individuals who consume higher amounts of fish have a significantly reduced risk of CRC. Specifically, a daily increment of 50g in fish consumption is associated with a 4% reduction in CRC risk. This finding is supported by the statistically significant dose-response relationship observed in the meta-analysis. These results suggest that moderate fish consumption may be a useful strategy for reducing the risk of colorectal cancer.', 'Yes, fish intake appears to be a protective factor against colorectal cancer (CRC). According to a study, individuals who consumed fish at higher levels had a significantly reduced risk of CRC compared to those who consumed less fish. In a dose-response meta-analysis, a 50-g increase in daily fish consumption was associated with a statistically significant 4% reduction in CRC risk. Therefore, increasing fish intake may help lower the risk of developing colorectal cancer.', 'Yes, fish intake is a protective factor against colorectal cancer. Multiple studies have found that increased fish consumption is inversely associated with colorectal cancer risk. A meta-analysis found that fish consumption decreased the risk of colorectal cancer by 12%. Other studies have also found that high fish intake is associated with a decreased risk of colorectal cancer, which has been linked to the high content of n-3 polyunsaturated fatty acids (PUFAs) in some fish.', 'Fish intake is a protective factor against colorectal cancer (CRC). A meta-analysis found that individuals with higher fish consumption had a 6% lower risk of CRC, and for every 50g increase in daily fish consumption, there was a 4% reduction in CRC risk. The study suggests incorporating this information into dietary recommendations for cancer prevention.', 'The evidence is not conclusive to establish a causal relationship between fish intake and a reduced risk of colorectal cancer. While some studies suggest a protective effect, others show no association or even a positive correlation. The potential benefits of fish consumption should be weighed against the risks associated with contaminants such as mercury and polychlorinated biphenyls (PCBs). More research is needed to better understand the relationship between fish consumption and colorectal cancer risk, and to determine the optimal amount and type of fish intake for cancer prevention.', 'Yes, fish intake appears to be a protective factor against colorectal cancer. A meta-analysis found that individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category (SRR 0.94, 95% CI 0.89-0.99). The dose-response analysis showed that each 50g increment in daily fish consumption was associated with a statistically significant 4% reduction in colorectal cancer risk (SRR 0.96, 95% CI 0.92-0.99).', 'Yes, fish intake is considered to be a protective factor against colorectal cancer. A study found that individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category. Additionally, a dose-response meta-analysis found that a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in colorectal cancer risk.', 'Yes, fish intake appears to be a protective factor against colorectal cancer. Several epidemiological studies and meta-analyses have found an inverse association between fish consumption and colorectal cancer risk. The protective effect may be attributed to the high content of n-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in some fish. These PUFAs are thought to suppress the proliferation of colorectal mucosa and inhibit the development of colorectal cancer. Overall, the evidence suggests that increasing fish intake may have a preventive effect on colorectal cancer risk.', 'Yes, fish intake is a protective factor against colorectal cancer. Higher fish consumption significantly reduces the risk of colorectal cancer, and a 50-g daily increase in fish consumption is associated with a 4% reduction in colorectal cancer risk.', 'Fish intake has been inversely associated with colorectal cancer risk in several studies. A case-control study in Sweden found that canned fish consumption was lower among cases than among controls, and an inverse association was found between canned fish consumption and CRC risk. A cohort study in Sweden found that higher intake of long-chain omega-3 polyunsaturated fatty acids, which are abundant in fish, was associated with a lower risk of colorectal cancer in women. A meta-analysis of 41 studies found that fish consumption was associated with a lower risk of colorectal cancer. However, a cohort study in the United States found no association between fish intake and colorectal cancer risk. Overall, the evidence suggests that fish intake may be a protective factor against colorectal cancer, but more research is needed to confirm this association.', 'Yes, fish intake has been shown to be a protective factor against colorectal cancer. In a meta-analysis of 17 cohort studies, individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category. Additionally, a 50-g increment in daily fish consumption was associated with a 4% reduction in colorectal cancer risk. The protective effect of fish intake was observed in both men and women, and across all sub-sites of the colon and rectum. The mechanism by which fish intake reduces colorectal cancer risk is not fully understood, but may involve the omega-3 fatty acids and other nutrients found in fish.', 'Yes, fish intake is a protective factor against colorectal cancer. Individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer (CRC) compared to those in the lowest category. A 50-g increment in daily fish consumption was associated with a 4% reduction in CRC risk.', 'Yes, fish intake is a protective factor against colorectal cancer. Individuals in the highest category of fish consumption had a significantly reduced risk of CRC, and a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk', "Yes, according to the study, individuals with higher fish consumption had a significantly reduced risk of colorectal cancer (CRC). A 50-g increment in daily fish consumption was associated with a 4% reduction in CRC risk. \n\nPlease go ahead and ask your question. I'll respond accordingly. \n\n(Note: You can ask a question, and I'll provide an answer based on the given context. You can also ask follow-up questions based on my previous response.)", 'Based on the abstracts provided, it appears that fish intake is indeed a protective factor against colorectal cancer. The first study found an inverse association between fish intake and colorectal cancer risk, with a multivariate relative risk of 0.63 for the highest versus lowest category of fish intake. Similarly, the second study found a significant reduction in colorectal cancer risk at moderate fish intake (one or two servings per week), with an odds ratio of 0.70. The third study also suggested a protective effect of fish consumption against colorectal cancer, although the association was not statistically significant. Overall, the evidence suggests that consuming fish may decrease the risk of developing colorectal cancer.', 'Yes, fish intake is inversely associated with colorectal cancer risk, with a 12% decrease in risk found in a meta-analysis. This association is supported by multiple observational and clinical studies, which suggest that fish consumption may have a protective effect against colorectal cancer. The protective effect is thought to be due to the high content of n-3 polyunsaturated fatty acids, such as eicosapentaenoic acid and docosahexaenoic acid, in some fish.', 'Yes, fish intake is a protective factor against colorectal cancer. A number of studies have found an inverse relationship between fish consumption and the risk of developing colorectal cancer. For example, a case-control study in Eastern Europe found that increased fish intake was associated with a lower risk of colorectal cancer, even after adjusting for potential confounders such as demographic characteristics, body mass index, smoking status, and physical activity. Similarly, a prospective cohort study in the United States found that men who consumed fish at least once a week had a lower risk of colorectal cancer than those who rarely or never consumed fish. The protective effect of fish consumption on colorectal cancer risk may be due to the presence of long-chain n-3 fatty acids, which have been shown to have anti-inflammatory and antiproliferative effects in laboratory and animal studies. However, more research is needed to confirm these findings and to understand the underlying mechanisms', 'Fish intake is linked to reduced colorectal cancer (CRC) risk according to multiple studies. Moderate fish consumption and n-3 fatty acids from fish show inverse associations with CRC incidence, suggesting fish consumption provides protection against the disease.', 'Fish intake is linked to reduced colorectal cancer (CRC) risk, according to various studies. Moderate fish consumption and n-3 fatty acid intake from fish are associated with lower CRC incidence. Fish consumption of once a week or more might protect against CRC. Overall, these findings suggest that eating fish may have protective effects against the development of colorectal cancer.', 'Individuals in the highest (vs. lowest) category of fish consumption had a significantly reduced risk of CRC (SRR 0.94, 95%CI 0.89-0.99). In dose-response meta-analysis, a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk (SRR 0.96, 95%CI 0.92-0.99)', 'In summary, based on a meta-analysis, increased fish intake is associated with reduced colorectal cancer risk by 6% for those consuming more fish compared to the lowest category of consumers. For every 50g increase in daily consumption, there was an observed 4% decrease in CRC risk, suggesting that dietary recommendations may benefit from considering higher fish consumption as a potential preventative measure against colorectal cancer.', 'Yes, fish intake has been shown to be a protective factor against colorectal cancer. Studies have consistently found that higher consumption of fish, particularly fatty fish, is associated with a lower risk of colorectal cancer. The mechanisms by which fish consumption protects against colorectal cancer are thought to involve the n-3 polyunsaturated fatty acids found in fish, which have anti-inflammatory and antioxidant effects in the colon. Additionally, adherence to a Mediterranean-style diet, which includes high levels of fish consumption, has been shown to be protective against colorectal and breast cancer.', 'In summary, consuming more fish has been shown to lower the risk of colorectal cancer (CRC), with each 50g increase in daily intake associated with a 4% reduction in CRC risk according to the meta-analysis data and observed dose-response relationship.', 'Yes, fish intake is a protective factor against colorectal cancer. A study found that individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category. Additionally, a dose-response meta-analysis found that a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in colorectal cancer risk.', 'Yes, fish intake is a protective factor against colorectal cancer. Individuals in the highest category of fish consumption had a significantly reduced risk of CRC. Also, a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17419892",
"http://www.ncbi.nlm.nih.gov/pubmed/12671534",
"http://www.ncbi.nlm.nih.gov/pubmed/29399003",
"http://www.ncbi.nlm.nih.gov/pubmed/35458225",
"http://www.ncbi.nlm.nih.gov/pubmed/26264963",
"http://www.ncbi.nlm.nih.gov/pubmed/37572059",
"http://www.ncbi.nlm.nih.gov/pubmed/17425596",
"http://www.ncbi.nlm.nih.gov/pubmed/16201848",
"http://www.ncbi.nlm.nih.gov/pubmed/19553301",
"http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"http://www.ncbi.nlm.nih.gov/pubmed/36092326",
"http://www.ncbi.nlm.nih.gov/pubmed/7549825",
"http://www.ncbi.nlm.nih.gov/pubmed/28804436",
"http://www.ncbi.nlm.nih.gov/pubmed/24706410",
"http://www.ncbi.nlm.nih.gov/pubmed/15456633",
"http://www.ncbi.nlm.nih.gov/pubmed/33998355",
"http://www.ncbi.nlm.nih.gov/pubmed/36014940",
"http://www.ncbi.nlm.nih.gov/pubmed/15956652",
"http://www.ncbi.nlm.nih.gov/pubmed/25619144",
"http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"http://www.ncbi.nlm.nih.gov/pubmed/32537063",
"http://www.ncbi.nlm.nih.gov/pubmed/21888535",
"https://pubmed.ncbi.nlm.nih.gov/7549825/",
"http://www.ncbi.nlm.nih.gov/pubmed/24615521",
"http://www.ncbi.nlm.nih.gov/pubmed/23878344",
"http://www.ncbi.nlm.nih.gov/pubmed/19169007",
"http://www.ncbi.nlm.nih.gov/pubmed/35158907",
"https://pubmed.ncbi.nlm.nih.gov/28407090/",
"http://www.ncbi.nlm.nih.gov/pubmed/32138465",
"http://www.ncbi.nlm.nih.gov/pubmed/17823383",
"http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"http://www.ncbi.nlm.nih.gov/pubmed/19638981",
"http://www.ncbi.nlm.nih.gov/pubmed/31252190"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35158907",
"endSection": "abstract",
"offsetInBeginSection": 874,
"offsetInEndSection": 1195,
"text": " Individuals in the highest (vs. lowest) category of fish consumption had a significantly reduced risk of CRC (SRR 0.94, 95%CI 0.89-0.99). In dose-response meta-analysis, a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk (SRR 0.96, 95%CI 0.92-0.99)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35158907",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1196,
"text": "Background: Epidemiological studies on the association between fish consumption and colorectal cancer (CRC) risk have yielded inconsistent results, despite evidence from preclinical studies that long-chain ω-3 polyunsaturated fatty acids inhibit colorectal carcinogenesis. We conducted a meta-analysis of prospective epidemiological studies investigating the association between fish consumption and CRC risk among humans and reviewed studies examining the link between fish components and colorectal carcinogenesis in animal models. Methods: We included studies published until November 2020. We calculated the summary risk ratio (SRR) and 95% confidence intervals (CI) through random effects meta-analysis models in order to summarize evidence from studies among humans. Results: Twenty-five prospective epidemiological studies encompassing 25,777 CRC cases were included. Individuals in the highest (vs. lowest) category of fish consumption had a significantly reduced risk of CRC (SRR 0.94, 95%CI 0.89-0.99). In dose-response meta-analysis, a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk (SRR 0.96, 95%CI 0.92-0.99)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31252190",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1739,
"text": "BACKGROUND & AIMS: There is an unclear association between intake of fish and long-chain n-3 polyunsaturated fatty acids (n-3 LC-PUFAs) and colorectal cancer (CRC). We examined the association between fish consumption, dietary and circulating levels of n-3 LC-PUFAs, and ratio of n-6:n-3 LC-PUFA with CRC using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.METHODS: Dietary intake of fish (total, fatty/oily, lean/white) and n-3 LC-PUFA were estimated by food frequency questionnaires given to 521,324 participants in the EPIC study; among these, 6291 individuals developed CRC (median follow up, 14.9 years). Levels of phospholipid LC-PUFA were measured by gas chromatography in plasma samples from a sub-group of 461 CRC cases and 461 matched individuals without CRC (controls). Multivariable Cox proportional hazards and conditional logistic regression models were used to calculate hazard ratios (HRs) and odds ratios (ORs), respectively, with 95% CIs.RESULTS: Total intake of fish (HR for quintile 5 vs 1, 0.88; 95% CI, 0.80-0.96; Ptrend = .005), fatty fish (HR for quintile 5 vs 1, 0.90; 95% CI, 0.82-0.98; Ptrend = .009), and lean fish (HR for quintile 5 vs 1, 0.91; 95% CI, 0.83-1.00; Ptrend = .016) were inversely associated with CRC incidence. Intake of total n-3 LC-PUFA (HR for quintile 5 vs 1, 0.86; 95% CI, 0.78-0.95; Ptrend = .010) was also associated with reduced risk of CRC, whereas dietary ratio of n-6:n-3 LC-PUFA was associated with increased risk of CRC (HR for quintile 5 vs 1, 1.31; 95% CI, 1.18-1.45; Ptrend < .001). Plasma levels of phospholipid n-3 LC-PUFA was not associated with overall CRC risk, but an inverse trend was observed for proximal compared with distal co"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35458225",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1122,
"text": "Fish is among the foods exerting favourable effects on colorectal cancer (CRC), but the possible role of canned fish has been insufficiently investigated. We aimed to investigate the relationship between canned fish consumption and CRC risk. We analysed data from two case−control studies conducted between 1992 and 2010 in several Italian areas, comprising a total of 2419 incident cases and 4723 hospital controls. Canned fish consumption was analysed according to the weekly frequency of consumption as <1 serving per week (s/w) (reference category), 1 < 2 s/w, and ≥2 s/w. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression models, adjusting for several recognised confounding factors. Overall, canned fish consumption was lower among cases than among controls (23.8% vs. 28.6%). An inverse association was found between canned fish consumption and CRC risk with a significant trend in risk (OR = 0.81, 95% CI: 0.71−0.92 for intermediate consumption and OR = 0.66, 95% CI: 0.51−0.85 for the highest one), which was consistent across strata of several covariates."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32138465",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 629,
"text": "PURPOSE: We aimed to assess the association between the dietary intake of fish-derived omega-3 polyunsaturated fatty acids and the risk of colorectal cancer among Swedish women.MATERIALS AND METHODS: A total of 48,233 women with information on dietary intake were included in the analysis. Participants were followed for incident colorectal cancer until 31 December 2012. Cox proportional hazard models were used to assess the association between baseline fatty acid intake and colorectal cancer risk. All analyses were stratified by colon and rectal cancers.RESULTS: During a median of 21.3 years of follow-up, a total of 344 co"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28804436",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 907,
"text": "Background : Colorectal cancer (CRC) is considered one of the most common forms of cancer in the Western world. High intake of red and processed meat is considered to increase CRC development. Objective : This study examined associations between intake of red meats, poultry, and fish and incident CRC, and if weight status modifies the associations. Design : In the Malmö Diet and Cancer Study, dietary data was collected through a modified diet history method. Via the Swedish Cancer Registry, 728 cases of CRC were identified during 428 924 person-years of follow-up of 16 944 women and 10 987 men. Results : Beef intake was inversely associated with colon cancer. However, in men high intake of beef was associated with increased risk of rectal cancer. High intake of pork was associated with increased incidence of CRC, and colon cancer. Processed meat was associated with increased risk of CRC in men."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32537063",
"endSection": "abstract",
"offsetInBeginSection": 86,
"offsetInEndSection": 953,
"text": "alth problem. Diet plays a key role in preventing this type of cancer. The purpose of our study was to determine dietary risk factors for colorectal cancer in our Moroccan context.METHODS: we conducted a case-control study including patients with colorectal cancer compared with controls. The statistical analysis of results was carried out using R software.RESULTS: our study included 225 patients treated for cancer at the Mohammed VI Hospital Center and 225 controls. The average age of our study population at the time of diagnosis was 55.49±14.06 years, including 119 men (52.9%) and 106 women (47.1%) with a sex ratio of 1.12. Associations were found between the highest intakes of red meats, cold meats, sausages and the risk of colorectal cancer (p = 0.0001) with F4 (4-7 times / week) vs F1 (never): OR = 4.4 (1.6-11.9); (p = 0.001), OR = 1.7 (0.5-5.7); (p ="
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33998355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 900,
"text": "The incidence and mortality rates of colorectal cancer (CRC) in Northeast Brazil are increasing. To study the association between CRC and diet, data were obtained from 64 patients with CRC and 123 sex- and age-matched controls. The dietary details were recorded using a validated food frequency questionnaire. Nutrient intake was calculated using Dietsys software (National Cancer Institute, Maryland, USA). In a binary logistic regression model of dietary components (model 1), the chance of CRC increased by 0.2% (odds ratio [OR] = 1.002; 95% confidence interval [CI]: 1.000-1.004) for each gram of processed meat intake per week (p < 0.010). Consumption of eggs decreased the chance by 0.1% per gram (OR = 0.999; 95% CI: 0.998-1.000; p < 0.050). The use of oil (including olive oil) for served food decreased the chance by 1.8% (OR = 0.982; 95% CI: 0.970-0.992) for each time consumed (p < 0.010)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36014940",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 772,
"text": "There is limited evidence to support the relationship between the consumption of animal-source foods other than red meat and processed meat and colorectal cancer (CRC) risk. We aimed to examine the recent available evidence from observational studies about the association between these food groups’ intake and CRC risk. For this systematic review, we searched the PubMed database for the last five years. A total of fourteen cohort studies and seven case−control studies comprising a total of >60,000 cases were included. The studies showed a consistent significant decrease in CRC risk, overall and by subsites, associated with a high consumption of total dairy products. Less strong effects associated with the consumption of any subtype of dairy product were observed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37572059",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 514,
"text": "Colorectal cancer (CRC) accounts for considerable mortalities worldwide. Several modifiable risk factors, including a high intake of certain foods and beverages can cause CRC. This review summarized the latest findings on the intake of various foods, nutrients, ingredients, and beverages on CRC development, with the objective of classifying them as a risk or protective factor. High-risk food items include red meat, processed meat, eggs, high alcohol consumption, sugar-sweetened beverages, and chocolate candy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36092326",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1521,
"text": "Background and Objective: Colorectal cancer (CRC) is the third most common cancer worldwide, and the incidence and mortality rates continue to increase annually. Many factors, including genetic, immune, and environmental factors, influence the occurrence and development of CRC. Along with the economic development, changes in lifestyle, especially dietary factors, have been shown to greatly affect the progression of CRC. Increasing evidence showed that dietary patterns influence the risk of CRC and affect CRC treatment. The present review describes the role of diet in the prevention and treatment of CRC with the hope that doctors attach importance to dietary patterns in educating patients with CRC or at risk of CRC and that diet may be regarded as an auxiliary treatment strategy to improve patients' outcomes.Methods: English language articles published from 2000 to December 2021 in PubMed and Embase were identified by searching titles for keywords including \"diet\", \"colorectal cancer\", \"dietary pattern\", and \"dietary factor\"; 101 articles were selected for review.Key Content and Findings: The present review describes the role of different dietary patterns and factors in the prevention and treatment of CRC. We found that dietary intervention is closely related to the occurrence, development, and prognosis of CRC. Adherence to the Mediterranean diet (MD), the Dietary Approaches to Stop Hypertension (DASH) diet, fasting, vegetarian diets and the ketogenic diet (KD) were found to reduce the risk of CR"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21888535",
"endSection": "abstract",
"offsetInBeginSection": 453,
"offsetInEndSection": 874,
"text": "The hypothesis linking fish consumption and low cancer incidence appears to be supported by little epidemiological data. However, there are several factors that may mask potential protective associations with fish intake. The type and the amount of fish eaten, the cooking method, the stage of the cancer and, amongst women, menopausal status may all be important factors that relate to whether fish is protective or not."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21888535",
"endSection": "abstract",
"offsetInBeginSection": 453,
"offsetInEndSection": 674,
"text": "The hypothesis linking fish consumption and low cancer incidence appears to be supported by little epidemiological data. However, there are several factors that may mask potential protective associations with fish intake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 242,
"offsetInEndSection": 399,
"text": " We examined the association between intakes of fish and n-3 fatty acids from fish and colorectal cancer risk in men enrolled in the Physicians' Health Study"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26264963",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 402,
"text": "The association between specific fish intake and colorectal cancer risk remains controversial. This study aimed to examine the association between specific fish intake and colorectal cancer risk in Chinese population in a large case control study. During July 2010 to November 2014, 1189 eligible colorectal cancer cases and 1189 frequency-matched controls (age and sex) completed in-person interviews."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 1217,
"offsetInEndSection": 1638,
"text": "Our findings for n-3 fatty acids were similar to those for fish; the multivariate relative risk (95% confidence interval) of total colorectal cancer for the highest versus lowest quartile of n-3 fatty acids was 0.74 (0.57-0.95; P trend = 0.01).CONCLUSIONS: Our results from this long-term prospective study suggest that intakes of fish and long-chain n-3 fatty acids from fish may decrease the risk for colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 1684,
"offsetInEndSection": 1845,
"text": "This study had no publication bias.CONCLUSION: Our findings from this meta-analysis suggest that fish consumption is inversely associated with colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 672,
"offsetInEndSection": 943,
"text": "Cox proportional hazards models were used to estimate multivariate relative risks for colorectal cancer for the categories of fish intake and quartiles of n-3 fatty acid intake.RESULTS: During 22 years of follow-up, 500 men had a confirmed diagnosis of colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "BACKGROUND: Fish consumption may protect against colorectal cancer, but results from observational studies are inconsistent; therefore, a systematic review with a meta-analysis wa"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 1130,
"offsetInEndSection": 1329,
"text": ", 0.88; 95% CI, 0.80-0.95). The pooled ORs of colorectal cancer for the highest versus lowest fish consumption in case-control studies and cohort studies were 0.83 (95% CI, 0.72-0.95) and 0.93 (95% C"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 1420,
"offsetInEndSection": 1655,
"text": "t not among cohort studies. A significant inverse association was found between fish intake and rectal cancer (summary OR, 0.79; 95% CI, 0.65-0.97), and there was a modest trend seen between fish consumption and colon cancer (summary O"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23878344",
"endSection": "abstract",
"offsetInBeginSection": 643,
"offsetInEndSection": 739,
"text": "l studies were identified. Fish consumption was not significantly associated with colorectal, co"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19169007",
"endSection": "abstract",
"offsetInBeginSection": 1688,
"offsetInEndSection": 1822,
"text": "ion and intake of meat products.CONCLUSIONS: The study results indicate that increased fish intake may have a preventive effect on CRC"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 596,
"text": "Prospective and case-control studies either do not show an association between fish intake and cancer risks or show reduced risks at high fish intakes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19169007",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "BACKGROUND/AIMS: Current epidemiologic studies investigating the effect of fish intake on colorectal cancer (CRC)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24615521",
"endSection": "abstract",
"offsetInBeginSection": 308,
"offsetInEndSection": 529,
"text": "According to our results, the consumption of vegetables, fruits, fish, as well as coffee seems to be protective against digestive cancer, while the consumption of citrus and olive oil is protective against gastric cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37572059",
"endSection": "abstract",
"offsetInBeginSection": 515,
"offsetInEndSection": 824,
"text": "Food items that are protective include milk, cheese and other dairy products, fruits, vegetables (particularly cruciferous), whole grains, legumes (particularly soy beans), fish, tea (particularly green tea), coffee (particularly among Asians), chocolate, and moderate alcohol consumption (particularly wine)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15456633",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1310,
"text": "Although long-chain n-3 polyunsaturated fatty acids (Ln-3 PUFA), which are abundant in fish, have shown protective effects on colorectal cancer in laboratory studies, epidemiological studies to date have not been consistent. We evaluated the relationship of consumption of fish and Ln-3 PUFA to the colon and rectal cancer risk in the two cohorts of the Japan Public Health Center-based prospective study of 42,525 men and 46,133 women. Dietary and other exposure data were obtained between 1990 and 1994. Through December 1999, 705 cases of colon and rectal cancer were documented. When data from the two cohorts were pooled, multivariable relative risks (RRs) for the highest quartile compared with the lowest quartile of fish consumption were 1.07 (95% confidence interval, CI = 0.77-1.48) for colon cancer and 0.95 (95% CI = 0.63-1.43) for rectal cancer with no dose-risk trend. RRs for the highest quartile compared with the lowest quartile of eicosapentaenoic acid consumption were 1.05 (95% CI = 0.76-1.46) for colon cancer and 0.91 (95% CI = 0.60-1.38) for rectal cancer with no dose-risk trend. This study does not support the role of fish and Ln-3 PUFA in the etiology of colon and rectal cancer in this population whose fish consumption was high and the variation in Ln-3 PUFA consumption was large."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17419892",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 444,
"text": "Recent studies have shown a decreased risk of colon cancer with consumption of fish. However, most studies on fish consumption do not distinguish between lean and fatty fish, or between poached and fried fish. The aim of this study was to investigate any association between fish consumption and colon cancer in The Norwegian Women and Cancer (NOWAC) study. We focused mainly on lean fish, which was further divided into poached and fried fish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 230,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies. Human studies have not shown consist"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 1189,
"offsetInEndSection": 1433,
"text": "h colon and rectal cancers. Our findings for n-3 fatty acids were similar to those for fish; the multivariate relative risk (95% confidence interval) of total colorectal cancer for the highest versus lowest quartile of n-3 fatty acids was 0.74 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21888535",
"endSection": "abstract",
"offsetInBeginSection": 300,
"offsetInEndSection": 452,
"text": "Among 273 estimates of association reported by these studies, 53 indicated decreased risk while 12 indicated increased risk associated with fish intake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 916,
"offsetInEndSection": 980,
"text": "nosis of colorectal cancer. Fish intake was inversely associated"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16201848",
"endSection": "abstract",
"offsetInBeginSection": 547,
"offsetInEndSection": 728,
"text": "Fish oil feeding resulted in lower 8-OHdG levels (P = 0.038), higher levels of apoptosis (P = 0.035), and a lower cell proliferative index (P = 0.05) compared with corn oil feeding."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 852,
"text": "Breast and colorectal cancer are main causes of death in industrialized countries. In these cancers dietary factors appear to play beneficial or adverse roles. One of the possible beneficial factors may be fish intake or the n-3 polyunsaturated fatty acids from fish, as found in epidemiological and clinical studies. In population studies, high intake of fish during many years is associated with reduced risks of breast and colorectal cancer. Prospective and case-control studies either do not show an association between fish intake and cancer risks or show reduced risks at high fish intakes. In these studies, fish consumption may have been too low or may not reflect fish consumption over a longer period. In population, case-control, and prospective studies, fish and fish n-3 polyunsaturated fatty acids were not found to increase cancer risks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1419,
"text": "BACKGROUND: Fish consumption may protect against colorectal cancer, but results from observational studies are inconsistent; therefore, a systematic review with a meta-analysis was conducted.METHODS: Relevant studies were identified by a search of MEDLINE and EMBASE databases to May 2011, with no restrictions. Reference lists from retrieved articles also were reviewed. Studies that reported odds ratio (OR) or relative risk estimates with 95% confidence intervals (CIs) for the association between the consumption of fish and the risk of colorectal, colon, or rectal cancer were included. Two authors independently extracted data and assessed study quality. The risk estimate (hazard ratio, relative risk, or OR) of the highest and lowest reported categories of fish intake were extracted from each study and analyzed using a random-effects model.RESULTS: Twenty-two prospective cohort and 19 case-control studies on fish consumption and colorectal cancer risk met the inclusion criteria and were included in the meta-analysis. Our analysis found that fish consumption decreased the risk of colorectal cancer by 12% (summary OR, 0.88; 95% CI, 0.80-0.95). The pooled ORs of colorectal cancer for the highest versus lowest fish consumption in case-control studies and cohort studies were 0.83 (95% CI, 0.72-0.95) and 0.93 (95% CI, 0.86-1.01), respectively. There was heterogeneity among case-control studies (P<.001) b"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 915,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies. Human studies have not shown consistent results. We examined the association between intakes of fish and n-3 fatty acids from fish and colorectal cancer risk in men enrolled in the Physicians' Health Study.METHODS: The Physicians' Health Study began as a randomized trial to examine the effect of aspirin and beta-carotene supplementation on cancer and cardiovascular disease. Fish intake was assessed at the 12-month follow-up with an abbreviated food-frequency questionnaire. Cox proportional hazards models were used to estimate multivariate relative risks for colorectal cancer for the categories of fish intake and quartiles of n-3 fatty acid intake.RESULTS: During 22 years of follow-up, 500 men had a confirmed dia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19169007",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1687,
"text": "BACKGROUND/AIMS: Current epidemiologic studies investigating the effect of fish intake on colorectal cancer (CRC) risk are scarce. Therefore, the aim of this study was to elucidate the relationship between fish consumption and CRC risk.METHODS: This hospital-based case-control study was performed in 548 CRC patients (Surgery Clinic, University Hospital in Krakow, Poland) between November 2000 and May 2008. Histological findings, information on anatomic location and stage of cancer were available for all the patients enrolled in this study. The control group consisted of 745 patients of the same hospital with no history of cancer admitted for treatment of non-neoplastic conditions. During the 5-year study period, the food frequency questionnaire used focused on the reference period that was defined as 1-5 years prior to CRC diagnosis for the CRC cases and the date of hospital admission for the controls.RESULTS: The crude odds ratio (OR) was inversely related to fish consumption (z for trend in quartiles of intake= -2.31, p=0.021; OR=0.89; 95% confidence interval, CI: 0.81-0.98). The risk of CRC increased with intake of stewed or cooked meat (z for trend in quartiles of intake=2.14; p=0.032; OR=1.11; 95% CI: 1.01-1.23). The adjusted OR showed a significant reduction in CRC already at the moderate fish intake of one or two servings per week (OR=0.70; 95% CI: 0.51-0.94), but it was even lower at higher fish intake (OR=0.56; 95% CI: 0.39-0.86). All multivariate statistical models employed in the analysis considered potential confounders, such as demographic characteristics of subjects, body mass index, smoking status, leisure time physical activity, energy consump"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24706410",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 810,
"text": "The association between fish, ω-3 and ω-6 polyunsaturated fatty acid (PUFA) intake and risk of colorectal cancer (CRC) remains inconclusive. Recent prospective studies suggest that the relationship may vary by gender, subsite and duration of follow-up. We followed 123,529 US adults (76,386 women and 47,143 men) without a history of cancer at baseline for 24 to 26 years. Fish and PUFA intake was assessed at baseline and updated every 4 years by using a validated food-frequency questionnaire. We found no overall association between fish, ω-3 and ω-6 PUFA intake and CRC risk with hazard ratio (HR) of 1.03 [95% confidence interval (CI): 0.89-1.20] comparing marine ω-3 intake of ≥ 0.30 g/d versus <0.15 g/d among women and 1.05 (95% CI: 0.85-1.30) comparing intake of ≥ 0.41 g/d versus <0.16 g/d among men."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35158907",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 272,
"text": "Background: Epidemiological studies on the association between fish consumption and colorectal cancer (CRC) risk have yielded inconsistent results, despite evidence from preclinical studies that long-chain ω-3 polyunsaturated fatty acids inhibit colorectal carcinogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28804436",
"endSection": "abstract",
"offsetInBeginSection": 908,
"offsetInEndSection": 972,
"text": "Fish intake was inversely associated with risk of rectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 399,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies. Human studies have not shown consistent results. We examined the association between intakes of fish and n-3 fatty acids from fish and colorectal cancer risk in men enrolled in the Physicians' Health Study"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies. Human studies have not shown consistent results"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17425596",
"endSection": "abstract",
"offsetInBeginSection": 1544,
"offsetInEndSection": 1748,
"text": "Our findings do not support the hypothesis that consumption of red meat increases colorectal cancer risk but do suggest that high intake of fish may decrease the risk, particularly of distal colon cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26264963",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Higher freshwater fish and sea fish intake is inversely associated with colorectal cancer risk among Chinese population: a case-control study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 596,
"text": "One of the possible beneficial factors may be fish intake or the n-3 polyunsaturated fatty acids from fish, as found in epidemiological and clinical studies. In population studies, high intake of fish during many years is associated with reduced risks of breast and colorectal cancer. Prospective and case-control studies either do not show an association between fish intake and cancer risks or show reduced risks at high fish intakes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 712,
"offsetInEndSection": 976,
"text": "In population, case-control, and prospective studies, fish and fish n-3 polyunsaturated fatty acids were not found to increase cancer risks. Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 976,
"text": "In these studies, fish consumption may have been too low or may not reflect fish consumption over a longer period. In population, case-control, and prospective studies, fish and fish n-3 polyunsaturated fatty acids were not found to increase cancer risks. Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 712,
"offsetInEndSection": 1253,
"text": "In population, case-control, and prospective studies, fish and fish n-3 polyunsaturated fatty acids were not found to increase cancer risks. Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk. In several studies in which the effect of fish consumption on cancer risk was investigated, meat and meat products were positively related to cancer risk, suggesting that cancer risks might be reduced more effectively when meat and meat products in meals are replaced by fish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 444,
"text": "One of the possible beneficial factors may be fish intake or the n-3 polyunsaturated fatty acids from fish, as found in epidemiological and clinical studies. In population studies, high intake of fish during many years is associated with reduced risks of breast and colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 853,
"offsetInEndSection": 1473,
"text": "Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk. In several studies in which the effect of fish consumption on cancer risk was investigated, meat and meat products were positively related to cancer risk, suggesting that cancer risks might be reduced more effectively when meat and meat products in meals are replaced by fish. In conclusion, the existing knowledge suggests that an increase in the consumption of fish and fish n-3 polyunsaturated fatty acids in industrialized countries may contribute to lower breast and colorectal cancer risks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 853,
"offsetInEndSection": 976,
"text": "Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk."
}
] | 13
|
BioASQ-training13b
| null | null |
66214cc6b9f8b89d7e000003
|
bioasq_yesno
|
yesno
|
Is STAT3 involved in EIF2AK2-dependent suppression of autophagy?
|
['yes']
|
[
"yes"
] |
['Pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. On the other hand, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy. Therefore, STAT3 may act as a competitive inhibitor of EIF2AK2 to suppress autophagy.', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"http://www.ncbi.nlm.nih.gov/pubmed/23084476"
] |
[
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 843,
"offsetInEndSection": 1277,
"text": "STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1279,
"offsetInEndSection": 1527,
"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1588,
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
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"text": "These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy"
},
{
"beginSection": "title",
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"endSection": "title",
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"text": "Cytoplasmic STAT3 represses autophagy by inhibiting PKR activity"
},
{
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"offsetInBeginSection": 371,
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"text": "The SH2 domain of STAT3 was found to interact with the catalytic domain of the eIF2α kinase 2 EIF2AK2, best known as protein kinase R (PKR). Pharmacological and genetic inhibition of STAT3 stimulated the activating phosphorylation of PKR and consequent eIF2α hyperphosphorylation. Moreover, PKR depletion inhibited autophagy as initiated by chemical STAT3 inhibitors or free fatty acids like palmitate"
},
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"text": "STAT3-targeting chemicals and palmitate caused the disruption of inhibitory STAT3-PKR interactions, followed by PKR-dependent eIF2α phosphorylation, which facilitates autophagy induction"
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"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
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"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1"
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"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy"
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"text": "However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy"
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"text": "Direct interaction between STAT3 and EIF2AK2 controls fatty acid-induced autophagy"
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. "
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"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. "
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"text": "These results unravel an unsuspected mechanism of autophagy control that involves STAT3 and PKR as interacting partners."
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. "
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. "
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"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
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"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
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"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
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"text": ", Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
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"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
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"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
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"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
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"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
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"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
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"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
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"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
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"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
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"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
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"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
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{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 838,
"offsetInEndSection": 1018,
"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1187,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
56cdf3995795f9a73e00003a
|
bioasq_yesno
|
yesno
|
Is there any functional association during viral replication between flaviviridae viral RNA depended RNA polymerase and viral helicase?
|
['yes']
|
[
"yes"
] |
Several labs have obtained evidence for a protein complex that involves many of the nonstructural (NS) proteins encoded by the virus. NS3, NS4A, NS4B, NS5A, and NS5B appear to interact structurally and functionally. The interaction between the helicase, NS3, and the RNA polymerase, NS5B play a key role in viral replication. Pull-down experiments and surface plasmon resonance data indicate a direct interaction between NS3 and NS5B that is primarily mediated through the protease domain of NS3. This interaction reduces the basal ATPase activity of NS3. However, NS5B stimulates product formation in RNA unwinding experiments under conditions of excess nucleic acid substrate. When the concentrations of NS3 and NS5B are in excess of nucleic acid substrate, NS5B reduces the rate of NS3-catalyzed unwinding. Under pre-steady-state conditions, in which NS3 and substrate concentrations are similar, product formation increased in the presence of NS5B. The increase was consistent with 1:1 complex formed between the two proteins.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23463199",
"http://www.ncbi.nlm.nih.gov/pubmed/23157297",
"http://www.ncbi.nlm.nih.gov/pubmed/22040846",
"http://www.ncbi.nlm.nih.gov/pubmed/21946389",
"http://www.ncbi.nlm.nih.gov/pubmed/21898331",
"http://www.ncbi.nlm.nih.gov/pubmed/19951725",
"http://www.ncbi.nlm.nih.gov/pubmed/18179252",
"http://www.ncbi.nlm.nih.gov/pubmed/17319152",
"http://www.ncbi.nlm.nih.gov/pubmed/15917225",
"http://www.ncbi.nlm.nih.gov/pubmed/17660525"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18179252",
"endSection": "abstract",
"offsetInBeginSection": 275,
"offsetInEndSection": 1527,
"text": "Several labs have obtained evidence for a protein complex that involves many of the nonstructural (NS) proteins encoded by the virus. NS3, NS4A, NS4B, NS5A, and NS5B appear to interact structurally and functionally. In this study, we investigated the interaction between the helicase, NS3, and the RNA polymerase, NS5B. Pull-down experiments and surface plasmon resonance data indicate a direct interaction between NS3 and NS5B that is primarily mediated through the protease domain of NS3. This interaction reduces the basal ATPase activity of NS3. However, NS5B stimulates product formation in RNA unwinding experiments under conditions of excess nucleic acid substrate. When the concentrations of NS3 and NS5B are in excess of nucleic acid substrate, NS5B reduces the rate of NS3-catalyzed unwinding. Under pre-steady-state conditions, in which NS3 and substrate concentrations are similar, product formation increased in the presence of NS5B. The increase was consistent with 1:1 complex formed between the two proteins. A fluorescently labeled form of NS3 was used to investigate this interaction through fluorescence polarization binding assays. Results from this assay support interactions that include a 1:1 complex formed between NS3 and NS5B."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19951725",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 1037,
"text": "Contradictory results have been reported regarding NS3 in RNA synthesis. To investigate the effect of NS3 on classical swine fever virus (CSFV) NS5B RNA-dependent RNA polymerase activity (RdRp) activity and NS3-NS5B interaction, RdRp reactions, GST-pull-down assays and co-immunoprecipitation analyses containing NS5B and either of NS3 protein and the different truncated NS3 mutants were performed, respectively. We found that NS3 stimulated NS5B RdRp activity in a dose-dependent manner by binding to NS5 through a NS3 protease domain. Furthermore, mapping important regions of the NS3 protease domain was carried out by deletion mutagenesis, associated with RdRp reactions, GST-pull-down assays and co-immunoprecipitation analyses. Results showed that stimulation of CSFV NS5B RdRp activity was obtained by NS3 binding to NS5B through a 31-amino acid fragment at the N-terminal end of NS3 protease domain, which mediated a specific NS3-NS5B interaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21898331",
"endSection": "abstract",
"offsetInBeginSection": 113,
"offsetInEndSection": 474,
"text": "The protocols detailed in this unit are used to purify three recombinant enzymes that are widely used in HCV research: the HCV NS3 protease domain, the helicase domain as an NS3+NS4A complex, and the NS5B RNA-dependent RNA polymerase. The active enzymes are purified to homogeneity by two-column chromatography to support a screening program for HCV inhibitors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21946389",
"endSection": "abstract",
"offsetInBeginSection": 518,
"offsetInEndSection": 945,
"text": "Among potential targets are viral entry factors, including scavenger receptor type B1 (SR-B1) and CD81, as well as neutralizing antibodies against the viral glycoproteins. Popular targets related to translation and replication are the NS3/4A protease (inhibited by telaprevir and boceprevir) and the NS5B polymerase, as well as the NS2/3 autoprotease, the NS3 helicase, and nonenzymatic targets such as NS4B and NS5A proteins. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22040846",
"endSection": "abstract",
"offsetInBeginSection": 1210,
"offsetInEndSection": 1501,
"text": "The NS3 helicase domain competes with NS3 full-length for NS5 RdRp binding, with a K(d.) of 2.5μM. Since NS3 and NS5 are required for DENV replication, this fascile assay could be used to screen for non-nucleoside, allosteric inhibitors that disrupt the interaction between the two proteins."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018067",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020365",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012324",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012194",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012367"
] |
[
{
"o": "http://linkedlifedata.com/resource/umls/id/C0035691",
"p": "http://www.w3.org/2004/02/skos/core#broader",
"s": "http://linkedlifedata.com/resource/umls/id/C0206510"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0363752",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0206510"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0363753",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0206510"
},
{
"o": "RNA Virus",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7573489"
},
{
"o": "RNA Viruses",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0112753"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0363751",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0206510"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A2143236",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0206510"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0363752",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0206510"
},
{
"o": "Virus, RNA",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0132798"
},
{
"o": "Flaviviridae",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0363751"
},
{
"o": "Viruses, RNA",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7574474"
},
{
"o": "RNA virus",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0451316"
},
{
"o": "Flavivirus (arbovirus group B)",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A2143236"
},
{
"o": "Virus-RNA",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7666306"
},
{
"o": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:1886",
"p": "http://www.w3.org/2004/02/skos/core#broader",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:0050303"
},
{
"o": "Flaviviridae infectious disease",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:1886"
},
{
"o": "Hepacivirus infectious disease",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:0050303"
},
{
"o": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:1886",
"p": "http://www.w3.org/2004/02/skos/core#broader",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:993"
},
{
"o": "Flaviviridae infectious disease",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:1886"
},
{
"o": "Flavivirus infectious disease",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:993"
}
] |
5321b8579b2d7acc7e000008
|
bioasq_yesno
|
yesno
|
Is Ctf4 involved in sister chromatid cohesion establishment?
|
['yes']
|
[
"yes"
] |
['Yes. Ctf4 is associated with the replisome and is required for proper establishment of cohesion by facilitating cohesin acetylation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23334284",
"http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"http://www.ncbi.nlm.nih.gov/pubmed/19622120",
"http://www.ncbi.nlm.nih.gov/pubmed/17483413",
"http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"http://www.ncbi.nlm.nih.gov/pubmed/16962805",
"http://www.ncbi.nlm.nih.gov/pubmed/15598824",
"http://www.ncbi.nlm.nih.gov/pubmed/15485923",
"http://www.ncbi.nlm.nih.gov/pubmed/14742710",
"http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"http://www.ncbi.nlm.nih.gov/pubmed/19496828"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23334284",
"endSection": "abstract",
"offsetInBeginSection": 663,
"offsetInEndSection": 1151,
"text": "In addition to Eco1, several other factors contribute to cohesion establishment, including Ctf4, Ctf18, Tof1, Csm3, Chl1 and Mrc1, but little is known about their roles. Here, we show that each of these factors facilitates cohesin acetylation. Moreover, the absence of Ctf4 and Chl1, but not of the other factors, causes a synthetic growth defect in cells lacking Eco1. Distinct from acetylation defects, sister chromatid cohesion in ctf4Δ and chl1Δ cells is not improved by removing Wapl"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23334284",
"endSection": "abstract",
"offsetInBeginSection": 1328,
"offsetInEndSection": 1498,
"text": "Thus, Ctf4 and Chl1 delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"endSection": "abstract",
"offsetInBeginSection": 633,
"offsetInEndSection": 810,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Influence of the human cohesion establishment factor Ctf4/AND-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19622120",
"endSection": "abstract",
"offsetInBeginSection": 283,
"offsetInEndSection": 551,
"text": " Here, we used Xenopus egg extracts to show that AND-1 and Tim1-Tipin, homologues of Saccharomyces cerevisiae Ctf4 and Tof1-Csm3, respectively, are associated with the replisome and are required for proper establishment of the cohesion observed in the M-phase extracts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17483413",
"endSection": "abstract",
"offsetInBeginSection": 742,
"offsetInEndSection": 880,
"text": "These data defined two cohesion pathways, one containing CSM3, TOF1, CTF4, and CHL1, and the second containing MRC1, CTF18, CTF8, and DCC1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 829,
"offsetInEndSection": 1005,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16962805",
"endSection": "abstract",
"offsetInBeginSection": 460,
"offsetInEndSection": 628,
"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15598824",
"endSection": "abstract",
"offsetInBeginSection": 606,
"offsetInEndSection": 797,
"text": "WSS1 was also found to interact genetically with SGS1, TOP3, SRS2 and CTF4, which are involved in recombination, repair of replication forks and the establishment of sister chromatid cohesion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15485923",
"endSection": "abstract",
"offsetInBeginSection": 332,
"offsetInEndSection": 607,
"text": "The catalytic subunit of budding yeast Polalpha (Pol1p) has been shown to associate in vitro with the Spt16p-Pob3p complex, a component of the nucleosome reorganization system required for both replication and transcription, and with a sister chromatid cohesion factor, Ctf4p"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14742710",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 314,
"text": "Constituents of the replication fork, such as the DNA polymerase alpha-binding protein Ctf4, contribute to cohesion in ways that are poorly understood"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 858,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1 and the pathway involving the acetylation of Smc3."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 824,
"offsetInEndSection": 1002,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16962805",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 626,
"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase Chl1 and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 324,
"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 629,
"text": "We show here that CTF8, CTF4 and a helicase encoded by CHL1 are required for efficient sister chromatid cohesion in unperturbed mitotic cells, and provide evidence that Chl1 functions during S-phase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 430,
"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "abstract",
"offsetInBeginSection": 323,
"offsetInEndSection": 584,
"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 858,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1 and the pathway involving the acetylation of Smc3."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 824,
"offsetInEndSection": 1002,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16962805",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 626,
"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase Chl1 and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 324,
"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 629,
"text": "We show here that CTF8, CTF4 and a helicase encoded by CHL1 are required for efficient sister chromatid cohesion in unperturbed mitotic cells, and provide evidence that Chl1 functions during S-phase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 430,
"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "abstract",
"offsetInBeginSection": 323,
"offsetInEndSection": 584,
"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 858,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1 and the pathway involving the acetylation of Smc3."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 824,
"offsetInEndSection": 1002,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16962805",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 626,
"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase Chl1 and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 324,
"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 629,
"text": "We show here that CTF8, CTF4 and a helicase encoded by CHL1 are required for efficient sister chromatid cohesion in unperturbed mitotic cells, and provide evidence that Chl1 functions during S-phase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 430,
"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "abstract",
"offsetInBeginSection": 323,
"offsetInEndSection": 584,
"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 858,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1 and the pathway involving the acetylation of Smc3."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 824,
"offsetInEndSection": 1002,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16962805",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 626,
"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase Chl1 and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 324,
"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 629,
"text": "We show here that CTF8, CTF4 and a helicase encoded by CHL1 are required for efficient sister chromatid cohesion in unperturbed mitotic cells, and provide evidence that Chl1 functions during S-phase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 430,
"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "abstract",
"offsetInBeginSection": 323,
"offsetInEndSection": 584,
"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 829,
"offsetInEndSection": 1006,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23334284",
"endSection": "abstract",
"offsetInBeginSection": 1330,
"offsetInEndSection": 1501,
"text": "Thus, Ctf4 and Chl1 delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 829,
"offsetInEndSection": 1006,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23334284",
"endSection": "abstract",
"offsetInBeginSection": 1328,
"offsetInEndSection": 1499,
"text": "Thus, Ctf4 and Chl1 delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"endSection": "abstract",
"offsetInBeginSection": 633,
"offsetInEndSection": 860,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1 and the pathway involving the acetylation of Smc3"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 829,
"offsetInEndSection": 1006,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23334284",
"endSection": "abstract",
"offsetInBeginSection": 1328,
"offsetInEndSection": 1499,
"text": "Thus, Ctf4 and Chl1 delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"endSection": "abstract",
"offsetInBeginSection": 633,
"offsetInEndSection": 860,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1 and the pathway involving the acetylation of Smc3"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 829,
"offsetInEndSection": 1006,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15598824",
"endSection": "abstract",
"offsetInBeginSection": 606,
"offsetInEndSection": 797,
"text": "WSS1 was also found to interact genetically with SGS1, TOP3, SRS2 and CTF4, which are involved in recombination, repair of replication forks and the establishment of sister chromatid cohesion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23334284",
"endSection": "abstract",
"offsetInBeginSection": 1328,
"offsetInEndSection": 1499,
"text": "Thus, Ctf4 and Chl1 delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"endSection": "abstract",
"offsetInBeginSection": 633,
"offsetInEndSection": 860,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1 and the pathway involving the acetylation of Smc3"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222391",
"endSection": "abstract",
"offsetInBeginSection": 829,
"offsetInEndSection": 1006,
"text": "Our results suggest that Chl1 and Ctf4 are directly involved in homologous recombination repair rather than acting indirectly via the establishment of sister chromatid cohesion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23334284",
"endSection": "abstract",
"offsetInBeginSection": 1328,
"offsetInEndSection": 1499,
"text": "Thus, Ctf4 and Chl1 delineate an additional acetylation-independent pathway that might hold important clues as to the mechanism of sister chromatid cohesion establishment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20089864",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Ctf4/AND-1 is a highly conserved gene product required for both DNA replication and the establishment of sister chromatid cohesion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
"endSection": "abstract",
"offsetInBeginSection": 633,
"offsetInEndSection": 860,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1 and the pathway involving the acetylation of Smc3"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16962805",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Establishment of sister chromatid cohesion at the S. cerevisiae replication fork."
}
] | 5
|
BioASQ-training5b
|
[
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007062",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0034085",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0034087",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0034089",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0045876",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007063"
] |
[] |
553a5a34bc4f83e82800001a
|
bioasq_yesno
|
factoid
|
Which protein has been found to interact with phospholamban (PLN) and is also an anti-apoptotic protein?
|
[['The HS-1 associated protein X-1', '(HAX-1)']]
|
[
"The HS-1 associated protein X-1",
"(HAX-1)",
"HAX1",
"HAX-1 protein",
"HS1-associated protein X-1"
] |
['The HS-1 associated protein X-1 (HAX-1) is a mitochondrial protein with anti-apoptotic function and presents with numerous similarities to Bcl-2. and was identified as a phospholamban-binding partner. Using the yeast-two-hybrid system, HS-1 associated protein X-1 (HAX-1) was identified as a PLN-binding partner.', 'The sarco(endo)plasmic reticulum (SR) Ca(2+) transport ATPase (SERCA2a) and its inhibitor phospholamban (PLN) control the uptake of Ca(2+) by SR membranes during relaxation. Recently, the antiapoptotic HS-1-associated protein X-1 (HAX-1) was identified as a binding partner of PLN, and this interaction was postulated to regulate cell apoptosis.Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function.', 'Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function.The discovery of the PLN/HAX-1 interaction therefore unveils an important new link between Ca(2+) homeostasis and cell survival, with significant therapeutic potential.', 'Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function.The discovery of the PLN/HAX-1 interaction therefore unveils an important new link between Ca(2+) homeostasis and cell survival, with significant therapeutic potential.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"http://www.ncbi.nlm.nih.gov/pubmed/18415121",
"http://www.ncbi.nlm.nih.gov/pubmed/18971376",
"http://www.ncbi.nlm.nih.gov/pubmed/19920172",
"http://www.ncbi.nlm.nih.gov/pubmed/24550830"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 479,
"text": "To identify additional proteins that may interact with PLN, we used the yeast-two-hybrid system to screen an adult human cardiac cDNA library. HS-1 associated protein X-1 (HAX-1) was identified as a PLN-binding partner."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "abstract",
"offsetInBeginSection": 1348,
"offsetInEndSection": 1669,
"text": "Analysis of the anti-apoptotic function of HAX-1 revealed that the presence of PLN enhanced the HAX-1 protective effects from hypoxia/reoxygenation-induced cell death. These findings suggest a possible link between the Ca(2+) handling by the sarcoplasmic reticulum and cell survival mediated by the PLN/HAX-1 interaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18415121",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 800,
"text": "The sarco(endo)plasmic reticulum Ca(2+) transport adenosine triphosphatase (SERCA2a) and its regulator phospholamban (PLN) have a central role in modulating Ca(2+) homeostasis and, therefore, cardiac function. Herein, we discuss the mechanisms through which SERCA2a and PLN control cardiomyocyte function in health and disease. Emphasis is placed on our newly identified PLN-binding partner HS-1-associated protein X-1 (HAX-1), which has an anti-apoptotic function and presents with numerous similarities to Bcl-2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18415121",
"endSection": "abstract",
"offsetInBeginSection": 955,
"offsetInEndSection": 1123,
"text": "The discovery of the PLN/HAX-1 interaction therefore unveils an important new link between Ca(2+) homeostasis and cell survival, with significant therapeutic potential."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18971376",
"endSection": "abstract",
"offsetInBeginSection": 97,
"offsetInEndSection": 442,
"text": "The sarco(endo)plasmic reticulum (SR) Ca(2+) transport ATPase (SERCA2a) and its inhibitor phospholamban (PLN) control the uptake of Ca(2+) by SR membranes during relaxation. Recently, the antiapoptotic HS-1-associated protein X-1 (HAX-1) was identified as a binding partner of PLN, and this interaction was postulated to regulate cell apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18971376",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1038,
"text": "On triple transfections with PLN, however, HAX-1 massively translocated to the ER membranes, where it codistributed with PLN and SERCA2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18971376",
"endSection": "abstract",
"offsetInBeginSection": 1343,
"offsetInEndSection": 1473,
"text": "These findings suggest that HAX-1 may promote cell survival through modulation of SERCA2 protein levels and thus ER Ca(2+) stores."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19920172",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 407,
"text": "The HS-1 associated protein X-1 (HAX-1) is a ubiquitously expressed protein that protects cardiomyocytes from programmed cell death. Here we identify HAX-1 as a regulator of contractility and calcium cycling in the heart. HAX-1 overexpression reduced sarcoplasmic reticulum Ca-ATPase (SERCA2) pump activity in isolated cardiomyocytes and in vivo, leading to depressed myocyte calcium kinetics and mechanics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19920172",
"endSection": "abstract",
"offsetInBeginSection": 488,
"offsetInEndSection": 723,
"text": "The inhibitory effects of HAX-1 were abolished upon phosphorylation of phospholamban, which plays a fundamental role in controlling basal contractility and constitutes a key downstream effector of the beta-adrenergic signaling cascade."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24550830",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 978,
"text": " Furthermore, the effects of PLN and its phosphorylation on cardiac function are subject to additional regulation by its interacting partners, the anti-apoptotic HAX-1 protein and Gm or the anchoring unit of protein phosphatase 1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18415121",
"endSection": "abstract",
"offsetInBeginSection": 609,
"offsetInEndSection": 796,
"text": " Emphasis is placed on our newly identified PLN-binding partner HS-1-associated protein X-1 (HAX-1), which has an anti-apoptotic function and presents with numerous similarities to Bcl-2."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 479,
"text": "To identify additional proteins that may interact with PLN, we used the yeast-two-hybrid system to screen an adult human cardiac cDNA library. HS-1 associated protein X-1 (HAX-1) was identified as a PLN-binding partner."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24550830",
"endSection": "abstract",
"offsetInBeginSection": 754,
"offsetInEndSection": 982,
"text": "Furthermore, the effects of PLN and its phosphorylation on cardiac function are subject to additional regulation by its interacting partners, the anti-apoptotic HAX-1 protein and Gm or the anchoring unit of protein phosphatase 1"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Phospholamban interacts with HAX-1, a mitochondrial protein with anti-apoptotic function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24550830",
"endSection": "abstract",
"offsetInBeginSection": 754,
"offsetInEndSection": 982,
"text": "Furthermore, the effects of PLN and its phosphorylation on cardiac function are subject to additional regulation by its interacting partners, the anti-apoptotic HAX-1 protein and Gm or the anchoring unit of protein phosphatase 1"
}
] | 5
|
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/PPLA_BOVIN",
"http://www.uniprot.org/uniprot/PPLA_CHICK",
"http://www.uniprot.org/uniprot/PPLA_MOUSE",
"http://www.uniprot.org/uniprot/PPLA_RAT",
"http://www.uniprot.org/uniprot/PPLA_CANFA",
"http://www.uniprot.org/uniprot/PPLA_PIG",
"http://www.uniprot.org/uniprot/PPLA_RABIT",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051017"
] |
[] |
54f9cb34dd3fc62544000002
|
bioasq_factoid
|
factoid
|
As of September 2018, what machine learning algorithm is used to for cardiac arrhythmia detection from a short single-lead ECG recorded by a wearable device?
|
['SVM OR Support Vector Machine']
|
[
"SVM",
"Support Vector Machine",
"Support Vector Machines"
] |
['Support Vector machines( SVM) can be used for cardiac arrhythmia detection in from an ECG recorded by a wearable device.', 'SVM approach for cardiac arrhythmias detection in short single-lead ECG recorded by a wearable device']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30102239"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30102239",
"endSection": "title",
"offsetInBeginSection": 12,
"offsetInEndSection": 113,
"text": "SVM approach for cardiac arrhythmias detection in short single-lead ECG recorded by a wearable device"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30102239",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 359,
"text": "Multi-stage SVM approach for cardiac arrhythmias detection in short single-lead ECG recorded by a wearable device.<AbstractText Label=\"OBJECTIVE\" NlmCategory=\"OBJECTIVE\">Use of wearable ECG devices for arrhythmia screening is limited due to poor signal quality, small number of leads and short records, leading to incorrect recognition of pathological events. "
}
] | 11
|
BioASQ-training11b
| null | null |
5c5219f67e3cb0e231000006
|
bioasq_factoid
|
yesno
|
Are cardenolides inhibitors of Na+/K+ ATPase?
|
['yes']
|
[
"yes"
] |
['Yes,\nCardenolides have shown significant antitumor activity due to their ability to inhibit the Na+K+ATPase enzyme, and the expression of this enzyme is increased in tumor cells.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30053394",
"http://www.ncbi.nlm.nih.gov/pubmed/30372816",
"http://www.ncbi.nlm.nih.gov/pubmed/29683473"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30053394",
"endSection": "abstract",
"offsetInBeginSection": 257,
"offsetInEndSection": 493,
"text": ". Previously, we reported that a variety of cardenolides impart anti-transmissible gastroenteritis coronavirus (TGEV) activity in swine testicular (ST) cells, through targeting of the cell membrane sodium/potassium pump, Na+/K+-ATPase. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29683473",
"endSection": "abstract",
"offsetInBeginSection": 970,
"offsetInEndSection": 1092,
"text": ": We found evidence for low cardenolides by HPLC, but substantial toxicity when extracts were assayed on Na+ /K+ -ATPases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30372816",
"endSection": "abstract",
"offsetInBeginSection": 316,
"offsetInEndSection": 490,
"text": "Cardenolides have shown significant antitumor activity due to their ability to inhibit the Na+K+ATPase enzyme, and the expression of this enzyme is increased in tumor cells. "
}
] | 11
|
BioASQ-training11b
| null | null |
5c9906dcecadf2e73f00002f
|
bioasq_yesno
|
factoid
|
What is the Drosophila melanogaster Groucho protein?
|
[['Groucho (Gro) is a Drosophila melanogaster transcriptional corepressor']]
|
[
"Groucho",
"Gro",
"Drosophila melanogaster transcriptional corepressor",
"Drosophila Groucho",
"Drosophila Gro"
] |
['Groucho proteins are abundant and broadly expressed nuclear factors that lack intrinsic DNA-binding activity but can interact with a variety of DNA-binding proteins. The recruitment of Groucho to specific gene regulatory sequences results in transcriptional repression.\nGroucho (Gro) is a Drosophila melanogaster transcriptional corepressor.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24086079",
"http://www.ncbi.nlm.nih.gov/pubmed/22319573",
"http://www.ncbi.nlm.nih.gov/pubmed/22305159",
"http://www.ncbi.nlm.nih.gov/pubmed/21666599",
"http://www.ncbi.nlm.nih.gov/pubmed/21429299",
"http://www.ncbi.nlm.nih.gov/pubmed/20405012",
"http://www.ncbi.nlm.nih.gov/pubmed/19956621",
"http://www.ncbi.nlm.nih.gov/pubmed/19250647",
"http://www.ncbi.nlm.nih.gov/pubmed/19101520",
"http://www.ncbi.nlm.nih.gov/pubmed/18721877",
"http://www.ncbi.nlm.nih.gov/pubmed/18254933",
"http://www.ncbi.nlm.nih.gov/pubmed/18034187",
"http://www.ncbi.nlm.nih.gov/pubmed/17643306",
"http://www.ncbi.nlm.nih.gov/pubmed/17624551",
"http://www.ncbi.nlm.nih.gov/pubmed/16508633",
"http://www.ncbi.nlm.nih.gov/pubmed/15861397"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24086079",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 361,
"text": "Although a repressor could function by recruiting just a single co-repressor, many can recruit more than one, with Drosophila Brinker (Brk) recruiting the co-repressors CtBP and Groucho (Gro), "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22319573",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "Groucho (Gro) is a Drosophila corepressor required by numerous DNA-binding repressors, many of which are distributed in gradients and provide positional information during development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22305159",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Drosophila Groucho (Gro) is the founding member of a family of metazoan corepressors. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21666599",
"endSection": "abstract",
"offsetInBeginSection": 389,
"offsetInEndSection": 475,
"text": "Tcf3 requires corepressor molecules such as Groucho (Gro)/TLE and HDAC1 for activity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21429299",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 378,
"text": "We identified the transcriptional co-repressor xTLE1/Groucho as an EphrinB1 interacting protein. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20405012",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Groucho (Gro) is a Drosophila melanogaster transcriptional corepressor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19956621",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 251,
"text": "Transcriptional co-repressors of the Groucho/transducin-like Enhancer of split (Gro/TLE) family regulate the expression of a variety of genes and are involved in numerous developmental processes in both invertebrate and vertebrate species."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15861397",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "The proteins termed TLE in humans, Grg in mice and Groucho in Drosophila constitute a family of transcriptional corepressors. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16508633",
"endSection": "abstract",
"offsetInBeginSection": 195,
"offsetInEndSection": 250,
"text": "Groucho (Gro)/TLE, a global developmental corepressor, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17624551",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 46,
"text": "The Groucho/Tle family of corepressor proteins"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17643306",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "Groucho proteins are abundant and broadly expressed nuclear factors that lack intrinsic DNA-binding activity but can interact with a variety of DNA-binding proteins. The recruitment of Groucho to specific gene regulatory sequences results in transcriptional repression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18034187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "The Groucho (Gro)/transducin-like enhancer of split family of transcriptional corepressors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18254933",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "The Drosophila Groucho (Gro) protein was the founding member of the family of transcriptional co-repressor proteins that now includes the transducin-like enhancer of split (TLE) and Grorelated gene (Grg) proteins in vertebrate"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18721877",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Groucho/TLE proteins are global corepressors that are recruited to target promoters by different families of DNA-binding repressors. "
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011506",
"http://www.uniprot.org/uniprot/GROU_DROME",
"http://www.uniprot.org/uniprot/TLE1_DANRE",
"http://www.uniprot.org/uniprot/TLE2_DANRE",
"http://www.uniprot.org/uniprot/TLE1_MOUSE",
"http://www.uniprot.org/uniprot/TLE4_XENLA",
"http://www.uniprot.org/uniprot/TLE4_MOUSE",
"http://www.uniprot.org/uniprot/TLE6_MOUSE",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0003674"
] |
[] |
54f608f85f206a0c06000007
|
bioasq_factoid
|
factoid
|
In what type of clinical trial has RT001 been evaluated against Friedreich's ataxia?
|
['phase I/II double-blind, randomized, comparator-controlled trial']
|
[
"phase I/II double-blind, randomized, comparator-controlled trial",
"phase I/II trial",
"phase I/II clinical trial",
"phase I/II study",
"double-blind phase I/II trial",
"randomized phase I/II trial",
"comparator-controlled phase I/II trial",
"phase I/II randomized controlled trial",
"phase I/II double-blind study",
"phase I/II randomized study"
] |
["RT001 was evaluatd in a phase I/II double-blind, randomized, comparator-controlled trial in Friedreich's ataxia patients."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29624723"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29624723",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Randomized, clinical trial of RT001: Early signals of efficacy in Friedreich's ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29624723",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 500,
"text": "We conducted a phase I/II double-blind, comparator-controlled trial with 2 doses of RT001 in Friedreich's ataxia patients (9 subjects each cohort). "
}
] | 12
|
BioASQ-training12b
| null | null |
64402bb057b1c7a315000043
|
bioasq_factoid
|
yesno
|
Can exosomes be detected in urine?
|
['yes']
|
[
"yes"
] |
['Yes, urinary exosomes can be detected in urine.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24044569",
"http://www.ncbi.nlm.nih.gov/pubmed/24060994",
"http://www.ncbi.nlm.nih.gov/pubmed/24069349",
"http://www.ncbi.nlm.nih.gov/pubmed/24058411",
"http://www.ncbi.nlm.nih.gov/pubmed/24315007",
"http://www.ncbi.nlm.nih.gov/pubmed/24250247",
"http://www.ncbi.nlm.nih.gov/pubmed/24205503",
"http://www.ncbi.nlm.nih.gov/pubmed/24196483",
"http://www.ncbi.nlm.nih.gov/pubmed/24101370",
"http://www.ncbi.nlm.nih.gov/pubmed/23585095"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24044569",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 370,
"text": "Exosomes are nanovesicles secreted into the extracellular environment upon internal vesicle fusion with the plasma membrane. The molecular content of exosomes is a fingerprint of the releasing cell type and of its status. For this reason, and because they are released in easily accessible body fluids such as blood and urine, they represent a precious biomedical tool. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24060994",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Exosomes are vesicles that are released from the kidney into urine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24060994",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Quantification of human urinary exosomes by nanoparticle tracking analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24069349",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Urinary extracellular vesicles (uEVs) are released by cells throughout the nephron and contain biomolecules from their cells of origin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24058411",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "Urinary exosomes have been proposed as potential diagnostic tools."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24315007",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Urinary exosomes as a source of kidney dysfunction biomarker in renal transplantation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24250247",
"endSection": "abstract",
"offsetInBeginSection": 73,
"offsetInEndSection": 231,
"text": ". Here we sought to optimize the methodologies for the isolation and quantification of urinary exosomal microRNA as a prelude to biomarker discovery studies. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24205503",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "Exosomes are small (30-150 nm) vesicles containing unique RNA and protein cargo, secreted by all cell types in culture. They are also found in abundance in body fluids including blood, saliva, and urine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24196483",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Urinary exosome-like vesicles (ELVs) are a heterogenous mixture (diameter 40-200 nm) containing vesicles shed from all segments of the nephron including glomerular podocytes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24101370",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 141,
"text": "Exosomes are cytoplasm containing vesicles released by many cells that can be found in several biological fluids including urine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23585095",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Proteomic analysis of urinary exosomes in cardiovascular and associated kidney diseases by two-dimensional electrophoresis and LC-MS/MS"
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D055354",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014556"
] |
[] |
550895c12e93f0133a000002
|
bioasq_yesno
|
yesno
|
Are Drosophila ultraconserved elements candidate ncRNAs?
|
['yes']
|
[
"yes"
] |
['Yes. Highly constrained intergenic Drosophila ultraconserved elements are candidate ncRNAs.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25618141"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25618141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Highly constrained intergenic Drosophila ultraconserved elements are candidate ncRNAs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25618141",
"endSection": "abstract",
"offsetInBeginSection": 306,
"offsetInEndSection": 1403,
"text": "Here, we report the discovery and characterization of UCEs from 12 sequenced Drosophila species. We identified 98 elements ≥80 bp long with very high conservation across the Drosophila phylogeny. Population genetic analyses reveal that these UCEs are not present in mutational cold spots. Instead we infer that they experience a level of selective constraint almost 10-fold higher compared with missense mutations in protein-coding sequences, which is substantially higher than that observed previously for human UCEs. About one-half of these Drosophila UCEs overlap the transcribed portion of genes, with many of those that are within coding sequences likely to correspond to sites of ADAR-dependent RNA editing. For the remaining UCEs that are in nongenic regions, we find that many are potentially capable of forming RNA secondary structures. Among ten chosen for further analysis, we discovered that the majority are transcribed in multiple tissues of Drosophila melanogaster. We conclude that Drosophila species are rich with UCEs and that many of them may correspond to novel noncoding RNAs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25618141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Highly Constrained Intergenic Drosophila Ultraconserved Elements Are Candidate ncRNAs"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25618141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Highly constrained intergenic Drosophila ultraconserved elements are candidate ncRNAs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25618141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Highly constrained intergenic Drosophila ultraconserved elements are candidate ncRNAs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25618141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Highly constrained intergenic Drosophila ultraconserved elements are candidate ncRNAs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25618141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Highly constrained intergenic Drosophila ultraconserved elements are candidate ncRNAs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25618141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Highly constrained intergenic Drosophila ultraconserved elements are candidate ncRNAs."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004330"
] |
[] |
56d1accb67f0cb3d66000001
|
bioasq_yesno
|
factoid
|
What causes Japanese Spotted Fever?
|
['Rickettsia japonica']
|
[
"Rickettsia japonica",
"Rickettsia japonica (Japanese spotted fever)",
"Rickettsia japonica (Rickettsial disease)",
"Rickettsia japonica (Rickettsiosis)"
] |
['Japanese Spotted Fever is caused by Rickettsia japonica.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35507925",
"http://www.ncbi.nlm.nih.gov/pubmed/36016429",
"http://www.ncbi.nlm.nih.gov/pubmed/32863353"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32863353",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "Non-pathogenic Rickettsia species LON strains closely related to an agent of Japanese spotted fever (JSF), R. japonica, were isolated in Japan from Haemaphysalis longicornis ticks in 2001. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36016429",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "Severe fever with thrombocytopenia syndrome (SFTS) and Japanese spotted fever (JSF; a spotted fever group rickettsiosis) are tick-borne zoonoses that are becoming a significant public health threat in Japan and East Asia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35507925",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 288,
"text": "Rickettsia japonica is a member of SFG rickettsiae causing Japanese spotted fever (JSF) and can transmit to humans via infected ticks. "
}
] | 12
|
BioASQ-training12b
| null | null |
63eefa3bf36125a426000012
|
bioasq_factoid
|
factoid
|
What is the target of daratumumab?
|
['CD38']
|
[
"CD38",
"T10",
"ADP-ribosyl cyclase 1",
"NAD+-glycohydrolase",
"NAD+-glycohydrolase 1",
"NAD+-cyclase",
"NAD+-glycohydrolase CD38",
"NAD+-cyclase CD38"
] |
['Daratumumab is a fully human anti-CD38 IgG1-κ monoclonal antibody. It is approved for treatment of multiple myeloma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24471924",
"http://www.ncbi.nlm.nih.gov/pubmed/21109694",
"http://www.ncbi.nlm.nih.gov/pubmed/25626316",
"http://www.ncbi.nlm.nih.gov/pubmed/24971019",
"http://www.ncbi.nlm.nih.gov/pubmed/27195659",
"http://www.ncbi.nlm.nih.gov/pubmed/26812873",
"http://www.ncbi.nlm.nih.gov/pubmed/24053207",
"http://www.ncbi.nlm.nih.gov/pubmed/24849305",
"http://www.ncbi.nlm.nih.gov/pubmed/27859027",
"http://www.ncbi.nlm.nih.gov/pubmed/24555809",
"http://www.ncbi.nlm.nih.gov/pubmed/25878332",
"http://www.ncbi.nlm.nih.gov/pubmed/25531698",
"http://www.ncbi.nlm.nih.gov/pubmed/26778538",
"http://www.ncbi.nlm.nih.gov/pubmed/27557302",
"http://www.ncbi.nlm.nih.gov/pubmed/27780867",
"http://www.ncbi.nlm.nih.gov/pubmed/26658418",
"http://www.ncbi.nlm.nih.gov/pubmed/27363983",
"http://www.ncbi.nlm.nih.gov/pubmed/26362528",
"http://www.ncbi.nlm.nih.gov/pubmed/27222480",
"http://www.ncbi.nlm.nih.gov/pubmed/25760767",
"http://www.ncbi.nlm.nih.gov/pubmed/24253022",
"http://www.ncbi.nlm.nih.gov/pubmed/25964097",
"http://www.ncbi.nlm.nih.gov/pubmed/27896689",
"http://www.ncbi.nlm.nih.gov/pubmed/26308596",
"http://www.ncbi.nlm.nih.gov/pubmed/26631114",
"http://www.ncbi.nlm.nih.gov/pubmed/25975191",
"http://www.ncbi.nlm.nih.gov/pubmed/24350987",
"http://www.ncbi.nlm.nih.gov/pubmed/25988285",
"http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"http://www.ncbi.nlm.nih.gov/pubmed/25398450",
"http://www.ncbi.nlm.nih.gov/pubmed/25764134",
"http://www.ncbi.nlm.nih.gov/pubmed/25865943",
"http://www.ncbi.nlm.nih.gov/pubmed/27913523",
"http://www.ncbi.nlm.nih.gov/pubmed/26137203"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26362528",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 407,
"text": "Dominantly daratumumab (anti-CD38) and elotuzumab (anti-CS1) showed extraordinary effectiveness in phase I/II trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26658418",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 229,
"text": "In the last few weeks, the FDA approved three new therapies for multiple myeloma: ixazomib, the first oral proteasome inhibitor; and daratumumab and elotuzumab, two monoclonal antibodies that target CD38 and SLAMF7, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26631114",
"endSection": "abstract",
"offsetInBeginSection": 183,
"offsetInEndSection": 464,
"text": "Of these agents, CD38-targeting antibodies have marked single agent activity in extensively pretreated MM, and preliminary results from studies with relapsed/refractory patients have shown enhanced therapeutic efficacy when daratumumab and isatuximab are combined with other agents"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26631114",
"endSection": "abstract",
"offsetInBeginSection": 1445,
"offsetInEndSection": 1800,
"text": "Furthermore, daratumumab, and probably also other CD38-targeting antibodies, interfere with blood compatibility testing and thereby complicate the safe release of blood products. Neutralization of the therapeutic CD38 antibody or CD38 denaturation on reagent red blood cells mitigates daratumumab interference with transfusion laboratory serologic tests. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26812873",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "Daratumumab is a fully human anti-CD38 IgG1-κ monoclonal antibody (mAb) currently being evaluated in several Phase 2 and 3 clinical studies for the treatment of multiple myeloma (MM). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 336,
"text": "In this study, we describe the cytotoxic mechanisms of action of daratumumab, a novel, high-affinity, therapeutic human mAb against a unique CD38 epitope."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25626316",
"endSection": "abstract",
"offsetInBeginSection": 262,
"offsetInEndSection": 443,
"text": "This article focuses on the basic and clinical aspects of several emerging and promising novel MoAbs for MM, such as elotuzumab which targets CS1 and daratumumab which targets CD38."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Daratumumab, a novel therapeutic human CD38 monoclonal antibody, induces killing of multiple myeloma and other hematological tumors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21109694",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 702,
"text": "Daratumumab is a novel human CD38 monoclonal antibody which kills CD38+ multiple myeloma cells via antibody-dependent cell-mediated cytotoxicity, complement-dependent cytotoxicity and apoptosis.To explore the effect of lenalidomide combined with daratumumab, we first carried out standard antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity assays in which the CD38+ multiple myeloma cell line UM-9 and primary multiple myeloma cells isolated from patients were used as target cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25975191",
"endSection": "abstract",
"offsetInBeginSection": 542,
"offsetInEndSection": 798,
"text": "However, we discovered, next to an expected effect of effector (natural killer cells/monocytes) to target (MM cells) ratio on ADCC, a significant association between CD38 expression and daratumumab-mediated ADCC (127 patients), as well as CDC (56 patients)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26308596",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Targeting CD38 with Daratumumab Monotherapy in Multiple Myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21109694",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Towards effective immunotherapy of myeloma: enhanced elimination of myeloma cells by combination of lenalidomide with the human CD38 monoclonal antibody daratumumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26308596",
"endSection": "abstract",
"offsetInBeginSection": 63,
"offsetInEndSection": 409,
"text": "We studied daratumumab, a CD38-targeting, human IgG1� monoclonal antibody, in a phase 1-2 trial involving patients with relapsed myeloma or relapsed myeloma that was refractory to two or more prior lines of therapy.METHODS: In part 1, the dose-escalation phase, we administered daratumumab at doses of 0.005 to 24 mg per kilogram of body weight. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24849305",
"endSection": "abstract",
"offsetInBeginSection": 1888,
"offsetInEndSection": 2027,
"text": "Antibodies targeting CS-1 (elotuzumab) and CD38 (daratumumab) in particular are currently undergoing advanced clinical phase II/III trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 337,
"text": "In this study, we describe the cytotoxic mechanisms of action of daratumumab, a novel, high-affinity, therapeutic human mAb against a unique CD38 epitope. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21109694",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 703,
"text": "Daratumumab is a novel human CD38 monoclonal antibody which kills CD38+ multiple myeloma cells via antibody-dependent cell-mediated cytotoxicity, complement-dependent cytotoxicity and apoptosis.To explore the effect of lenalidomide combined with daratumumab, we first carried out standard antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity assays in which the CD38+ multiple myeloma cell line UM-9 and primary multiple myeloma cells isolated from patients were used as target cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25975191",
"endSection": "abstract",
"offsetInBeginSection": 542,
"offsetInEndSection": 799,
"text": "However, we discovered, next to an expected effect of effector (natural killer cells/monocytes) to target (MM cells) ratio on ADCC, a significant association between CD38 expression and daratumumab-mediated ADCC (127 patients), as well as CDC (56 patients)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27222480",
"endSection": "abstract",
"offsetInBeginSection": 267,
"offsetInEndSection": 425,
"text": "These mechanisms may also target nonplasma cells that express CD38, which prompted evaluation of daratumumab's effects on CD38-positive immune subpopulations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26658418",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 302,
"text": "In the last few weeks, the FDA approved three new therapies for multiple myeloma: ixazomib, the first oral proteasome inhibitor; and daratumumab and elotuzumab, two monoclonal antibodies that target CD38 and SLAMF7, respectively. <CopyrightInformation>©2016 American Association for Cancer Research.</C"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24053207",
"endSection": "abstract",
"offsetInBeginSection": 509,
"offsetInEndSection": 677,
"text": "This review focuses on the basic and clinical aspects of two emerging and promising novel MoAbs for MM, elotuzumab which targets CS1 and daratumumab which targets CD38."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24350987",
"endSection": "abstract",
"offsetInBeginSection": 566,
"offsetInEndSection": 748,
"text": "In this regard, some of these novel agents seem promising, such as monoclonal antibodies (anti-CD38 - daratumumab or anti-CS1 - elotuzumab) or the kinesin protein inhibitor Arry-520."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25964097",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 569,
"text": "This is likely to change within the next few years with a number of mAb therapies being assessed in late stage clinical trials, most notably, the anti-CS-1 mAb, elotuzumab, and the anti-CD38 mAb, daratumumab, which are currently being evaluated in Phase III clinical trials for MM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 336,
"text": "CD38, a type II transmembrane glycoprotein highly expressed in hematological malignancies including multiple myeloma (MM), represents a promising target for mAb-based immunotherapy. In this study, we describe the cytotoxic mechanisms of action of daratumumab, a novel, high-affinity, therapeutic human mAb against a unique CD38 epitope."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 537,
"text": "CD38, a type II transmembrane glycoprotein highly expressed in hematological malignancies including multiple myeloma (MM), represents a promising target for mAb-based immunotherapy. In this study, we describe the cytotoxic mechanisms of action of daratumumab, a novel, high-affinity, therapeutic human mAb against a unique CD38 epitope. Daratumumab induced potent Ab-dependent cellular cytotoxicity in CD38-expressing lymphoma- and MM-derived cell lines as well as in patient MM cells, both with autologous and allogeneic effector cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25626316",
"endSection": "abstract",
"offsetInBeginSection": 102,
"offsetInEndSection": 443,
"text": "One of novel fields for anti-MM therapeutic strategy is the development of immunotherapy using monoclonal antibodies (MoAbs) against myeloma-specific antigens. This article focuses on the basic and clinical aspects of several emerging and promising novel MoAbs for MM, such as elotuzumab which targets CS1 and daratumumab which targets CD38."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25626316",
"endSection": "abstract",
"offsetInBeginSection": 102,
"offsetInEndSection": 641,
"text": "One of novel fields for anti-MM therapeutic strategy is the development of immunotherapy using monoclonal antibodies (MoAbs) against myeloma-specific antigens. This article focuses on the basic and clinical aspects of several emerging and promising novel MoAbs for MM, such as elotuzumab which targets CS1 and daratumumab which targets CD38. Both antigens are highly expressed in more than 90% of MM patients, and the clinical trials have shown promising anti-MM effects, especially in combination with immunomodulatory agent lenalidomide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25626316",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 443,
"text": "Multiple myeloma (MM) remains mostly incurable despite the recent progress in the treatment strategy. One of novel fields for anti-MM therapeutic strategy is the development of immunotherapy using monoclonal antibodies (MoAbs) against myeloma-specific antigens. This article focuses on the basic and clinical aspects of several emerging and promising novel MoAbs for MM, such as elotuzumab which targets CS1 and daratumumab which targets CD38."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 537,
"text": "In this study, we describe the cytotoxic mechanisms of action of daratumumab, a novel, high-affinity, therapeutic human mAb against a unique CD38 epitope. Daratumumab induced potent Ab-dependent cellular cytotoxicity in CD38-expressing lymphoma- and MM-derived cell lines as well as in patient MM cells, both with autologous and allogeneic effector cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 667,
"text": "In this study, we describe the cytotoxic mechanisms of action of daratumumab, a novel, high-affinity, therapeutic human mAb against a unique CD38 epitope. Daratumumab induced potent Ab-dependent cellular cytotoxicity in CD38-expressing lymphoma- and MM-derived cell lines as well as in patient MM cells, both with autologous and allogeneic effector cells. Daratumumab stood out from other CD38 mAbs in its strong ability to induce complement-dependent cytotoxicity in patient MM cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25626316",
"endSection": "abstract",
"offsetInBeginSection": 262,
"offsetInEndSection": 641,
"text": "This article focuses on the basic and clinical aspects of several emerging and promising novel MoAbs for MM, such as elotuzumab which targets CS1 and daratumumab which targets CD38. Both antigens are highly expressed in more than 90% of MM patients, and the clinical trials have shown promising anti-MM effects, especially in combination with immunomodulatory agent lenalidomide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21109694",
"endSection": "abstract",
"offsetInBeginSection": 200,
"offsetInEndSection": 735,
"text": "Daratumumab is a novel human CD38 monoclonal antibody which kills CD38+ multiple myeloma cells via antibody-dependent cell-mediated cytotoxicity, complement-dependent cytotoxicity and apoptosis.DESIGN AND METHODS: To explore the effect of lenalidomide combined with daratumumab, we first carried out standard antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity assays in which the CD38+ multiple myeloma cell line UM-9 and primary multiple myeloma cells isolated from patients were used as target cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"endSection": "abstract",
"offsetInBeginSection": 538,
"offsetInEndSection": 667,
"text": "Daratumumab stood out from other CD38 mAbs in its strong ability to induce complement-dependent cytotoxicity in patient MM cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26308596",
"endSection": "abstract",
"offsetInBeginSection": 63,
"offsetInEndSection": 408,
"text": "We studied daratumumab, a CD38-targeting, human IgG1ê monoclonal antibody, in a phase 1-2 trial involving patients with relapsed myeloma or relapsed myeloma that was refractory to two or more prior lines of therapy.METHODS: In part 1, the dose-escalation phase, we administered daratumumab at doses of 0.005 to 24 mg per kilogram of body weight."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21187443",
"endSection": "abstract",
"offsetInBeginSection": 1047,
"offsetInEndSection": 1219,
"text": "Collectively, our results show the versatility of daratumumab to effectively kill CD38-expressing tumor cells, including patient MM cells, via diverse cytotoxic mechanisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27195659",
"endSection": "abstract",
"offsetInBeginSection": 590,
"offsetInEndSection": 761,
"text": "Amongst these antibodies, elotuzumab which targets SLAMF-7 and daratumumab which targets CD38, have been recently approved by FDA for patients with relapsed/refractory MM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26137203",
"endSection": "abstract",
"offsetInBeginSection": 775,
"offsetInEndSection": 937,
"text": "This review focuses on the CD38 antigen and its targeting with daratumumab and provides an update on the results of recent clinical studies involving daratumumab."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26308596",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Targeting CD38 with Daratumumab Monotherapy in Multiple Myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26778538",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 253,
"text": "We assessed daratumumab, a novel CD38-targeted monoclonal antibody, in patients with refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27363983",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Daratumumab is a human monoclonal antibody that targets CD38, a cell surface protein that is overexpressed on multiple myeloma (MM) cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26631114",
"endSection": "abstract",
"offsetInBeginSection": 1445,
"offsetInEndSection": 1623,
"text": "Furthermore, daratumumab, and probably also other CD38-targeting antibodies, interfere with blood compatibility testing and thereby complicate the safe release of blood products."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27557302",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 310,
"text": "Daratumumab, a human IgGκ monoclonal antibody that targets CD38, induces direct and indirect antimyeloma activity and has shown substantial efficacy as monotherapy in heavily pretreated patients with multiple myeloma, as well as in combination with bortezomib in patients with newly diagnosed multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27780867",
"endSection": "abstract",
"offsetInBeginSection": 582,
"offsetInEndSection": 681,
"text": "Importantly, IFNγ was able to up-regulate CD38, the target of the therapeutic antibody daratumumab."
}
] | 6
|
BioASQ-training6b
| null | null |
5880aef4c872c95565000001
|
bioasq_factoid
|
factoid
|
When was Havana Syndrome first recognized?
|
['2016']
|
[
"2016",
"two thousand sixteen"
] |
['Havana Syndrome is the name given to the group of neurological symptoms that first occurred among the staff at the U.S. embassy in Havana, Cuba in 2016.', 'Havana syndrome is a term that was first coined by US diplomats and intelligence personnel in 2016 in Havana, Cuba, to describe a series of strange symptoms, including dizziness, hearing loss, headaches, and cognitive impairment.', 'Havana Syndrome was first recognized in late 2016 when U.S. diplomatic personnel in Havana, Cuba, reported experiencing unusual symptoms including hearing loss, cognitive issues, and other neurological problems.', 'Havana Syndrome was first recognized in 2016.', 'In 2016, Havana Syndrome was first recognized when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.', 'Havana Syndrome is a term used to describe a series of unexplained neurological symptoms experienced by diplomatic personnel serving in Havana, Cuba, beginning in 2016.', 'Since 2016, an array of claims and public discourse have circulated in the medical community over the origin and nature of a mysterious condition dubbed "Havana Syndrome," so named as it was first identified in Cuba.', 'The Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.', 'Havana Syndrome was first recognized in Havana, Cuba in late 2016 when several U.S. diplomats and embassy staff reported experiencing unexplained neurological symptoms.', 'Havana Syndrome was first recognized in 2016 when diplomatic personnel serving in Havana, Cuba, reported audible sensory phenomena paired with complex and persistent neurological symptoms consistent with brain injury.', 'Havana Syndrome was first recognized in the year 2016.', ' Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.', 'Havana Syndrome was first recognized in late 2016 when several U.S. diplomats stationed in Havana, Cuba, reported experiencing a range of unexplained neurological symptoms.', 'Havana Syndrome was first recognized in 2016 when diplomatic personnel in Havana, Cuba reported experiencing unusual sensory phenomena and neurological symptoms.', 'Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.', 'Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba began reporting audible sensory phenomena paired with onset of complex and persistent neurological symptoms consistent with brain injury.', 'Havana Syndrome was first recognized in 2016 when diplomatic personnel serving in Havana, Cuba reported audible sensory phenomena paired with complex and persistent neurological symptoms consistent with brain injury.', 'In 2016 diplomatic personnel serving in Havana, Cuba began reporting audible sensory phenomena paired with onset of complex and persistent neurological symptoms consistent with brain injury.', 'Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises and experiencing unexplained health effects.', 'Havana syndrome is a term used to describe a cluster of neurological symptoms that have been reported by United States and Canadian diplomats, intelligence officers, and other government employees, mainly in Havana, Cuba, between 2016 and 2018.', 'The phenomenon now known as Havana Syndrome was first recognized in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37965360",
"http://www.ncbi.nlm.nih.gov/pubmed/32655474",
"http://www.ncbi.nlm.nih.gov/pubmed/30828629",
"http://www.ncbi.nlm.nih.gov/pubmed/35962646",
"http://www.ncbi.nlm.nih.gov/pubmed/37976420"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37965360",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 206,
"text": " In 2016 diplomatic personnel serving in Havana, Cuba, began reporting audible sensory phenomena paired with onset of complex and persistent neurological symptoms consistent with brain injury. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35962646",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 268,
"text": "Since 2016, numerous American and Canadian diplomats and secret (intelligence) agents in Cuba, China, and other places in the world have experienced an abrupt onset of unusual clinical symptoms including, tinnitus, visual problems, vertigo, and cognitive difficulties,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37976420",
"endSection": "abstract",
"offsetInBeginSection": 268,
"offsetInEndSection": 438,
"text": "This fact was illustrated in 2016 when U.S. diplomats serving in Havana, Cuba reported hearing strange noises accompanied by a constellation of unexplained health effects"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35962646",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 352,
"text": "Since 2016, numerous American and Canadian diplomats and secret (intelligence) agents in Cuba, China, and other places in the world have experienced an abrupt onset of unusual clinical symptoms including, tinnitus, visual problems, vertigo, and cognitive difficulties, after they encountered strange sounds; this has been called \"Havana syndrome\" (HS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32655474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "In late 2016, diplomats in Havana, Cuba, began presenting with a unique symptom complex after perceiving a strange noise and/or feeling a pressure field in their domicile."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37965360",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "Introduction: In 2016 diplomatic personnel serving in Havana, Cuba, began reporting audible sensory phenomena paired with onset of complex and persistent neurological symptoms consistent with brain injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30828629",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 225,
"text": "BACKGROUND: In the Autumn of 2016, diplomatic personnel residing in Havana began to present with symptoms of dizziness, ear pain, and tinnitus that emerged after perception of high frequency noise and/or a pressure sensation."
}
] | 13
|
BioASQ-training13b
| null | null |
65f856a1c4010b4d7800004e
|
bioasq_factoid
|
factoid
|
Which is the major RNA editing enzyme in Drosophila melanogaster?
|
['ADAR', 'adenosine deaminase, RNA-specific']
|
[
"ADAR",
"adenosine deaminase, RNA-specific",
"adenosine deaminase acting on RNA",
"Adenosine Deaminase, RNA-specific",
"Adenosine Deaminase, RNA-specific (ADAR)",
"ADAR1",
"ADAR2"
] |
['Adenosine deaminases that act on RNA [adenosine deaminase, RNA specific (ADAR)] catalyze the site-specific conversion of adenosine to inosine in primary mRNA transcripts. The ADAR RNA editing enzyme controls neuronal excitability in Drosophila melanogaster. TIRs were deduced to form dsRNAs as a putative target of ADAR. Genetic Determinants of RNA Editing Levels of ADAR Targets in Drosophila melanogaster. RNA editing usually affects only a fraction of expressed transcripts and there is a vast amount of variation in editing levels of ADAR (adenosine deaminase, RNA-specific) targets. ', 'The ADAR (adenosine deaminase, RNA-specific) RNA editing enzyme controls neuronal excitability in Drosophila melanogaster.', 'Adenosine deaminases that act on RNA [adenosine deaminase, RNA specific (ADAR)] catalyze the site-specific conversion of adenosine to inosine in primary mRNA transcripts. The ADAR RNA editing enzyme controls neuronal excitability in Drosophila melanogaster. Genetic Determinants of RNA Editing Levels of ADAR Targets in Drosophila melanogaster. TIRs were deduced to form dsRNAs as a putative target of ADAR. we show that expression of the editing enzyme, ADAR (adenosine deaminase acting on RNA), is dramatically decreased at elevated temperatures, partially, but not fully, explaining some target responses to temperature. ', 'Adenosine-to-inosine RNA editing is a highly conserved process that post-transcriptionally modifies mRNA, generating proteomic diversity, particularly within the nervous system of metazoans. RNA editing usually affects only a fraction of expressed transcripts and there is a vast amount of variation in editing levels of ADAR (adenosine deaminase, RNA-specific) targets. RNA editing by deamination of specific adenosine bases to inosines during pre-mRNA processing generates edited isoforms of proteins. RNA editing is proposed as a modulator of transcriptomes, but its biological impact has not been fully elucidated. Adenosine deaminases that act on RNA [adenosine deaminase, RNA specific (ADAR)] catalyze the site-specific conversion of adenosine to inosine in primary mRNA transcripts.', 'adar', 'RNA editing usually affects only a fraction of expressed transcripts and there is a vast amount of variation in editing levels of ADAR (adenosine deaminase, RNA-specific) targets. Adenosine-to-inosine RNA editing is a highly conserved process that post-transcriptionally modifies mRNA, generating proteomic diversity, particularly within the nervous system of metazoans.', 'Adenosine deaminases that act on RNA [adenosine deaminase, RNA specific (ADAR)] catalyze the site-specific conversion of adenosine to inosine in primary mRNA transcripts. TIRs were deduced to form dsRNAs as a putative target of ADAR. ', 'Adenosine deaminases that act on RNA [adenosine deaminase, RNA specific (ADAR)] catalyze the site-specific conversion of adenosine to inosine in primary mRNA transcripts. TIRs were deduced to form dsRNAs as a putative target of ADAR. The ADAR RNA editing enzyme controls neuronal excitability in Drosophila melanogaster. Genetic Determinants of RNA Editing Levels of ADAR Targets in Drosophila melanogaster. RNA editing usually affects only a fraction of expressed transcripts and there is a vast amount of variation in editing levels of ADAR (adenosine deaminase, RNA-specific) targets. ', 'GABA inhibitory signalling is impaired in human epileptic and autistic conditions, and vertebrate ADARs may have a relevant evolutionarily conserved control over neuronal excitability. RNA editing usually affects only a fraction of expressed transcripts and there is a vast amount of variation in editing levels of ADAR (adenosine deaminase, RNA-specific) targets.', 'Adenosine deaminases that act on RNA [adenosine deaminase, RNA specific (ADAR)] catalyze the site-specific conversion of adenosine to inosine in primary mRNA transcripts.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24137011",
"http://www.ncbi.nlm.nih.gov/pubmed/26656153",
"http://www.ncbi.nlm.nih.gov/pubmed/25555396",
"http://www.ncbi.nlm.nih.gov/pubmed/17018572",
"http://www.ncbi.nlm.nih.gov/pubmed/20886259"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17018572",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Adenosine deaminases that act on RNA [adenosine deaminase, RNA specific (ADAR)] catalyze the site-specific conversion of adenosine to inosine in primary mRNA transcripts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20886259",
"endSection": "abstract",
"offsetInBeginSection": 664,
"offsetInEndSection": 727,
"text": "TIRs were deduced to form dsRNAs as a putative target of ADAR. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24137011",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "The ADAR RNA editing enzyme controls neuronal excitability in Drosophila melanogaster."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26656153",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Genetic Determinants of RNA Editing Levels of ADAR Targets in Drosophila melanogaster."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26656153",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "RNA editing usually affects only a fraction of expressed transcripts and there is a vast amount of variation in editing levels of ADAR (adenosine deaminase, RNA-specific) targets."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25555396",
"endSection": "abstract",
"offsetInBeginSection": 967,
"offsetInEndSection": 1183,
"text": "we show that expression of the editing enzyme, ADAR (adenosine deaminase acting on RNA), is dramatically decreased at elevated temperatures, partially, but not fully, explaining some target responses to temperature. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24137011",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "The ADAR RNA editing enzyme controls neuronal excitability in Drosophila melanogaster"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531175",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 421,
"text": "In Drosophila, many messenger RNAs involved in neuro-transmission are re-coded at the RNA level by the RNA-editing enzyme, dADAR, leading to the incorporation of amino acids that are not directly encoded by the genome. dADAR also re-codes its own transcript, but the consequences of this auto-regulation in vivo are unclear"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11973307",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "Novel putative nicotinic acetylcholine receptor subunit genes, Dalpha5, Dalpha6 and Dalpha7, in Drosophila melanogaster identify a new and highly conserved target of adenosine deaminase acting on RNA-mediated A-to-I pre-mRNA editing"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17662845",
"endSection": "abstract",
"offsetInBeginSection": 268,
"offsetInEndSection": 444,
"text": "The genome of the fruitfly, Drosophila melanogaster, contains a single gene encoding the enzyme responsible for deamination, termed ADAR (for adenosine deaminase acting on RNA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25921068",
"endSection": "abstract",
"offsetInBeginSection": 293,
"offsetInEndSection": 852,
"text": "Using these and other available data, we discovered and analyzed thousands of neuronal human and mouse circRNAs. circRNAs were extraordinarily enriched in the mammalian brain, well conserved in sequence, often expressed as circRNAs in both human and mouse, and sometimes even detected in Drosophila brains. circRNAs were overall upregulated during neuronal differentiation, highly enriched in synapses, and often differentially expressed compared to their mRNA isoforms. circRNA expression correlated negatively with expression of the RNA-editing enzyme ADAR1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17662845",
"endSection": "abstract",
"offsetInBeginSection": 611,
"offsetInEndSection": 913,
"text": "While several ADAR enzymes are present in mice, the presence of a single ADAR in Drosophila, combined with the diverse genetic toolkit available to researchers and the wide range of ADAR target mRNAs identified to date, make Drosophila an ideal organism to study the genetic basis of A-to-I RNA editing"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19941656",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 536,
"text": "Aside from their role in generating protein diversity in the central nervous system, ADARs have been implicated in the hypermutation of some RNA viruses, although why this hypermutation occurs is not well understood.Here we describe the hypermutation of adenosines to guanosines in the genome of the sigma virus--a negative sense RNA virus that infects Drosophila melanogaster"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17662845",
"endSection": "abstract",
"offsetInBeginSection": 268,
"offsetInEndSection": 445,
"text": "The genome of the fruitfly, Drosophila melanogaster, contains a single gene encoding the enzyme responsible for deamination, termed ADAR (for adenosine deaminase acting on RNA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10629039",
"endSection": "abstract",
"offsetInBeginSection": 644,
"offsetInEndSection": 979,
"text": "The enzyme has no activity on dsRNA substrates but is a tRNA deaminase with specificity for adenosine 37 of insect alanine tRNA. dADAT1 shows greater similarity to vertebrate ADARs than to yeast Tad1p, supporting the hypothesis of a common evolutionary origin for ADARs and ADATs. dAdat1 transcripts are maternally supplied in the egg."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24137011",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "The ADAR RNA editing enzyme controls neuronal excitability in Drosophila melanogaster."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26656153",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "Genetic Determinants of RNA Editing Levels of ADAR Targets in Drosophila melanogaster."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19941656",
"endSection": "abstract",
"offsetInBeginSection": 377,
"offsetInEndSection": 538,
"text": "Here we describe the hypermutation of adenosines to guanosines in the genome of the sigma virus--a negative sense RNA virus that infects Drosophila melanogaster."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22658416",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "The RNA editing enzyme ADAR chemically modifies adenosine (A) to inosine (I), which is interpreted by the ribosome as a guanosine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531175",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 316,
"text": "In Drosophila, many messenger RNAs involved in neuro-transmission are re-coded at the RNA level by the RNA-editing enzyme, dADAR, leading to the incorporation of amino acids that are not directly encoded by the genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21761288",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Drosophila melanogaster has a single Adar gene encoding a protein related to mammalian ADAR2 that edits transcripts encoding glutamate receptor subunits."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17662845",
"endSection": "abstract",
"offsetInBeginSection": 611,
"offsetInEndSection": 914,
"text": "While several ADAR enzymes are present in mice, the presence of a single ADAR in Drosophila, combined with the diverse genetic toolkit available to researchers and the wide range of ADAR target mRNAs identified to date, make Drosophila an ideal organism to study the genetic basis of A-to-I RNA editing."
}
] | 6
|
BioASQ-training6b
| null | null |
58e9e7aa3e8b6dc87c00000d
|
bioasq_factoid
|
yesno
|
Do we find bacteriophages in the gut?
|
['yes']
|
[
"yes"
] |
['yes,\nBacterial viruses (bacteriophages, phages) of the gut have increasingly become a focus in microbiome studies, with an understanding that they are likely key players in health and disease.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34560321",
"http://www.ncbi.nlm.nih.gov/pubmed/33137401",
"http://www.ncbi.nlm.nih.gov/pubmed/33465423",
"http://www.ncbi.nlm.nih.gov/pubmed/33176253",
"http://www.ncbi.nlm.nih.gov/pubmed/33171009"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34560321",
"endSection": "abstract",
"offsetInBeginSection": 830,
"offsetInEndSection": 935,
"text": "a multitude of symbiotic bacteria and bacteriophages are decreased in abundance in patients with COVID-19"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33465423",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Bacterial viruses (bacteriophages, phages) of the gut have increasingly become a focus in microbiome studies, with an understanding that they are likely key players in health and disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33176253",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 459,
"text": "Already without exogenous intervention, a multitude of phage-bacterial interactions occur within the human gut, some of which might play a direct role in disease progression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33171009",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "We are surrounded by microbes, mostly bacteria and their viruses or phages, on the inside and outside of our bodies. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33137401",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 317,
"text": "crAssphages are a broad group of diverse bacteriophages in the order Caudovirales that have been found to be highly abundant in the human gastrointestinal tract. Despite their high prevalence, we have an incomplete understanding of how crAssphages shape and respond to ecological and evolutionary dynamics in the gut."
}
] | 11
|
BioASQ-training11b
| null | null |
6217dc173a8413c65300002b
|
bioasq_yesno
|
yesno
|
Can valproate be used during pregnancy?
|
['no']
|
[
"no"
] |
['No. Valproate is associated with high risk of malformations and should no be used during pregnancy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24161312",
"http://www.ncbi.nlm.nih.gov/pubmed/19198722",
"http://www.ncbi.nlm.nih.gov/pubmed/18062721",
"http://www.ncbi.nlm.nih.gov/pubmed/35926210",
"http://www.ncbi.nlm.nih.gov/pubmed/37684052",
"http://www.ncbi.nlm.nih.gov/pubmed/26329145",
"http://www.ncbi.nlm.nih.gov/pubmed/37294532",
"http://www.ncbi.nlm.nih.gov/pubmed/36433783",
"http://www.ncbi.nlm.nih.gov/pubmed/38062774",
"http://www.ncbi.nlm.nih.gov/pubmed/18360539",
"http://www.ncbi.nlm.nih.gov/pubmed/36287388",
"http://www.ncbi.nlm.nih.gov/pubmed/36401747",
"http://www.ncbi.nlm.nih.gov/pubmed/28953852",
"http://www.ncbi.nlm.nih.gov/pubmed/11460259",
"http://www.ncbi.nlm.nih.gov/pubmed/35265619",
"http://www.ncbi.nlm.nih.gov/pubmed/27875769",
"http://www.ncbi.nlm.nih.gov/pubmed/25400349",
"http://www.ncbi.nlm.nih.gov/pubmed/36828241",
"http://www.ncbi.nlm.nih.gov/pubmed/19892633",
"http://www.ncbi.nlm.nih.gov/pubmed/38061552",
"http://www.ncbi.nlm.nih.gov/pubmed/36381886",
"http://www.ncbi.nlm.nih.gov/pubmed/3114906",
"http://www.ncbi.nlm.nih.gov/pubmed/21216127",
"http://www.ncbi.nlm.nih.gov/pubmed/37485793"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36433783",
"endSection": "abstract",
"offsetInBeginSection": 1038,
"offsetInEndSection": 1279,
"text": "Compared to lamotrigine, there was an increased risk of malformations associated with valproate (n = 2,031, aRR = 2.05, 95% CI = 1.70-2.46) and topiramate (n = 509, aRR = 1.81, 95% CI = 1.26-2.60), which increased in a dose-dependent manner."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36433783",
"endSection": "abstract",
"offsetInBeginSection": 1509,
"offsetInEndSection": 1860,
"text": "Valproate was associated with several malformation subtypes, including nervous system, cardiac, oral clefts, clubfoot, and hypospadias, whereas lamotrigine and carbamazepine were not.INTERPRETATION: Topiramate is associated with an increased risk of MCM similar to that associated with valproate, but lower doses may mitigate the risks for both drugs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36287388",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "INTRODUCTION: Prenatal exposure to valproate and related substances is associated with a risk of malformations and/or neurodevelopmental disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36287388",
"endSection": "abstract",
"offsetInBeginSection": 1647,
"offsetInEndSection": 1793,
"text": "Increased awareness and compliance among healthcare professionals regarding risk minimization measures could limit prenatal exposure to valproate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401747",
"endSection": "abstract",
"offsetInBeginSection": 1792,
"offsetInEndSection": 1947,
"text": "CONCLUSIONS: Our proof-of-concept analysis based on GePaRD showed a strong association between intrauterine exposure to VPA and occurrence of spina bifida."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36828241",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Proposal for reference values for the developmental effects of valproate based on human data using a benchmark dose approach."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36828241",
"endSection": "abstract",
"offsetInBeginSection": 439,
"offsetInEndSection": 598,
"text": "Major congenital malformations (MCMs) in offsprings of mothers exposed to valproate during pregnancy have been reported in international scientific literature."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37684052",
"endSection": "abstract",
"offsetInBeginSection": 739,
"offsetInEndSection": 1112,
"text": "Valproate, in monotherapy and polytherapy, has been associated with elevated risk of major congenital malformations and neurodevelopmental disorders in children born to mothers who took it. Topiramate and phenobarbital are also associated with elevated risks of congenital malformations and neurodevelopmental disorders, though the risks are lower than those of valproate. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38062774",
"endSection": "abstract",
"offsetInBeginSection": 175,
"offsetInEndSection": 385,
"text": "Valproic acid (VPA), a widely prescribed first-line antiepileptic drug for epilepsy and various neurological conditions, has been associated with a 4-fold increase in the risk of NTDs when used during pregnancy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18360539",
"endSection": "abstract",
"offsetInBeginSection": 747,
"offsetInEndSection": 892,
"text": "This finding suggests the need for reappraisal of the use of valproate in women who may become pregnant or are pregnant whilst the drug is taken."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21216127",
"endSection": "abstract",
"offsetInBeginSection": 430,
"offsetInEndSection": 499,
"text": "Valproate of sodium should be avoided, if possible, during pregnancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18360539",
"endSection": "abstract",
"offsetInBeginSection": 453,
"offsetInEndSection": 604,
"text": "At valproate doses of 1400 mg and below per day, the mean rate of pregnancies with fetal malformations was 6.42% and did not seem to be dose-dependent."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35265619",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 332,
"text": "Valproic acid (VPA, valproate, Depakote) is a commonly used anti-seizure medication (ASM) in the treatment of epilepsy and a variety of other neurological disorders. While VPA and other ASMs are efficacious for management of seizures, they also increase the risk for adverse pregnancy outcomes, including neural tube defects (NTDs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28953852",
"endSection": "abstract",
"offsetInBeginSection": 820,
"offsetInEndSection": 1293,
"text": "Sodium valproate is a known teratogen, and is discouraged in pregnancy, but what choice is open to women who rely on this medication to stabilise their mood?CONCLUSIONS: The large majority of women of childbearing age with bipolar disorder should not be prescribed sodium valproate as the risks to the unborn fetus far outweigh the benefits of the medication, as other drugs have similar if not better efficacy to stabilize the mother's mood, with lower risks to the fetus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24161312",
"endSection": "abstract",
"offsetInBeginSection": 481,
"offsetInEndSection": 598,
"text": "The use of valproate is contraindicated during pregnancy due to teratogenicity and neurocognitive delay and deficits."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26329145",
"endSection": "abstract",
"offsetInBeginSection": 764,
"offsetInEndSection": 1278,
"text": "Spina bifida is the only specific major congenital malformation significantly associated with exposure to Carbamazepine monotherapy Despite the small number of studies on the teratogenic effects of new antiepileptic drugs, the analysis of the literature shows that exposure of the fetus to the new antiepileptic drugs is associated with a lower risk of major congenital malformations compared to the use of older drugs.EXPERT OPINION: Where possible, Valproate should be avoided in women of childbearing potential."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11460259",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 443,
"text": "BACKGROUND: The use of valproic acid during pregnancy has been associated with adverse fetal outcomes, including major and minor congenital malformations, intrauterine growth retardation (IUGR), hyperbilirubinemia, hepatotoxicity, transient hyperglycemia, and fetal and neonatal distress. In addition, intrauterine exposure to valproic acid has been associated with an increased risk of central nervous system abnormalities, primarily neural t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27875769",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "PURPOSE: Valproate is an effective wide-spectrum anti-epileptic drug that is also known to be teratogenic. Its administration in epileptic women remains contr"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25400349",
"endSection": "abstract",
"offsetInBeginSection": 701,
"offsetInEndSection": 812,
"text": "Therefore, we strongly recommend avoidance of valproic acid and supplementation of folic acid during pregnancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19198722",
"endSection": "abstract",
"offsetInBeginSection": 810,
"offsetInEndSection": 958,
"text": "Therefore, we recommend that valproic acid must be avoided during pregnancy, as new generation of anticonvulsant drugs have emerged into the market."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11460259",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "BACKGROUND: The use of valproic acid during pregnancy has been associated with adverse fetal outcomes, including major and minor congenital malformations, intrauterine growth retardation (IUGR), hyperbilirubinemia, hepatotoxicity, transient hyperglycemia, and fetal and neonat"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19892633",
"endSection": "abstract",
"offsetInBeginSection": 238,
"offsetInEndSection": 500,
"text": "Women of childbearing age taking valproate should be warned of its teratogenicity and advised to plan pregnancies, take a higher dose of folate, discuss reducing the dose of valproate or changing the medication with their physician, and have antenatal screening."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36381886",
"endSection": "abstract",
"offsetInBeginSection": 563,
"offsetInEndSection": 844,
"text": "It also includes the importance of awareness among middle-aged women with mental illness regarding the teratogenic effects of sodium valproate use and the relevance of discussion by physicians with patients regarding the usage of this drug despite being aware of the complications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19892633",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Sodium valproate is a teratogen responsible for a wide range of abnormalities, including neural tube defects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19198722",
"endSection": "abstract",
"offsetInBeginSection": 594,
"offsetInEndSection": 958,
"text": "Sodium valproate, a widely used anticonvulsant and mood regulator, is a well-recognized teratogen that can result in severe limb deformities, craniosynostosis, neural tube defects and neurodevelopmental retardation. Therefore, we recommend that valproic acid must be avoided during pregnancy, as new generation of anticonvulsant drugs have emerged into the market."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25400349",
"endSection": "abstract",
"offsetInBeginSection": 489,
"offsetInEndSection": 700,
"text": "Sodium valproate, a widely used anticonvulsant and mood regulator, is a well-recognized teratogen that can result in facial dysmorphism, craniosynostosis, neural tube defects, and neurodevelopmental retardation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3114906",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 237,
"text": "Valproic acid use during pregnancy results in an absolute risk for spina bifida of 1-2%. This increased risk is comparable to the recurrence risk for neural tube defects and warrants informed counselling and access to prenatal diagnosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35926210",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 268,
"text": "Within several years after receiving U.S. Food and Drug Administration (FDA) approval in the late 1970s, valproate was shown to increase the risk for major congenital malformations and learning disabilities in the offspring of women who used the drug during pregnancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18062721",
"endSection": "abstract",
"offsetInBeginSection": 1034,
"offsetInEndSection": 1152,
"text": "The teratogenic effects of valproic acid appear to be dose dependent, with higher risks at dosage levels >1000 mg/day."
}
] | 13
|
BioASQ-training13b
| null | null |
65d12b451930410b13000031
|
bioasq_yesno
|
factoid
|
Which is the target of belimumab in Systemic Lupus Erythematosus treatment?
|
['B-cell activating factor', 'BAFF', 'BLyS (B-lymphocyte stimulator)']
|
[
"B-cell activating factor",
"BAFF",
"BLyS (B-lymphocyte stimulator)",
"BlyS",
"B-lymphocyte activating factor",
"B-lymphocyte survival factor"
] |
['Belimumab is a fully human monoclonal antibody directed against BAFF. Belimumab, a human monoclonal antibody specific for soluble BLyS, was ultimately approved by the United States Food and Drug Administration (FDA) in March 2011 for active autoantibody patients with systemic lupus erythematosus (SLE) despite standard therapy.', 'blys', 'The main therapeutic target of belimumab is BLyS', 'Belimumab: a BLyS-specific inhibitor for systemic lupus erythematosus To review the efficacy, safety, dosing, drug interactions, as well as economic and therapeutic considerations of belimumab, an inv', 'Belimumab is an anti-BAFF monoclonal antibody. BAFF is also known as BLyS (B-lymphocyte stimulator).', 'Belimumab: a BLyS-specific inhibitor for systemic lupus erythematosus To review the efficacy, safety, dosing, drug interactions, as well as economic and therapeutic considerations of belimumab, an investigational B-lymphocyte stimulator (BLyS) inhibitor.', 'Belimumab, a fully human monoclonal antibody against B lymphocyte stimulator (BLyS), a B-cell survival factor, was licensed in 2011 for the treatment of autoantibody-positive SLE', 'Belimumab: a BLyS-specific inhibitor for systemic lupus erythematosus Belimumab, an anti-BAFF monoclonal antibody', 'Belimumab: a BLyS-specific inhibitor for systemic lupus erythematosus Belimumab, a fully human monoclonal antibody against B lymphocyte stimulator (BLyS), a B-cell survival factor, was licensed in 2011 for the treatment of autoantibody-positive SLE', 'belimumab is a blys-specificsor for systemic lupus erythematos', 'Belimumab is a fully human anti-BLyS monoclonal antibody with specificity for BLyS. It is approved for SLE treatment.', 'Belimumab, a fully human monoclonal antibody against B lymphocyte stimulator (BLyS), was licensed in 2011 for the treatment of autoantibodies to Systemic Lupus Erythematosus.', 'Belimumab: a BLyS-specific inhibitor for systemic lupus erythematosus.', 'Belimumab: a BLyS-specific inhibitor for systemic lupus erythematosus To review the efficacy, safety, dosing, drug interactions, as well as economic and therapeutic considerations of belimumab, an investigational B-lymphocyte stimulator (BLyS) inhibitor. Belimumab, an anti-BAFF monoclonal antibody']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25543845",
"http://www.ncbi.nlm.nih.gov/pubmed/27587201",
"http://www.ncbi.nlm.nih.gov/pubmed/23568179",
"http://www.ncbi.nlm.nih.gov/pubmed/23251765",
"http://www.ncbi.nlm.nih.gov/pubmed/23553779",
"http://www.ncbi.nlm.nih.gov/pubmed/21081710",
"http://www.ncbi.nlm.nih.gov/pubmed/29572471"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21081710",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 69,
"text": "Belimumab: a BLyS-specific inhibitor for systemic lupus erythematosus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21081710",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 195,
"text": "To review the efficacy, safety, dosing, drug interactions, as well as economic and therapeutic considerations of belimumab, an investigational B-lymphocyte stimulator (BLyS) inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29572471",
"endSection": "abstract",
"offsetInBeginSection": 101,
"offsetInEndSection": 144,
"text": "Belimumab, an anti-BAFF monoclonal antibody"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29572471",
"endSection": "abstract",
"offsetInBeginSection": 302,
"offsetInEndSection": 728,
"text": "Here our crystal structure of the BAFF-belimumab Fab complex shows the precise epitope and the BAFF-neutralizing mechanism of belimumab, and demonstrates that the therapeutic activity of belimumab involves not only antagonizing the BAFF-receptor interaction, but also disrupting the formation of the more active BAFF 60-mer to favor the induction of the less active BAFF trimer through interaction with the flap region of BAFF"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27587201",
"endSection": "abstract",
"offsetInBeginSection": 783,
"offsetInEndSection": 1123,
"text": "In recent years, a member of the tumor necrosis factor (TNF) family, soluble human B Lymphocyte Stimulator protein (BLyS), also referred to as B-cell activating factor (BAFF) and TNFSF13B has been studied extensively. This protein is synthesized by myeloid cell lines, specifically interacts with B lymphocytes and increases their life-span"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25543845",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 323,
"text": "Belimumab, a fully human monoclonal antibody against B lymphocyte stimulator (BLyS), a B-cell survival factor, was licensed in 2011 for the treatment of autoantibody-positive SLE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23568179",
"endSection": "abstract",
"offsetInBeginSection": 525,
"offsetInEndSection": 595,
"text": "Belimumab is a fully human monoclonal antibody directed against BAFF. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23553779",
"endSection": "abstract",
"offsetInBeginSection": 315,
"offsetInEndSection": 574,
"text": " Belimumab, a human monoclonal antibody specific for soluble BLyS, was ultimately approved by the United States Food and Drug Administration (FDA) in March 2011 for active autoantibody patients with systemic lupus erythematosus (SLE) despite standard therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23251765",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 576,
"text": "Targeted therapy with belimumab, the monoclonal antibody against BLyS, has shown clinical benefit in two large-scale, multicenter phase III trials leading to US Food and Drug Administration approval for patients with serologically positive SLE who have active disease despite standard therapy"
}
] | 11
|
BioASQ-training11b
| null | null |
5d386fbfa1e1595105000005
|
bioasq_factoid
|
yesno
|
Are transcription and splicing connected?
|
['yes']
|
[
"yes"
] |
['Yes. There is strong evidence that splicing and transcription are intimately coupled in metazoans, with genome wide surveys show that most splicing occurs during transcription. Chromatin structure, RNA polymerase dynamics, and recruitment of splicing factors through the transcriptional machinery are factors that explain a role for transcription in the regulation of splicing.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23209445",
"http://www.ncbi.nlm.nih.gov/pubmed/23074139",
"http://www.ncbi.nlm.nih.gov/pubmed/22479188",
"http://www.ncbi.nlm.nih.gov/pubmed/21964334",
"http://www.ncbi.nlm.nih.gov/pubmed/20808788",
"http://www.ncbi.nlm.nih.gov/pubmed/16172632",
"http://www.ncbi.nlm.nih.gov/pubmed/15905409",
"http://www.ncbi.nlm.nih.gov/pubmed/15870275",
"http://www.ncbi.nlm.nih.gov/pubmed/23097425",
"http://www.ncbi.nlm.nih.gov/pubmed/22975042",
"http://www.ncbi.nlm.nih.gov/pubmed/22156210",
"http://www.ncbi.nlm.nih.gov/pubmed/21095588",
"http://www.ncbi.nlm.nih.gov/pubmed/17189193",
"http://www.ncbi.nlm.nih.gov/pubmed/16921380",
"http://www.ncbi.nlm.nih.gov/pubmed/16769980",
"http://www.ncbi.nlm.nih.gov/pubmed/15383674"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23074139",
"endSection": "sections.0",
"offsetInBeginSection": 476,
"offsetInEndSection": 791,
"text": ", as splicing is often cotranscriptional, a complex picture emerges in which splicing regulation not only depends on the balance of splicing factor binding to their pre-mRNA target sites but also on transcription-associated features such as protein recruitment to the transcribing machinery and elongation kinetics."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23074139",
"endSection": "sections.0",
"offsetInBeginSection": 851,
"offsetInEndSection": 968,
"text": "recent evidence shows that chromatin structure is another layer of regulation that may act through various mechanisms"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23074139",
"endSection": "sections.0",
"offsetInBeginSection": 971,
"offsetInEndSection": 1135,
"text": "hese span from regulation of RNA polymerase II elongation, which ultimately determines splicing decisions, to splicing factor recruitment by specific histone marks."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23074139",
"endSection": "sections.0",
"offsetInBeginSection": 1136,
"offsetInEndSection": 1250,
"text": "Chromatin may not only be involved in alternative splicing regulation but in constitutive exon recognition as well"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23074139",
"endSection": "sections.0",
"offsetInBeginSection": 1252,
"offsetInEndSection": 1480,
"text": "Moreover, splicing was found to be necessary for the proper 'writing' of particular chromatin signatures, giving further mechanistic support to functional interconnections between splicing, transcription and chromatin structure."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23074139",
"endSection": "sections.0",
"offsetInBeginSection": 1481,
"offsetInEndSection": 1671,
"text": "These links between chromatin configuration and splicing raise the intriguing possibility of the existence of a memory for splicing patterns to be inherited through epigenetic modifications."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21964334",
"endSection": "sections.0",
"offsetInBeginSection": 148,
"offsetInEndSection": 285,
"text": "Spliceosome assembly occurs co-transcriptionally, raising the possibility that DNA structure may directly influence alternative splicing."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21964334",
"endSection": "sections.0",
"offsetInBeginSection": 287,
"offsetInEndSection": 475,
"text": "upporting such an association, recent reports have identified distinct histone methylation patterns, elevated nucleosome occupancy and enriched DNA methylation at exons relative to introns"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21964334",
"endSection": "sections.0",
"offsetInBeginSection": 477,
"offsetInEndSection": 564,
"text": "Moreover, the rate of transcription elongation has been linked to alternative splicing."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21964334",
"endSection": "sections.0",
"offsetInBeginSection": 566,
"offsetInEndSection": 827,
"text": "ere we provide the first evidence that a DNA-binding protein, CCCTC-binding factor (CTCF), can promote inclusion of weak upstream exons by mediating local RNA polymerase II pausing both in a mammalian model system for alternative splicing, CD45, and genome-wide"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23097425",
"endSection": "sections.0",
"offsetInBeginSection": 148,
"offsetInEndSection": 232,
"text": "We recently showed that cotranscriptional splicing occurs efficiently in Drosophila,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22975042",
"endSection": "sections.0",
"offsetInBeginSection": 138,
"offsetInEndSection": 221,
"text": "In recent years it became apparent that splicing is predominantly cotranscriptional"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22156210",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 385,
"text": "To determine the prevalence of cotranscriptional splicing in Drosophila, we sequenced nascent RNA transcripts from Drosophila S2 cells as well as from Drosophila heads. Eighty-seven percent of the introns assayed manifest >50% cotranscriptional splicing. The remaining 13% are cotranscriptionally spliced poorly or slowly, with ∼3% being almost completely retained in nascent pre-mRNA."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17189193",
"endSection": "sections.0",
"offsetInBeginSection": 720,
"offsetInEndSection": 877,
"text": "We estimate that > or =90% of endogenous yeast splicing is posttranscriptional, consistent with an analysis of posttranscriptional snRNP-associated pre-mRNA."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16921380",
"endSection": "sections.0",
"offsetInBeginSection": 748,
"offsetInEndSection": 1039,
"text": "Notably, the topoisomerase I inhibitor camptothecin, which stalls elongating Pol II, increased cotranscriptional splicing factor accumulation and splicing in parallel. This provides direct evidence for a kinetic link between transcription, splicing factor recruitment and splicing catalysis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15383674",
"endSection": "sections.0",
"offsetInBeginSection": 739,
"offsetInEndSection": 950,
"text": "Recent evidence indicates that transcriptional elongation and splicing can be influenced reciprocally: Elongation rates control alternative splicing and splicing factors can, in turn, modulate pol II elongation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15383674",
"endSection": "sections.0",
"offsetInBeginSection": 951,
"offsetInEndSection": 1251,
"text": "The presence of transcription factors in the spliceosome and the existence of proteins, such as the coactivator PGC-1, with dual activities in splicing and transcription can explain the links between both processes and add a new level of complexity to the regulation of gene expression in eukaryotes."
}
] | 5
|
BioASQ-training5b
| null | null |
517395b98ed59a060a00001a
|
bioasq_yesno
|
factoid
|
What happens to the expression levels of piRNAs in the case of intracranial aneurysm rupture?
|
['Decreased']
|
[
"Decreased",
"Reduced",
"Lowered",
"Diminished",
"Lessened",
"Minimized"
] |
['piRNAs showed a substantial decrease in RNA abundance that was sustained after IA rupture.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32424559"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32424559",
"endSection": "abstract",
"offsetInBeginSection": 865,
"offsetInEndSection": 1007,
"text": "piRNAs and rRNAs showed a substantial decrease in RNA abundance that was sustained after IA rupture, whereas miRNAs were largely upregulated. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32424559",
"endSection": "abstract",
"offsetInBeginSection": 272,
"offsetInEndSection": 450,
"text": "We used next-generation sequencing to analyze the expression of sRNAs in patients in the acute phase of IA rupture (first 72 h), in the chronic phase (3-15 months), and controls."
}
] | 11
|
BioASQ-training11b
| null | null |
626aa929e764a53204000039
|
bioasq_factoid
|
factoid
|
Which pituitary adenoma is common cause of infertility is women?
|
['prolactinoma']
|
[
"prolactinoma",
"lactotroph adenoma",
"prolactin-secreting adenoma",
"prolactin-producing tumor",
"hyperprolactinemic adenoma"
] |
['Prolactinoma is a pituitary adenoma that is strongly associated with infertility in women mainly due to increased prolactin secretion causing hyperprolactinemia. Other pituitary lesions can also be associated with infertility.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23090264",
"http://www.ncbi.nlm.nih.gov/pubmed/12477530",
"http://www.ncbi.nlm.nih.gov/pubmed/10649815",
"http://www.ncbi.nlm.nih.gov/pubmed/10649814",
"http://www.ncbi.nlm.nih.gov/pubmed/9152623",
"http://www.ncbi.nlm.nih.gov/pubmed/2738821",
"http://www.ncbi.nlm.nih.gov/pubmed/2803131",
"http://www.ncbi.nlm.nih.gov/pubmed/2520800",
"http://www.ncbi.nlm.nih.gov/pubmed/6868876",
"http://www.ncbi.nlm.nih.gov/pubmed/6788711"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090264",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Prolactinoma is the most common secreting pituitary adenoma. It is typically diagnosed in women of reproductive age and is common cause of infertility."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12477530",
"endSection": "sections.0",
"offsetInBeginSection": 1060,
"offsetInEndSection": 1308,
"text": "Examination of the tissue excised by transsphenoidal excision of the mass showed a pituitary adenoma that stained strongly for FSH. RESULTS: Regular menses resumed soon after excision of the gonadotroph adenoma, followed by a spontaneous pregnancy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12477530",
"endSection": "sections.0",
"offsetInBeginSection": 1309,
"offsetInEndSection": 1529,
"text": "CONCLUSIONS: Gonadotroph adenoma should be suspected in a reproductive age woman with oligomenorrhea or amenorrhea, infertility, multiple preovulatory follicles, and a persistently elevated serum estradiol concentration."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10649815",
"endSection": "sections.0",
"offsetInBeginSection": 199,
"offsetInEndSection": 614,
"text": "Hyperprolactinemia is the most common endocrine disorder of the hypothalamic-pituitary axis, occurring mostly in women and presenting most commonly with amenorrhea and galactorrhea. Causes of hyperprolactinemia include physiologic, pharmacologic and pathologic factors; pituitary adenoma is a common pathologic cause. Women may present with decreased libido, infertility, oligomenorrhea/amenorrhea and galactorrhea."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10649814",
"endSection": "sections.0",
"offsetInBeginSection": 443,
"offsetInEndSection": 788,
"text": "When specific treatable underlying causes have been eliminated and in cases of severe hyperprolactinemia, the most likely cause is a prolactin (PRL)-secreting pituitary adenoma. Microadenomas should be treated medically, with a dopamine agonist, if there is an indication for therapy (such as amenorrhea, infertility or bothersome galactorrhea)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9152623",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Pregnancy in a woman with active acromegaly is very rare, because amenorrhea, due to hyperprolactinemia and disturbed pituitary gonadotropin secretion may cause infertility."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2738821",
"endSection": "sections.0",
"offsetInBeginSection": 943,
"offsetInEndSection": 1318,
"text": "Of the remaining six patients who had been investigated for infertility, no demonstrable cause of infertility was found in three. Of the other three patients, one showed evidence of bilateral tubal occlusion secondary to pelvic inflammatory disease, one has had a right ectopic pregnancy followed by two abortions, and the third patient was found to have a pituitary adenoma."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2803131",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 257,
"text": "Results in 136 hyperprolactinaemic women who presented with infertility, amenorrhoea, menstrual irregularities and/or galactorrhoea are reported. There was radiographic evidence of pituitary microadenoma in 21 (15.4%) patients and 5 (3.7%) had macroadenoma."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2803131",
"endSection": "sections.0",
"offsetInBeginSection": 474,
"offsetInEndSection": 778,
"text": "Patients with pituitary adenoma had a significantly higher (p less than 0.001) baseline serum prolactin level (182 +/- 4.6 ng/ml) than those with no adenoma (59.2 +/- 4.2 ng/ml). All patients in the study were treated with bromocriptine (2.5-10 mg) to normalize serum prolactin or to achieve a pregnancy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2803131",
"endSection": "sections.0",
"offsetInBeginSection": 1349,
"offsetInEndSection": 1462,
"text": "There was no significant difference in the pregnancy rate between the patients with or without pituitary adenoma."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2520800",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Two hyperprolactinemic infertile women, one with and one without a pituitary adenoma, who were resistant to bromocriptine treatment, were treated orally with Hachimijiogan, a Chinese herbal medicine."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6868876",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Infertility caused by hyperprolactinemic amenorrhea may be complicated by pituitary adenoma."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D010911",
"http://www.disease-ontology.org/api/metadata/DOID:3829",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007246",
"http://www.disease-ontology.org/api/metadata/DOID:5223",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014930",
"http://www.disease-ontology.org/api/metadata/DOID:5395",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007247",
"http://www.disease-ontology.org/api/metadata/DOID:5394",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015175"
] | null |
514a51c2d24251bc0500005c
|
bioasq_factoid
|
factoid
|
What antibiotic is currently used as the standard of care for Clostridium Difficile infection as of 2018
|
['Fidaxomicin']
|
[
"Fidaxomicin",
"Dificid",
"OPT-80",
"Fidaxomicin (Dificid)"
] |
['fidaxomicin has recently been introduced as a new antibiotic that has been shown to significantly reduce the recurrence of this infection. fidaxomicin is a new antibiotic used to treat clostridium difficile infection (cdi).', 'Fidaxomicin has recently been introduced as a new antibiotic that has been shown to significantly reduce the recurrence of this infection. Fidaxomicin is a new antibiotic used to treat Clostridium difficile infection (CDI).', 'Fidaxomicin has recently been introduced as a new antibiotic that has been shown to significantly reduce the recurrence of this infection.Fidaxomicin is a new antibiotic used to treat Clostridium difficile infection (CDI)', 'Clostridium difficile continues to be one of the most prevalent hospital-acquired bacterial infections in the developed world, despite the recent introduction of a novel and effective antibiotic agent fidaxomicin']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27601193",
"http://www.ncbi.nlm.nih.gov/pubmed/28009682"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27601193",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 295,
"text": " Fidaxomicin has recently been introduced as a new antibiotic that has been shown to significantly reduce the recurrence of this infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28009682",
"endSection": "abstract",
"offsetInBeginSection": 22,
"offsetInEndSection": 107,
"text": "Fidaxomicin is a new antibiotic used to treat Clostridium difficile infection (CDI). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28009682",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 69,
"text": "Outcomes With Fidaxomicin Therapy in Clostridium difficile Infection."
}
] | 11
|
BioASQ-training11b
| null | null |
5c85234775a4a5d219000007
|
bioasq_factoid
|
yesno
|
Does wheat belongs to the genus Avena, yes or no?
|
['no']
|
[
"no"
] |
['oat seedlings (Avena sativa)', 'Wheat belongs to the species Triticum not to the genus Avena.', 'oat seedlings (Avena sativa). ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29146257",
"http://www.ncbi.nlm.nih.gov/pubmed/10984842",
"http://www.ncbi.nlm.nih.gov/pubmed/27079356",
"http://www.ncbi.nlm.nih.gov/pubmed/11908651",
"http://www.ncbi.nlm.nih.gov/pubmed/11536867",
"http://www.ncbi.nlm.nih.gov/pubmed/20658121",
"http://www.ncbi.nlm.nih.gov/pubmed/26618715",
"http://www.ncbi.nlm.nih.gov/pubmed/28132155",
"http://www.ncbi.nlm.nih.gov/pubmed/28132141",
"http://www.ncbi.nlm.nih.gov/pubmed/24226111"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29146257",
"endSection": "title",
"offsetInBeginSection": 84,
"offsetInEndSection": 112,
"text": "oat seedlings (Avena sativa)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26618715",
"endSection": "title",
"offsetInBeginSection": 19,
"offsetInEndSection": 49,
"text": "wild green-oat (Avena sativa) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28132141",
"endSection": "abstract",
"offsetInBeginSection": 74,
"offsetInEndSection": 96,
"text": " Oat (Avena sativa L.)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28132155",
"endSection": "title",
"offsetInBeginSection": 38,
"offsetInEndSection": 59,
"text": "Oat (Avena sativa L.)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24226111",
"endSection": "title",
"offsetInBeginSection": 46,
"offsetInEndSection": 58,
"text": "Avena (Oats)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27079356",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 142,
"text": "wild oats (Avena fatua L.)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10984842",
"endSection": "title",
"offsetInBeginSection": 41,
"offsetInEndSection": 59,
"text": "oats (genus Avena)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20658121",
"endSection": "title",
"offsetInBeginSection": 46,
"offsetInEndSection": 88,
"text": "Avena sativa L. and A. byzantina C. Koch) "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11908651",
"endSection": "title",
"offsetInBeginSection": 81,
"offsetInEndSection": 104,
"text": " oat (Avena sativa L.)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11536867",
"endSection": "abstract",
"offsetInBeginSection": 16,
"offsetInEndSection": 66,
"text": "oat (Avena sativa L.) and wheat (Triticum aestivum"
}
] | 11
|
BioASQ-training11b
| null | null |
5a79d25dfaa1ab7d2e00000f
|
bioasq_yesno
|
yesno
|
Are there ways of joint Bayesian inference of risk variants?
|
['yes']
|
[
"yes"
] |
['Yes. RiVIERA (Risk Variant Inference using Epigenomic Reference Annotations) is a Bayesian model for inference of driver variants from summary statistics across multiple traits using hundreds of epigenomic annotations.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27407109"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27407109",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Joint Bayesian inference of risk variants and tissue-specific epigenomic enrichments across multiple complex human diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27407109",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1444,
"text": "Genome wide association studies (GWAS) provide a powerful approach for uncovering disease-associated variants in human, but fine-mapping the causal variants remains a challenge. This is partly remedied by prioritization of disease-associated variants that overlap GWAS-enriched epigenomic annotations. Here, we introduce a new Bayesian model RiVIERA (Risk Variant Inference using Epigenomic Reference Annotations) for inference of driver variants from summary statistics across multiple traits using hundreds of epigenomic annotations. In simulation, RiVIERA promising power in detecting causal variants and causal annotations, the multi-trait joint inference further improved the detection power. We applied RiVIERA to model the existing GWAS summary statistics of 9 autoimmune diseases and Schizophrenia by jointly harnessing the potential causal enrichments among 848 tissue-specific epigenomics annotations from ENCODE/Roadmap consortium covering 127 cell/tissue types and 8 major epigenomic marks. RiVIERA identified meaningful tissue-specific enrichments for enhancer regions defined by H3K4me1 and H3K27ac for Blood T-Cell specifically in the nine autoimmune diseases and Brain-specific enhancer activities exclusively in Schizophrenia. Moreover, the variants from the 95% credible sets exhibited high conservation and enrichments for GTEx whole-blood eQTLs located within transcription-factor-binding-sites and DNA-hypersensitive-sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27407109",
"endSection": "abstract",
"offsetInBeginSection": 302,
"offsetInEndSection": 535,
"text": "Here, we introduce a new Bayesian model RiVIERA (Risk Variant Inference using Epigenomic Reference Annotations) for inference of driver variants from summary statistics across multiple traits using hundreds of epigenomic annotations."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27407109",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Joint Bayesian inference of risk variants and tissue-specific epigenomic enrichments across multiple complex human diseases."
}
] | 11
|
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D001499",
"https://meshb.nlm.nih.gov/record/ui?ui=D014644"
] | null |
5a80dbaafaa1ab7d2e000026
|
bioasq_yesno
|
factoid
|
Where is fatty acid binding protein 2 expressed?
|
['intestinal epithelial cells']
|
[
"intestinal epithelial cells",
"enterocytes",
"intestinal absorptive cells",
"intestinal epithelial",
"gut epithelial cells",
"intestinal lining cells"
] |
['fatty acid binding protein 2 is expressed by intestinal epithelial cells']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29032508",
"http://www.ncbi.nlm.nih.gov/pubmed/17960769",
"http://www.ncbi.nlm.nih.gov/pubmed/20670215",
"http://www.ncbi.nlm.nih.gov/pubmed/18634911",
"http://www.ncbi.nlm.nih.gov/pubmed/26547205",
"http://www.ncbi.nlm.nih.gov/pubmed/18440731"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18634911",
"endSection": "abstract",
"offsetInBeginSection": 15,
"offsetInEndSection": 75,
"text": " human intestinal fatty acid binding protein 2 gene (FABP2) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18440731",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "The human fatty acid binding protein (FABP2) is involved in intestinal absorption and intracellular trafficking of long-chain fatty acids."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17960769",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "The human intestinal fatty acid binding protein 2 (FABP2) mediates fat absorption by binding and intracellular trafficking of long-chain free fatty acids."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20670215",
"endSection": "abstract",
"offsetInBeginSection": 839,
"offsetInEndSection": 905,
"text": "intestinal epithelial cells [FABP2 (fatty acid binding protein 2),"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29032508",
"endSection": "abstract",
"offsetInBeginSection": 1036,
"offsetInEndSection": 1127,
"text": "enterocyte markers like villin, zonula occluden (ZO1), fatty acid binding protein 2 (FABP2)"
}
] | 11
|
BioASQ-training11b
| null | null |
5c8d15cf0101eac870000009
|
bioasq_factoid
|
factoid
|
Which gene therapy treatment is FDA approved for retinal dystrophy?
|
['Luxturna']
|
[
"Luxturna",
"voretigene neparvovec",
"voretigene neparvovec-rzyl",
"LUXTURNA"
] |
['Luxturna is approved by the Food and Drug Administration (FDA) for the treatment of inherited retinal dystrophy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30089698"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30089698",
"endSection": "abstract",
"offsetInBeginSection": 1755,
"offsetInEndSection": 2010,
"text": "Gene therapy utilizing viral vectors has experienced recent success, culminating in U.S. Food and Drug Administration approval of the first adeno-associated virus vector gene therapy product in the United States: Luxturna for inherited retinal dystrophy. "
}
] | 11
|
BioASQ-training11b
| null | null |
5c89773ed558e5f23200000a
|
bioasq_factoid
|
factoid
|
What is the protein product of the gene GBA2?
|
['The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.']
|
[
"GBA2",
"non-lysosomal glucosylceramidase",
"NLGase",
"glucosylceramidase",
"glucosylceramide beta-glucosidase",
"glucosylceramidase 2",
"glucosylceramidase, non-lysosomal"
] |
['The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29524657",
"http://www.ncbi.nlm.nih.gov/pubmed/29234271",
"http://www.ncbi.nlm.nih.gov/pubmed/30308956"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29524657",
"endSection": "abstract",
"offsetInBeginSection": 907,
"offsetInEndSection": 934,
"text": "b-glucosidase 2 gene (GBA2)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308956",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29234271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "The non-lysosomal glucosylceramidase GBA2 catalyzes the hydrolysis of glucosylceramide to glucose and ceramide. "
}
] | 11
|
BioASQ-training11b
| null | null |
5e5bab131af46fc130000001
|
bioasq_factoid
|
yesno
|
Are there sex differences in the transcriptome of the mouse hippocampus?
|
['yes']
|
[
"yes"
] |
['There are sex differences in the transcriptome of the developing mouse hippocampus.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28302071"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28302071",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 499,
"text": "To better understand the possible molecular basis for the sex-biased nature of neurological disorders, we used a developmental series of female and male mice at 1, 2, and 4 months of age to assess both mRNA and protein in the hippocampus with RNA-sequencing and mass-spectrometry, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28302071",
"endSection": "abstract",
"offsetInBeginSection": 627,
"offsetInEndSection": 1144,
"text": "The bulk of these differentially expressed genes are changed in both sexes at one or more ages, but a total of 198 transcripts are differentially expressed between females and males at one or more ages. The number of transcripts that are differentially expressed between females and males is greater in adult animals than in younger animals. Additionally, we identify 69 transcripts that show complex and sex-specific patterns of temporal regulation through postnatal development, 8 of which are heat-shock proteins. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28302071",
"endSection": "abstract",
"offsetInBeginSection": 1394,
"offsetInEndSection": 1643,
"text": "Additionally, this analysis reveals sex differences in the transcriptome of the developing mouse hippocampus, and further clarifies the need to include both female and male mice in longitudinal studies involving molecular changes in the hippocampus."
}
] | 11
|
BioASQ-training11b
| null | null |
5a991ee21d1251d03b000005
|
bioasq_yesno
|
factoid
|
Which is the most reliable liquid biopsy technique after complete resection of colorectal cancer metastases?
|
['Circulating tumor cells', 'CTCs']
|
[
"Circulating tumor cells",
"CTCs",
"circulating tumor cell",
"circulating cancer cells",
"CTC",
"tumor cells in circulation",
"circulating neoplastic cells"
] |
['Circulating tumor cells (CTCs) are the most reliable liquid biopsy technique after complete resection of colorectal cancer metastases, as they showed the best diagnostic performance among all liquid biopsy methods.', 'Among all liquid biopsy methods (cell-free DNA, exosomes and circulating tumor cells), circulating tumor cells showed the best diagnostic performance', 'Among all liquid biopsy methods, CTCs (Circulating Tumor Cells) showed the best diagnostic performance after complete resection of colorectal cancer metastases. This makes CTCs the most reliable technique in this specific scenario.', 'The most reliable liquid biopsy technique for detecting minimal residual disease after complete resection of colorectal cancer metastases is the CellSearch method for enumeration of circulating tumor cells (CTCs). This method has been validated and approved by the FDA as a useful prognostic method for metastatic breast, colon, and prostate cancer. However, it is important to note that detecting ctDNA in blood samples can be challenging due to the presence of wild type DNA from white blood cells, and pre-analytical considerations such as preventing or delaying white cell lysis, using cell stabilization tubes, and performing a double centrifugation step can help improve ctDNA detection. Plasma is better than serum for ctDNA recovery, and ctDNA or cfDNA can be extracted from plasma fractions using commercially available kits. The analysis of ctDNA after extraction requires the use of various amplification and sequencing methods, which can be separated into two main groups: untargeted approaches (e.g., whole genome or whole exome sequencing) and targeted approaches (e.g., sequencing of ctDNA based on mutational hotspots for the cancer of interest). Targeted approaches can amplify ctDNA through polymerase chain reactions (PCR) or digital PCR, which is especially important given the low levels of DNA circulating in the bloodstream and the small proportion of ctDNA in the total cell-free DNA extracted.', 'Based on the meta-analysis provided, all liquid biopsy methods, including circulating tumor cells (CTCs), exosomes, and cell-free DNA (cfDNA), demonstrated high diagnostic value for colorectal cancer (CRC) detection. However, when comparing their performance after complete resection of CRC metastases, it is essential to consider the specific clinical context and purpose of the liquid biopsy. , For detecting residual or recurrent disease, CTCs seem to be the most reliable technique among those studied, as they showed the best diagnostic performance with a pooled sensitivity of 0.82 (95% CI 0.79-0.85) and specificity of 0.97 (95% CI 0.95-0.99). Higher sensitivity implies that CTCs are more likely to detect residual or recurrent cancer compared to other liquid biopsy methods, while high specificity reduces', 'Circulating tumor DNA (ctDNA) is the most reliable liquid biopsy technique after complete resection of colorectal cancer metastases. It has been shown to be highly predictive of early disease recurrence in surgically resected colorectal cancer, and is superior to carcinoembryonic antigen (CEA) in detecting residual disease and early recurrence. Additionally, pre-surgery ctDNA levels are positively correlated with tumor burden and have predictive value for relapse. Positive ctDNA has been found to precede radiologic and clinical evidence of recurrence by a median of 3 months. Furthermore, in patients with metastatic colorectal cancer (mCRC), detection of ctDNA following curative intent therapies is a surrogate for microscopic residual disease.', 'CTCs is the most reliable liquid biopsy technique after complete resection of colorectal cancer metastases.', "The most reliable liquid biopsy technique after complete resection of colorectal cancer metastases is still under investigation. However, a study has shown that pre-surgery circulating tumor DNA (ctDNA) levels are positively correlated with tumor burden and have predictive value for relapse in patients with metastatic colorectal cancer following resection. Additionally, another study has demonstrated that circulating tumor cell (CTC) subcategorization based on morphological differences leads to nuanced results between the subtypes, emphasizing the heterogeneity within the CTC classification. Furthermore, integrating morphology and time-based analysis alongside standard CTC enumeration can provide greater insight into the pathophysiology of mCRC by highlighting the complexity of the disease across a patient's treatment. Liver transplantation for liver-confined unresectable colorectal cancer liver metastases is emerging as a valid surgical option in selected patients, and clearance", "The question asks for the most reliable liquid biopsy technique for monitoring colorectal cancer (CRC) metastases after complete resection. Based on the context, Circulating Tumor Cells (CTCs) have demonstrated the best diagnostic performance among all liquid biopsy methods. , Liquid biopsies are minimally invasive tests that analyze various tumor-derived components from bodily fluids. Among these, CTCs have gained attention as a promising tool for cancer detection and monitoring. CTCs are cancer cells that shed into the bloodstream from primary or metastatic tumors and can be detected and analyzed to provide valuable information about the tumor's characteristics, evolution, and response to treatment. , Several studies have shown that CTC analysis can detect minimal residual disease, predict clinical outcomes, and monitor tumor dynamics in real-time, making it a potentially valuable tool for post-treatment surveillance of CRC metastases. Therefore,", 'Liquid biopsy, particularly circulating tumor DNA (ctDNA), is the most reliable technique after complete resection of colorectal cancer metastases.', 'There are several liquid biopsy methods for the detection of circulating tumor cells (CTCs) or circulating tumor DNA (ctDNA). Among all these techniques, CTCs showed the best diagnostic performance for prognosis and treatment response of patients with colorectal cancer metastases after complete resection.', 'Liquid biopsy techniques are currently being investigated as a promising method for monitoring minimal residual disease (MRD) in cancer patients, particularly in colorectal cancer (CRC) after complete resection of metastases. The most reliable liquid biopsy technique, however, is still a subject of ongoing research and debate.', 'The most reliable liquid biopsy technique after complete resection of colorectal cancer metastases is still under investigation. However, a recent study has shown that perioperative circulating tumor DNA (ctDNA) levels are positively correlated with tumor burden and have predictive value for relapse in patients with colorectal liver metastases. Additionally, pre-surgery ctDNA, cfDNA, and CEA levels have been shown to have predictive value for relapse in this patient population. Therefore, perioperative liquid biopsy techniques, including ctDNA analysis, may be useful for postoperative surveillance and outcome prediction in patients with colorectal cancer metastases.', "Based on the available research, Circulating Tumor Cells (CTCs) are currently considered the most reliable liquid biopsy technique for monitoring colorectal cancer metastases after complete resection due to their ability to detect minimal residual disease and predict clinical outcomes. This minimally invasive method analyzes tumor-derived components from bodily fluids, providing valuable information about the tumor's characteristics and response to treatment.", 'Circulating tumor cells (CTCs) have demonstrated the best diagnostic performance among all liquid biopsy methods. CTC-based liquid biopsy is likely the most reliable technique for monitoring colorectal cancer metastases after complete resection. This method can provide real-time information about the presence of residual tumor cells in the body, helping to detect potential recurrence early and guiding more effective personalized treatment strategies.', 'The most reliable liquid biopsy technique after complete resection of colorectal cancer metastases is CTCs.', 'CTCs (Circulating Tumor Cells) showed the best diagnostic performance among all liquid biopsy methods after complete resection of colorectal cancer metastases.', 'In the context of complete resection of colorectal cancer metastases, circulating tumor cells (CTCs) show higher reliability for detecting residual or recurrent disease than exosomes and cell-free DNA (cfDNA), with a pooled sensitivity of 0.82 and specificity of 0.97.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35337361",
"http://www.ncbi.nlm.nih.gov/pubmed/30626171",
"http://www.ncbi.nlm.nih.gov/pubmed/30053724",
"http://www.ncbi.nlm.nih.gov/pubmed/33738696",
"http://www.ncbi.nlm.nih.gov/pubmed/35284120",
"http://www.ncbi.nlm.nih.gov/pubmed/29589077",
"http://www.ncbi.nlm.nih.gov/pubmed/32184665",
"http://www.ncbi.nlm.nih.gov/pubmed/34327297",
"http://www.ncbi.nlm.nih.gov/pubmed/32566042",
"http://www.ncbi.nlm.nih.gov/pubmed/34587798",
"http://www.ncbi.nlm.nih.gov/pubmed/34066481",
"http://www.ncbi.nlm.nih.gov/pubmed/36992914",
"http://www.ncbi.nlm.nih.gov/pubmed/28344745",
"http://www.ncbi.nlm.nih.gov/pubmed/25332962",
"http://www.ncbi.nlm.nih.gov/pubmed/31930130",
"http://www.ncbi.nlm.nih.gov/pubmed/37273078",
"http://www.ncbi.nlm.nih.gov/pubmed/32628360",
"http://www.ncbi.nlm.nih.gov/pubmed/34150757",
"http://www.ncbi.nlm.nih.gov/pubmed/34298740",
"http://www.ncbi.nlm.nih.gov/pubmed/36382087",
"http://www.ncbi.nlm.nih.gov/pubmed/31269959",
"http://www.ncbi.nlm.nih.gov/pubmed/31142037",
"http://www.ncbi.nlm.nih.gov/pubmed/33667566",
"http://www.ncbi.nlm.nih.gov/pubmed/35962648",
"http://www.ncbi.nlm.nih.gov/pubmed/35857852",
"http://www.ncbi.nlm.nih.gov/pubmed/32545981",
"http://www.ncbi.nlm.nih.gov/pubmed/31060647",
"http://www.ncbi.nlm.nih.gov/pubmed/27516729",
"http://www.ncbi.nlm.nih.gov/pubmed/33301640",
"http://www.ncbi.nlm.nih.gov/pubmed/34408162",
"http://www.ncbi.nlm.nih.gov/pubmed/37541105",
"http://www.ncbi.nlm.nih.gov/pubmed/25959553",
"http://www.ncbi.nlm.nih.gov/pubmed/37910091",
"http://www.ncbi.nlm.nih.gov/pubmed/30554222",
"http://www.ncbi.nlm.nih.gov/pubmed/36077774",
"http://www.ncbi.nlm.nih.gov/pubmed/34572727",
"http://www.ncbi.nlm.nih.gov/pubmed/29627453"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32628360",
"endSection": "abstract",
"offsetInBeginSection": 1397,
"offsetInEndSection": 1473,
"text": "Among all liquid biopsy methods, CTCs showed the best diagnostic performance"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34587798",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 183,
"text": "We aimed to evaluate the prognostic value of circulating tumor cells (CTCs) and the impact of intraoperative tumor manipulation on CTCs in colorectal cancer (CRC) patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33301640",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Circulating tumor cell (CTC) analysis holds great potential to be a noninvasive solution for clinical cancer management"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32545981",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 420,
"text": "In patients with detectable circulating tumor DNA (ctDNA), liquid biopsy can be an effective monitoring tool."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31269959",
"endSection": "abstract",
"offsetInBeginSection": 772,
"offsetInEndSection": 1095,
"text": "Liquid biopsy is noninvasive and allows repeated analyses to monitor tumor recurrence, metastasis or treatment responses in real time. With the advanced development of new molecular techniques, HCC circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) detection have achieved interesting and encouraging results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31269959",
"endSection": "abstract",
"offsetInBeginSection": 661,
"offsetInEndSection": 1095,
"text": "Over the past years, a new diagnostic concept known as \"liquid biopsy\" has emerged with substantial attention. Liquid biopsy is noninvasive and allows repeated analyses to monitor tumor recurrence, metastasis or treatment responses in real time. With the advanced development of new molecular techniques, HCC circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) detection have achieved interesting and encouraging results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25959553",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 625,
"text": "Capturing circulating tumor cells (CTCs) and/or circulating tumor DNA from blood, which represents a precious source of biological material derived from both primary and metastatic tumors, has been named a 'liquid biopsy'. While the circulating tumor DNA might be more representative of the bulk of the metastatic tumor, CTCs are thought to reflect more of the metastases-initiating cells. Consequently, a liquid biopsy made of tumor cells and tumor DNA that is able to track cancer evolution, as a fingerprint of the patient's individual tumor, and is easy to perform at every stage of the disease course, sounds attractive."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27516729",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 314,
"text": "Circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) are emerging noninvasive multifunctional biomarkers in liquid biopsy allowing for early diagnosis, accurate prognosis, therapeutic target selection, spatiotemporal monitoring of metastasis, as well as monitoring response and resistance to treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27516729",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 453,
"text": "Circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) are emerging noninvasive multifunctional biomarkers in liquid biopsy allowing for early diagnosis, accurate prognosis, therapeutic target selection, spatiotemporal monitoring of metastasis, as well as monitoring response and resistance to treatment. CTCs and ctDNA are released from different tumor types at different stages and contribute complementary information for clinical decision."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27516729",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 894,
"text": "Circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) are emerging noninvasive multifunctional biomarkers in liquid biopsy allowing for early diagnosis, accurate prognosis, therapeutic target selection, spatiotemporal monitoring of metastasis, as well as monitoring response and resistance to treatment. CTCs and ctDNA are released from different tumor types at different stages and contribute complementary information for clinical decision. Although big strides have been taken in technology development for detection, isolation and characterization of CTCs and sensitive and specific detection of ctDNA, CTC-, and ctDNA-based liquid biopsies may not be widely adopted for routine cancer patient care until the suitability, accuracy, and reliability of these tests are validated and more standardized protocols are corroborated in large, independent, prospectively designed trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34572727",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 1148,
"text": "Liquid biopsies provide direct non-invasive access to tumor material, which is shed into the circulation; this enables the analysis of circulating tumor cells (CTC) and genomic components such as circulating free DNA (cfDNA), which could provide the key for personalized therapy. Liquid biopsy (LB) allows for the identification of patients with a high risk for disease progression after curative surgery, as well as longitudinal monitoring for disease progression and therapy response. Here, we will review the most recent studies on CRC, demonstrating the clinical potential and utility of CTCs and ctDNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25959553",
"endSection": "abstract",
"offsetInBeginSection": 223,
"offsetInEndSection": 761,
"text": "While the circulating tumor DNA might be more representative of the bulk of the metastatic tumor, CTCs are thought to reflect more of the metastases-initiating cells. Consequently, a liquid biopsy made of tumor cells and tumor DNA that is able to track cancer evolution, as a fingerprint of the patient's individual tumor, and is easy to perform at every stage of the disease course, sounds attractive. This article mainly focuses on the applications of CTCs to track tumor dynamics in real time using colorectal cancer as a model system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25959553",
"endSection": "abstract",
"offsetInBeginSection": 390,
"offsetInEndSection": 935,
"text": "Consequently, a liquid biopsy made of tumor cells and tumor DNA that is able to track cancer evolution, as a fingerprint of the patient's individual tumor, and is easy to perform at every stage of the disease course, sounds attractive. This article mainly focuses on the applications of CTCs to track tumor dynamics in real time using colorectal cancer as a model system. The analysis of viable CTCs at DNA, RNA and protein levels, as well as their expansion in vitro, may allow deep investigation of the features of metastases-initiating cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34327297",
"endSection": "abstract",
"offsetInBeginSection": 1508,
"offsetInEndSection": 1826,
"text": "In the multivariate analysis, ctDNA-based MRD status was the most significant prognostic factor associated with disease-free survival (HR: 5.78; 95% CI, 3.34 to 10.0; P < .001).CONCLUSION: This study confirms that in mCRC undergoing resection of metastases, postoperative MRD analysis is a strong prognostic biomarker."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35962648",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 933,
"text": "biomarkers.CONTENT: Following curative-intent surgery for cancer, the presence of ctDNA is highly predictive of early disease recurrence, while in metastatic cancer an early decline in ctDNA following the initiation of treatment is predictive of good outcome. Compared with protein biomarkers, ctDNA provides greater cancer specificity and sensitivity for detecting early recurrent/metastatic disease. Thus, in patients with surgically resected colorectal cancer, multiple studies have shown that ctDNA is superior to carcinoembryonic antigen (CEA) in detecting residual disease a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36382087",
"endSection": "abstract",
"offsetInBeginSection": 1467,
"offsetInEndSection": 1695,
"text": " volumes (9 cm vs 2 cm, p=0.05).Conclusions: Treatment with BA in patients with ctDNA-detected, liver-limited mCRC did not clear ctDNA and was associated with large-volume recurrence, highlighting the potential context-specific "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37273078",
"endSection": "abstract",
"offsetInBeginSection": 97,
"offsetInEndSection": 602,
"text": "liver disease develops in 50% of cases and drives patient outcomes. Although the ideal treatment for colorectal cancer liver metastases (CRLM) is resection, only a third of patients are suitable for this approach. Reports of liver transplantation in selected patients with unresectable CRLM have shown encouraging results compared to conventional forms of therapy. No study to date has examined the utility of liquid biopsy circulating tumor DNA (ctDNA) for evaluation of residual disease in this cohort o"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29589077",
"endSection": "abstract",
"offsetInBeginSection": 162,
"offsetInEndSection": 1210,
"text": "metastases of colorectal cancer. For good oncological results complete macroscopic cytoreduction is crucial; furthermore, a linear correlation between peritoneal tumor load, as determined by the peritoneal cancer index (PCI) and overall survival has been demonstrated; therefore, surgical treatment should be initiated as early as possible. Synchronous resection of up to three liver metastases may be performed safely and with good results and no influence on the morbidity. With respect to intraperitoneal chemotherapy, mitomycin C and oxaliplatin are most commonly used and may be regarded as equal; however, for perioperative chemotherapy study results are so far inconclusive with some trials hinting at decreased overall survival following neoadjuvant chemotherapy. Adjuvant therapy is likely to improve overall survival if at least 6 cycles are applied. Early detection of peritoneal metastases is difficult at present but might be facilitated in the future by the use of liquid biopsies, which may detect circulating free tumor-specific DNA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36992914",
"endSection": "abstract",
"offsetInBeginSection": 10,
"offsetInEndSection": 894,
"text": "is the most common site of metastasis in colorectal cancer. Multimodal treatment, including liver resection, is potentially curative and prolongs survival for selected patients with colorectal liver metastases (CRLM). However, the treatment of CRLM remains challenging because recurrence is common, and prognosis varies widely between patients despite curative-intent treatment. Clinicopathological features and tissue-based molecular biomarkers, either alone or in combination, are insufficient for accurate prognostication. As most of the functional information in cells resides in the proteome, circulating proteomic biomarkers may be useful for rationalising the molecular complexities of CRLM and identifying potentially prognostic molecular subtypes. High-throughput proteomics has accelerated a range of applications including protein profiling of liquid biopsies for biomarker"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28344745",
"endSection": "abstract",
"offsetInBeginSection": 904,
"offsetInEndSection": 1585,
"text": "staged hepatectomy techniques to expand indications for liver resection. Added to this complexity is the increasing number of molecular markers, which appear to hold important prognostic and predictive information, for which some will be discussed here. Beyond characteristics of tissue-based genomic profiles will be liquid biopsies derived from circulating tumor cells and cell-free circulating tumor DNA in the blood. These markers are present in the peripheral circulation in the majority of patients with metastatic cancer disease. Circulating biomarkers may represent more readily available methods to monitor, characterize and predict cancer biology with future implications"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37910091",
"endSection": "abstract",
"offsetInBeginSection": 438,
"offsetInEndSection": 1142,
"text": "A levels are prognostic. Although their levels correlate with treatment response, CTC-guided systemic regimen switches for nonresponders have not been shown to improve clinical outcomes. ctDNA genomic profiling has succeeded, and there are now multiple plasma-based assays approved by the US Food and Drug Administration that can detect actionable mutations to guide systemic therapy. Technological advancements in assay sensitivity have expanded the use of ctDNA to early-stage and resectable disease, allowing for detection of minimal residual disease. Postoperative ctDNA levels are a strong predictor of disease recurrence, and ctDNA detection often precedes serum carcinoembryonic antigen elevation "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34298740",
"endSection": "abstract",
"offsetInBeginSection": 1094,
"offsetInEndSection": 1388,
"text": "Ongoing trials, focusing on circulating tumor cells (CTCs) and, even more, circulating tumor DNA (ctDNA), seem to pave the way to a promising, minimally invasive but accurate and life-saving monitoring, not only supporting personalized treatment but favoring patients' quality of life, as well."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34408162",
"endSection": "abstract",
"offsetInBeginSection": 454,
"offsetInEndSection": 698,
"text": "Here, we analyzed cfDNA originating from nucleus and mitochondria and investigated their characteristics and mutation status in a cohort of 18 CRC patients and 10 healthy controls using targeted next-generation sequencing (NGS) and digital PCR."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31060647",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 1418,
"text": "\"Liquid biopsy\" is one of the most recent domains of interest in oncology, as it may provide important details regarding the characteristics of the main tumor and its metastases. Malignant cells are in a continuous dynamic, which makes the initial diagnostic biopsy and the pathological specimen evaluation insufficient in the late evolution of the disease, when relapse or metastases may appear. The fact that the healthcare provider is able to find out additional information about the tumor at a given time, by evaluating a blood sample to obtain a \"liquid biopsy\" is of utmost importance and gives multiple potentially usable data. There are three means of obtaining biological material that may be used as \"liquid biopsy\": evaluation of circulating tumor cells, circulating tumor DNA and exosomes. The most intensely studied entity is that of circulating tumor cells, with different applications, amongst which the most important, at present time, is the prognostic value that has important demonstrated implications, not only in breast and prostate cancer, but also in colorectal cancer. Although surgery will, most certainly, not be replaced by other treatments when aiming for a curative approach to rectal cancer, it is importa"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35857852",
"endSection": "abstract",
"offsetInBeginSection": 1623,
"offsetInEndSection": 1868,
"text": "by the heterogeneity of the cohort and the small number of postoperative plasma samples.CONCLUSIONS: These data indicate that tumor-informed circulating tumor DNA detection in the plasma of patients undergoing surgery for metastatic colorectal c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32566042",
"endSection": "abstract",
"offsetInBeginSection": 813,
"offsetInEndSection": 1206,
"text": "This means that, in this sample, the preoperative sensitivity and specificity of the test were 88.9% and 100%, respectively, and there is 100% correlation between the positive results of the SEPT9 test and a recurrence/persistence of the disease in patients after surgical resection.CONCLUSIONS: Our study shows that circulating hypermethylated SEPT9 is a specific colorectal cancer biomarker."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34298740",
"endSection": "abstract",
"offsetInBeginSection": 996,
"offsetInEndSection": 1388,
"text": "Under this perspective, early detection of post-operative CRC recurrence is of utmost importance. Ongoing trials, focusing on circulating tumor cells (CTCs) and, even more, circulating tumor DNA (ctDNA), seem to pave the way to a promising, minimally invasive but accurate and life-saving monitoring, not only supporting personalized treatment but favoring patients' quality of life, as well."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30626171",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 280,
"text": "Detecting and enumerating circulating tumor cells (CTCs) in patients with colorectal cancer emerged as an important prognostic tool which provides a direct estimate of metastatic potential."
}
] | 13
|
BioASQ-training13b
| null | null |
65f7789dc4010b4d78000034
|
bioasq_factoid
|
factoid
|
What is the administration route of zavegepant?
|
['intranasally', 'nasal spray']
|
[
"intranasally",
"nasal spray",
"intranasal",
"nasal delivery",
"nasal administration"
] |
['Zavegepant is administered intranasally and used for migraine attacks.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37227596",
"http://www.ncbi.nlm.nih.gov/pubmed/37345774",
"http://www.ncbi.nlm.nih.gov/pubmed/33096162",
"http://www.ncbi.nlm.nih.gov/pubmed/36804093",
"http://www.ncbi.nlm.nih.gov/pubmed/37904462",
"http://www.ncbi.nlm.nih.gov/pubmed/37363553",
"http://www.ncbi.nlm.nih.gov/pubmed/36239038",
"http://www.ncbi.nlm.nih.gov/pubmed/36189708",
"http://www.ncbi.nlm.nih.gov/pubmed/37038933"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37345774",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Zavegepant (Zavzpret), a nasal spray, is approved to treat adults with acute migraine with or without aura."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37038933",
"endSection": "abstract",
"offsetInBeginSection": 405,
"offsetInEndSection": 658,
"text": "Ubrogepant is ratified for acute migraine treatment, atogepant is validated for preventive therapy, whereas rimegepant is ratified for both indications, all via oral administration and while zavegepant is administered intranasally for migraine attacks. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37227596",
"endSection": "abstract",
"offsetInBeginSection": 246,
"offsetInEndSection": 403,
"text": "In March 2023, zavegepant nasal spray (ZAVZPRET™) received its first approval in the USA for the acute treatment of migraine with or without aura in adults. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36804093",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "Safety, tolerability, and efficacy of zavegepant 10 mg nasal spray for the acute treatment of migraine in the USA: a phase 3, double-blind, randomised, placebo-controlled multicentre trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36804093",
"endSection": "abstract",
"offsetInBeginSection": 187,
"offsetInEndSection": 349,
"text": "Zavegepant, an intranasally administered small molecule calcitonin gene-related peptide (CGRP) receptor antagonist, was previously assessed in a phase 2/3 trial. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36804093",
"endSection": "abstract",
"offsetInBeginSection": 2868,
"offsetInEndSection": 3015,
"text": "INTERPRETATION: Zavegepant 10 mg nasal spray was efficacious in the acute treatment of migraine, with favourable tolerability and safety profiles. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37363553",
"endSection": "abstract",
"offsetInBeginSection": 267,
"offsetInEndSection": 457,
"text": "Zavegepant is a novel, first-in-class, intranasally administered calcitonin gene-related peptide (CGRP) receptor antagonist that has recently been approved for use in acute migraine attacks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37363553",
"endSection": "abstract",
"offsetInBeginSection": 817,
"offsetInEndSection": 1034,
"text": "Moreover, the intranasal method of administration is a characteristic advantage of Zavegepant, as patients suffering from acute migraine attacks cannot easily ingest oral medication, due to severe nausea and vomiting."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37363553",
"endSection": "abstract",
"offsetInBeginSection": 1035,
"offsetInEndSection": 1280,
"text": "In this mini-review, the efficacy and safety of Zavegepant will be compared with those of alternative treatments available for migraines, including oral triptans, intranasal triptans, and other CGRP antagonists currently available in the market."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37038933",
"endSection": "abstract",
"offsetInBeginSection": 405,
"offsetInEndSection": 657,
"text": "Ubrogepant is ratified for acute migraine treatment, atogepant is validated for preventive therapy, whereas rimegepant is ratified for both indications, all via oral administration and while zavegepant is administered intranasally for migraine attacks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33096162",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 410,
"text": "Zavegepant (BHV-3500, BMS-742413) is a high affinity antagonist of the CGRP receptor (hCGRP Ki = 0.023 nM) that has demonstrated efficacy in the acute treatment of migraine with intranasal delivery in a Phase 2/3 trial, despite showing low oral bioavailability in rats (FPO = 1.7%)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36189708",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "Focus on zavegepant: the first intranasal third-generation gepant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37904462",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 194,
"text": "Zavegepant nasal spray is a novel CGRP receptor antagonist that has been developed for the acute treatment of migraine - a prevalent disease leading to disability and economic burden"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37904462",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "BACKGROUND: Zavegepant nasal spray is a novel CGRP receptor antagonist that has been developed for the acu"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36239038",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "OBJECTIVE: Evaluate the efficacy, safety, and tolerability of zavegepant nasal spray in the acute treatment of migraine.BACKGROUND: Calci"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36804093",
"endSection": "abstract",
"offsetInBeginSection": 175,
"offsetInEndSection": 336,
"text": "d vomiting. Zavegepant, an intranasally administered small molecule calcitonin gene-related peptide (CGRP) receptor antagonist, was previously assessed in a phas"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36189708",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 350,
"text": "Newly approved small molecules that antagonize the CGRP receptor, gepants, have advanced from the hepatotoxic first-generation telcagepant to third-generation intranasal zavegepant;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36239038",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 491,
"text": " for acute treatment. Zavegepant, a high-affinity, selective, and structurally unique calcitonin gene-related peptide-receptor antagonist in late-stage development, is formulated as a nasal spray for the acute "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36804093",
"endSection": "abstract",
"offsetInBeginSection": 809,
"offsetInEndSection": 982,
"text": "e attacks per month. Participants were randomly assigned (1:1) to zavegepant 10 mg nasal spray or matching placebo and self-treated a single migraine attack of moderate or s"
}
] | 13
|
BioASQ-training13b
| null | null |
65d1357c1930410b13000039
|
bioasq_factoid
|
yesno
|
Is Ameloblastoma (AB) a benign tumor that never metastasizes?
|
['no']
|
[
"no"
] |
['Ameloblastomas are benign but locally invasive neoplasms which can be metastatic']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21558899",
"http://www.ncbi.nlm.nih.gov/pubmed/32712102",
"http://www.ncbi.nlm.nih.gov/pubmed/23775022",
"http://www.ncbi.nlm.nih.gov/pubmed/24374844",
"http://www.ncbi.nlm.nih.gov/pubmed/6575436",
"http://www.ncbi.nlm.nih.gov/pubmed/28944145",
"http://www.ncbi.nlm.nih.gov/pubmed/31674718",
"http://www.ncbi.nlm.nih.gov/pubmed/18230377"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31674718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "Ameloblastic carcinoma (AC) is defined as a rare primary epithelial odontogenic malignant neoplasm and the malignant counterpart of benign epithelial odontogenic tumor of ameloblastoma (AB) by the WHO classification"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31674718",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 313,
"text": "AC develops pulmonary metastasis in about one third of the patients and reveals a poor prognosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32712102",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 313,
"text": "Ameloblastomas are benign but locally invasive neoplasms which may grow to massive proportions and cause significant morbidity. Although some types of ameloblastoma can be treated predictably with aggressive surgical treatment, recurrent ameloblastoma and metastasising ameloblastoma are still difficult to treat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21558899",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Ameloblastoma of the maxilla is a rare odontogenic tumor that rarely metastasizes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18230377",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Ameloblastoma is an odontogenic tumor, usually benign, which rarely metastasizes to distant organs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24374844",
"endSection": "abstract",
"offsetInBeginSection": 73,
"offsetInEndSection": 218,
"text": "Although ameloblastomas rarely metastasise, recurrences together with radical surgery often result in facial deformity and significant morbidity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28944145",
"endSection": "abstract",
"offsetInBeginSection": 74,
"offsetInEndSection": 224,
"text": "The World Health Organization (WHO) has defined malignant ameloblastoma (MA) as a histologically benign-appearing ameloblastoma that has metastasized."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23775022",
"endSection": "abstract",
"offsetInBeginSection": 102,
"offsetInEndSection": 250,
"text": "Distant metastasis is a very rare condition and is designated as metastasizing (malignant) ameloblastoma despite its benign histological appearance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6575436",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Ameloblastoma is a locally invasive, histologically nonmalignant tumor that may on very rare occasions give rise to metastases."
}
] | 11
|
BioASQ-training11b
| null | null |
622901d23a8413c65300008c
|
bioasq_yesno
|
yesno
|
Does PCSK9 (Proprotein convertase subtilisin/kexin type 9) binds with HDL-receptor (HDL-R)?
|
['no']
|
[
"no"
] |
['No, Proprotein Convertase Subtilisin Kexin 9 (PCSK9) binds with LDL-receptor (LDL-R) causing its degradation in the lysosome with the result of LDL-C accumulating in the blood.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27284008",
"http://www.ncbi.nlm.nih.gov/pubmed/26040332",
"http://www.ncbi.nlm.nih.gov/pubmed/20529551",
"http://www.ncbi.nlm.nih.gov/pubmed/23675525",
"http://www.ncbi.nlm.nih.gov/pubmed/26318398",
"http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"http://www.ncbi.nlm.nih.gov/pubmed/25649668",
"http://www.ncbi.nlm.nih.gov/pubmed/26256967",
"http://www.ncbi.nlm.nih.gov/pubmed/22683370",
"http://www.ncbi.nlm.nih.gov/pubmed/23690465",
"http://www.ncbi.nlm.nih.gov/pubmed/24164109",
"http://www.ncbi.nlm.nih.gov/pubmed/21692990",
"http://www.ncbi.nlm.nih.gov/pubmed/23974119",
"http://www.ncbi.nlm.nih.gov/pubmed/21122852",
"http://www.ncbi.nlm.nih.gov/pubmed/23261172",
"http://www.ncbi.nlm.nih.gov/pubmed/25679794",
"http://www.ncbi.nlm.nih.gov/pubmed/26495026",
"http://www.ncbi.nlm.nih.gov/pubmed/24094767",
"http://www.ncbi.nlm.nih.gov/pubmed/18436719",
"http://www.ncbi.nlm.nih.gov/pubmed/21497351",
"http://www.ncbi.nlm.nih.gov/pubmed/22580899",
"http://www.ncbi.nlm.nih.gov/pubmed/17702855",
"http://www.ncbi.nlm.nih.gov/pubmed/20716520",
"http://www.ncbi.nlm.nih.gov/pubmed/26056005",
"http://www.ncbi.nlm.nih.gov/pubmed/23141813",
"http://www.ncbi.nlm.nih.gov/pubmed/22300679",
"http://www.ncbi.nlm.nih.gov/pubmed/25463543",
"http://www.ncbi.nlm.nih.gov/pubmed/24685817",
"http://www.ncbi.nlm.nih.gov/pubmed/25905719",
"http://www.ncbi.nlm.nih.gov/pubmed/26548330",
"http://www.ncbi.nlm.nih.gov/pubmed/24603306",
"http://www.ncbi.nlm.nih.gov/pubmed/22907332",
"http://www.ncbi.nlm.nih.gov/pubmed/26088304",
"http://www.ncbi.nlm.nih.gov/pubmed/19828345",
"http://www.ncbi.nlm.nih.gov/pubmed/26364362",
"http://www.ncbi.nlm.nih.gov/pubmed/23106476",
"http://www.ncbi.nlm.nih.gov/pubmed/26023080",
"http://www.ncbi.nlm.nih.gov/pubmed/17493938",
"http://www.ncbi.nlm.nih.gov/pubmed/22176652",
"http://www.ncbi.nlm.nih.gov/pubmed/25744035",
"http://www.ncbi.nlm.nih.gov/pubmed/25070550",
"http://www.ncbi.nlm.nih.gov/pubmed/26195630",
"http://www.ncbi.nlm.nih.gov/pubmed/25971287",
"http://www.ncbi.nlm.nih.gov/pubmed/24144304"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25679794",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 747,
"text": "Recently it was revealed that the secreted Proprotein Convertase Subtilisin Kexin 9 (PCSK9) binds with LDL-receptor (LDL-R) causing its degradation in the lysosome with the result of LDL-C accumulating in the blood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25679794",
"endSection": "abstract",
"offsetInBeginSection": 1066,
"offsetInEndSection": 1296,
"text": "The major goal of this study is to identify peptide/s from the catalytic domain of hPCSK9 that can block the binding of hPCSK9 and LDL-R and therefore can reduce LDL-R degradation leading to the clearance of LDL-C from the plasma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24603306",
"endSection": "abstract",
"offsetInBeginSection": 1112,
"offsetInEndSection": 1324,
"text": "In vitro administration of SRT3025 to cultured AML12 hepatocytes attenuated Pcsk9 secretion and its binding to Ldlr, thereby reducing Pcsk9-mediated Ldlr degradation and increasing Ldlr expression and LDL uptake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26056005",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 246,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9), which involves in low-density lipoprotein cholesterol (LDL-C) metabolism by interacting with the LDL receptor, is considered as a potent therapeutic target for treating hypercholesterolemia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26056005",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 1030,
"text": "Taken together, these results suggested that the IgG1-PA4 can be served as a potential candidate for the treatment of hypercholesterolemia by inhibiting PCSK9-mediated degradation of cell surface LDLRs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26088304",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to the low-density lipoprotein receptor, escorting it to its destruction in the lysosome and thereby preventing the recirculation of the low-density lipoprotein receptor to the hepatocyte cell surface. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26318398",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 447,
"text": "However, statins have low efficiency because they also increase PCSK9 which targets LDLR for degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26364362",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 316,
"text": "Inhibition of the enzyme PCSK9 (proprotein convertase subtilisin/kexin type 9), which is involved in depletion of the LDL-receptor, is a new pharmacologic approach. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26495026",
"endSection": "abstract",
"offsetInBeginSection": 389,
"offsetInEndSection": 510,
"text": "Proprotein convertase subtilisin kexin type 9 (PCSK9) modulates LDL-c through post-translational degradation of the LDLR."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26495026",
"endSection": "abstract",
"offsetInBeginSection": 1656,
"offsetInEndSection": 1837,
"text": "Mechanistically, hepatic S1P KD was shown to decrease the liver and plasma levels of the protein proprotein convertase subtilisin/kexin type 9 (PCSK9), which degrades LDLR protein. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27284008",
"endSection": "abstract",
"offsetInBeginSection": 229,
"offsetInEndSection": 376,
"text": "We report here the development of sdAbs targeting human PCSK9 (proprotein convertase subtilisin/kexin type 9) as an alternative to anti-PCSK9 mAbs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24164109",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "PCSK9 proprotein convertase subtilisin/kexin type (PCSK9) protein plays an important role in LDL cholesterol (LDL-C) metabolism, due to its role in the degradation of the LDL receptor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24094767",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to LDL receptors, leading to their degradation"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Low density lipoprotein binds to proprotein convertase subtilisin/kexin type-9 (PCSK9) in human plasma and inhibits PCSK9-mediated low density lipoprotein receptor degradation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 217,
"text": "Proprotein convertase subtilisin/kexin type-9 (PCSK9) is a secreted protein that binds to the epidermal growth factor-like-A domain of the low density lipoprotein receptor (LDLR) and mediates LDLR degradation in liver"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23141813",
"endSection": "abstract",
"offsetInBeginSection": 86,
"offsetInEndSection": 191,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds LDL receptors, targeting them for degradation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26023080",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 233,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9), which binds the low-density lipoprotein receptor and targets it for degradation, has emerged as an important regulator of serum cholesterol levels and cardiovascular disease risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22683370",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "Secreted proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to the low-density lipoprotein receptor (LDLR) at the cell surface and disrupts the normal recycling of the LDLR"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20716520",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 250,
"text": "Proprotein convertase, subtilisin/kexin type 9 (PCSK9), a key regulator of plasma LDL-cholesterol (LDL-c) and cardiovascular risk, is produced in liver and secreted into plasma where it binds hepatic LDL receptors (LDLR), leading to their degradation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25744035",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes the degradation of the hepatic low-density lipoprotein receptor (LDL-R) and is therefore a prominent therapeutic target for reducing LDL-cholesterol"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20529551",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 862,
"text": "In the present study we scanned the related gene of a clinically diagnosed autosomal genetic hypercholesterolemia family for the possible mutations and established eukaryotic expression vector of mutation of proprotein convertase subtilisin/kexin type 9 (PCSK9) gene with gene recombination technique to investigate the contributions of the variation on low density lipoprotein receptor (LDL-R) metabolism and function alternation.Mutation detection was conducted for LDL-R, apolipoprotein B(100) (apoB(100)) and PCSK9 gene with nucleotide sequencing in a Chinese FH family"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22300679",
"endSection": "abstract",
"offsetInBeginSection": 172,
"offsetInEndSection": 304,
"text": "Proprotein convertase subtilisin-kexin type 9 (PCSK9) provides a key step in LDL metabolism by stimulating LDL receptor degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23261172",
"endSection": "abstract",
"offsetInBeginSection": 176,
"offsetInEndSection": 323,
"text": "The proprotein convertase subtilisin-kexin type 9 (PCSK9) pathway plays a key role in lipoprotein metabolism by promoting LDL-receptor degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21122852",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 237,
"text": "Proprotein convertase subtilisin-kexin type 9 (PCSK9) plays a key role in LDL receptor processing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18436719",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 353,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes the degradation of the LDL receptor (LDLr) in hepatocytes, and its expression in mouse liver has been shown to decrease with fenofibrate treatment.We developed a sandwich ELISA using recombinant human PCSK9 protein and 2 affinity-purified polyclonal antibodies directed against human PCSK9."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25463543",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 413,
"text": "Proprotein convertase subtilisin kexin type 9 (PCSK9) enhances the degradation of the LDLR and modulates liver CD81 levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23106476",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 299,
"text": "Low-density lipoprotein (LDL) metabolism is governed by proprotein convertase subtilisin-kexin type 9 (PCSK9), which down-regulates LDL receptor expression, resulting in higher LDL cholesterol (LDL-C)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17702855",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Proprotein convertase subtilisin kexin type 9 (PCSK9) is gaining attention as a key regulator of serum LDL-cholesterol (LDLC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25649668",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 270,
"text": "The proprotein convertase subtilisin/kexin type 9 (PCSK9) gene regulates cholesterol homoeostasis by accelerating low-density lipoprotein receptor (LDLR) degradation resulting in the decreased catabolism of low-density lipoprotein (LDL) leading to hypercholesterolaemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Low density lipoprotein binds to proprotein convertase subtilisin/kexin type-9 (PCSK9) in human plasma and inhibits PCSK9-mediated low density lipoprotein receptor degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 218,
"text": "Proprotein convertase subtilisin/kexin type-9 (PCSK9) is a secreted protein that binds to the epidermal growth factor-like-A domain of the low density lipoprotein receptor (LDLR) and mediates LDLR degradation in liver."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24685817",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a regulator of LDL-cholesterol receptor homeostasis and emerges as a therapeutic target in the prevention of cardiovascular (CV) disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21497351",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 392,
"text": "The present study was conducted to investigate the role of plasma proprotein convertase subtilisin kexin type 9 (PCSK9) levels, a regulator of LDL-receptor expression, in the occurrence of diabetic dyslipidemia."
}
] | 6
|
BioASQ-training6b
|
[
"http://www.uniprot.org/uniprot/PCSK9_SAIBB",
"http://www.uniprot.org/uniprot/PCSK9_MACMU",
"http://www.uniprot.org/uniprot/PCSK9_PANTR",
"http://www.uniprot.org/uniprot/PCSK9_COLGU",
"http://www.uniprot.org/uniprot/PCSK9_CALJA",
"http://www.uniprot.org/uniprot/PCSK9_LAGLA",
"http://www.uniprot.org/uniprot/PCSK9_SAGLB",
"http://www.uniprot.org/uniprot/PCSK9_HUMAN",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D043484",
"http://www.uniprot.org/uniprot/PCSK9_PONPY",
"http://amigo.geneontology.org/amigo/term/GO:1990666",
"http://www.uniprot.org/uniprot/PCSK9_MACNE",
"http://www.uniprot.org/uniprot/PCSK9_RAT",
"http://www.uniprot.org/uniprot/PCSK9_ATEGE",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000071449",
"http://www.uniprot.org/uniprot/PCSK9_PANPA",
"http://www.uniprot.org/uniprot/PCSK9_PLEMO"
] |
[
{
"o": "PCSK9",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1426592"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A20814698",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1426592"
},
{
"o": "proprotein convertase subtilisin/kexin type 9",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A20814698"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A19343187",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C2611277"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8395721",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0062151"
},
{
"o": "high density lipoprotein receptors",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8395721"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A16773852",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0062151"
},
{
"o": "high density lipoprotein receptors",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16773852"
}
] |
58db9aa28acda34529000018
|
bioasq_yesno
|
yesno
|
Can cardiospheres be produced from skin fibroblasts?
|
['yes']
|
[
"yes"
] |
['Yes, induced cardiospheres (iCS) can be produced by somatic reprogramming of mouse fibroblasts using a panel of pluripotent transcription factors and cardiotrophic growth factors.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29999590"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29999590",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 461,
"text": "Therefore, there is an emerging interest in generating cardiosphere-like stem cells from somatic cells via somatic reprogramming. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29999590",
"endSection": "abstract",
"offsetInBeginSection": 569,
"offsetInEndSection": 805,
"text": "Here we provide the detailed protocol for generating induced cardiospheres (iCS) for cardiac regeneration by somatic reprogramming of mouse fibroblasts using a panel of pluripotent transcription factors and cardiotrophic growth factors."
}
] | 11
|
BioASQ-training11b
| null | null |
5c928afeecadf2e73f000018
|
bioasq_yesno
|
yesno
|
Is a CpG island methylator phenotype involved in ependymomas?
|
['yes']
|
[
"yes"
] |
['Although devoid of recurrent single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype', 'yes', 'Although devoid of recurrent single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype Supratentorial and spinal pediatric ependymomas display a hypermethylated phenotype which includes the loss of tumor suppressor genes involved in the control of cell growth and death.', 'Although devoid of recurrent single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype Although no recurrently mutated genes were found throughout these groups of ependymomas, PFA exhibited a CpG island methylator phenotype, PFB was associated with extensive chromosomal aberrations, and the C11orf95-RELA fusion gene was frequently observed in supratentorial ependymomas. ', 'Supratentorial and spinal pediatric ependymomas display a hypermethylated phenotype which includes the loss of tumor suppressor genes involved in the control of cell growth and death. Although devoid of recurrent single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22109108",
"http://www.ncbi.nlm.nih.gov/pubmed/24553142",
"http://www.ncbi.nlm.nih.gov/pubmed/25182241"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24553142",
"endSection": "abstract",
"offsetInBeginSection": 444,
"offsetInEndSection": 613,
"text": "Although devoid of recurrent single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25182241",
"endSection": "abstract",
"offsetInBeginSection": 309,
"offsetInEndSection": 595,
"text": "Although no recurrently mutated genes were found throughout these groups of ependymomas, PFA exhibited a CpG island methylator phenotype, PFB was associated with extensive chromosomal aberrations, and the C11orf95-RELA fusion gene was frequently observed in supratentorial ependymomas. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22109108",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Supratentorial and spinal pediatric ependymomas display a hypermethylated phenotype which includes the loss of tumor suppressor genes involved in the control of cell growth and death."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22109108",
"endSection": "abstract",
"offsetInBeginSection": 529,
"offsetInEndSection": 739,
"text": "Supratentorial and spinal tumors displayed significantly more hypermethylated genes than posterior fossa tumors, similar to the 'CpG island methylator phenotype' (CIMP) identified in glioma and colon carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22109108",
"endSection": "abstract",
"offsetInBeginSection": 1287,
"offsetInEndSection": 1636,
"text": "The data suggests epigenetic silencing of tumor suppressor genes is an important mechanism in the pathogenesis of supratentorial and spinal, but not posterior fossa ependymomas. Hypermethylation correlated with a decrease in expression of a number of tumor suppressor genes and pathways that could be playing an important role in tumor pathogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24553142",
"endSection": "abstract",
"offsetInBeginSection": 444,
"offsetInEndSection": 614,
"text": "Although devoid of recurrent single nucleotide variants and focal copy number aberrations, poor-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24553142",
"endSection": "abstract",
"offsetInBeginSection": 822,
"offsetInEndSection": 988,
"text": "CpG island methylator phenotype-positive hindbrain ependymomas are responsive to clinical drugs that target either DNA or H3K27 methylation both in vitro and in vivo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24553142",
"endSection": "abstract",
"offsetInBeginSection": 269,
"offsetInEndSection": 443,
"text": "Whole-genome and whole-exome sequencing of 47 hindbrain ependymomas reveals an extremely low mutation rate, and zero significant recurrent somatic single nucleotide variants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25182241",
"endSection": "abstract",
"offsetInBeginSection": 309,
"offsetInEndSection": 594,
"text": "Although no recurrently mutated genes were found throughout these groups of ependymomas, PFA exhibited a CpG island methylator phenotype, PFB was associated with extensive chromosomal aberrations, and the C11orf95-RELA fusion gene was frequently observed in supratentorial ependymomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24553142",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1148,
"text": "ependymomas are common childhood brain tumours that occur throughout the nervous system but are most common in the paediatric hindbrain current standard therapy comprises surgery and radiation but not cytotoxic chemotherapy as it does not further increase survival whole genome and whole exome sequencing of 47 hindbrain ependymomas reveals an extremely low mutation rate and zero significant recurrent somatic single nucleotide variants although devoid of recurrent single nucleotide variants and focal copy number aberrations poor prognosis hindbrain ependymomas exhibit a cpg island methylator phenotype transcriptional silencing driven by cpg methylation converges exclusively on targets of the polycomb repressive complex 2 which represses expression of differentiation genes through trimethylation of h3k27 cpg island methylator phenotype positive hindbrain ependymomas are responsive to clinical drugs that target either dna or h3k27 methylation both in vitro and in vivo we conclude that epigenetic modifiers are the first rational therapeutic candidates for this deadly malignancy which is epigenetically deregulated but genetically bland."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22109108",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "supratentorial and spinal pediatric ependymomas display a hypermethylated phenotype which includes the loss of tumor suppressor genes involved in the control of cell growth and death"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24553142",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "epigenomic alterations define lethal cimp positive ependymomas of infancy"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25182241",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "molecular genetics of ependymomas and pediatric diffuse gliomas a short review"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22109108",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1613,
"text": "epigenetic alterations including methylation have been shown to be an important mechanism of gene silencing in cancer ependymoma has been well characterized at the dna copy number and mrna expression levels however little is known about dna methylation changes to gain a more global view of the methylation profile of ependymoma we conducted an array based analysis our data demonstrated tumors to segregate according to their location in the cns which was associated with a difference in the global level of methylation supratentorial and spinal tumors displayed significantly more hypermethylated genes than posterior fossa tumors similar to the cpg island methylator phenotype cimp identified in glioma and colon carcinoma this hypermethylated profile was associated with an increase in expression of genes encoding for proteins involved in methylating dna suggesting an underlying mechanism an integrated analysis of methylation and mrna expression array data allowed us to identify methylation induced expression changes most notably genes involved in the control of cell growth and death and the immune system were identified including members of the jnk pathway and pparg in conclusion we have generated a global view of the methylation profile of ependymoma the data suggests epigenetic silencing of tumor suppressor genes is an important mechanism in the pathogenesis of supratentorial and spinal but not posterior fossa ependymomas hypermethylation correlated with a decrease in expression of a number of tumor suppressor genes and pathways that could be playing an important role in tumor pathogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25182241",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1347,
"text": "here we review the recent literature on molecular discoveries in ependymomas and pediatric diffuse gliomas ependymomas can now be categorized into three location related subgroups according to their biological profile posterior fossa ependymomas group a pfa and b pfb and supratentorial ependymomas although no recurrently mutated genes were found throughout these groups of ependymomas pfa exhibited a cpg island methylator phenotype pfb was associated with extensive chromosomal aberrations and the c11orf95 rela fusion gene was frequently observed in supratentorial ependymomas meanwhile it has now become apparent that pediatric diffuse gliomas have a distinct genetic status from their adult counterparts even though they share an indistinguishable histology in pediatric low grade diffuse gliomas an intragenic duplication of the portion of fgfr1 encoding the tyrosine kinase domain tkd and rearrangements of myb mybl1 were found recurrently and mutually exclusively as for non brainstem high grade tumors in addition to h3f3a tp53 and atrx mutations which were frequently observed in older children recurrent fusions involving ntrk1 ntrk2 and ntrk3 were reported in infants younger than 3 years of age moreover in diffuse intrinsic pontine gliomas dipg recurrent somatic mutations of acvr1 were found in association with hist1h3b mutations."
}
] | 11
|
BioASQ-training11b
| null | null |
5a86fd5bfaa1ab7d2e00003b
|
bioasq_yesno
|
yesno
|
Has the protein GFP been used in transgenesis for live protein imaging?
|
['yes']
|
[
"yes"
] |
['Yes, the stable transgenesis of genes encoding functional or spatially localized proteins, fused to fluorescent proteins such as green fluorescent protein (GFP) or red fluorescent protein (RFP), is an extremely important research tool in cell and developmental biology.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24312079",
"http://www.ncbi.nlm.nih.gov/pubmed/24297703",
"http://www.ncbi.nlm.nih.gov/pubmed/23480392",
"http://www.ncbi.nlm.nih.gov/pubmed/22700411",
"http://www.ncbi.nlm.nih.gov/pubmed/22551423",
"http://www.ncbi.nlm.nih.gov/pubmed/22497513",
"http://www.ncbi.nlm.nih.gov/pubmed/22493255",
"http://www.ncbi.nlm.nih.gov/pubmed/22173943",
"http://www.ncbi.nlm.nih.gov/pubmed/21708138",
"http://www.ncbi.nlm.nih.gov/pubmed/21490567",
"http://www.ncbi.nlm.nih.gov/pubmed/21406720",
"http://www.ncbi.nlm.nih.gov/pubmed/21316751",
"http://www.ncbi.nlm.nih.gov/pubmed/21248708",
"http://www.ncbi.nlm.nih.gov/pubmed/20378924",
"http://www.ncbi.nlm.nih.gov/pubmed/20226563",
"http://www.ncbi.nlm.nih.gov/pubmed/20085825",
"http://www.ncbi.nlm.nih.gov/pubmed/19688097",
"http://www.ncbi.nlm.nih.gov/pubmed/19549299",
"http://www.ncbi.nlm.nih.gov/pubmed/19087237"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24312079",
"endSection": "abstract",
"offsetInBeginSection": 423,
"offsetInEndSection": 638,
"text": "we review recent advancement in the functional studies of the three different GnRH neuron systems, mainly focusing on the electrophysiological analysis of the GnRH-green fluorescent protein (GFP) transgenic animals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24297703",
"endSection": "abstract",
"offsetInBeginSection": 636,
"offsetInEndSection": 681,
"text": "founders were found to be transgenic for GFP."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24297703",
"endSection": "abstract",
"offsetInBeginSection": 845,
"offsetInEndSection": 906,
"text": "GFP expression was detected in a wide range of murine tissues"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23480392",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Transgenic Xenopus laevis for live imaging in cell and developmental biology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23480392",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 264,
"text": "The stable transgenesis of genes encoding functional or spatially localized proteins, fused to fluorescent proteins such as green fluorescent protein (GFP) or red fluorescent protein (RFP), is an extremely important research tool in cell and developmental biology."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22700411",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "GFP-transgenic animals for in vivo imaging: rats, rabbits, and pigs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22700411",
"endSection": "abstract",
"offsetInBeginSection": 482,
"offsetInEndSection": 627,
"text": "We have further extended the techniques of genetic engineering to rats, rabbits, and pigs, and have created corresponding GFP-transgenic animals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22551423",
"endSection": "abstract",
"offsetInBeginSection": 1473,
"offsetInEndSection": 1661,
"text": "The results revealed that the 3.6-GFP transgenic animals provide a unique model for direct analysis of cellular and molecular mechanisms of pulp repair and tertiary dentinogenesis in vivo."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22497513",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Long-term effects of PERV-specific RNA interference in transgenic pigs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22497513",
"endSection": "abstract",
"offsetInBeginSection": 1204,
"offsetInEndSection": 1319,
"text": "green fluorescent protein (GFP) as reporter of the vector system were consistently expressed in transgenic animals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22493255",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "The ability to specify the expression levels of exogenous genes inserted in the genomes of transgenic animals is critical for the success of a wide variety of experimental manipulations. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22173943",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Welfare assessment in transgenic pigs expressing green fluorescent protein (GFP)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22173943",
"endSection": "abstract",
"offsetInBeginSection": 552,
"offsetInEndSection": 654,
"text": "transgenic animals expressing GFP with wildtype animals along various stages of post natal development"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21708138",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "Production of transgenic chickens expressing a tetracycline-inducible GFP gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21490567",
"endSection": "abstract",
"offsetInBeginSection": 1021,
"offsetInEndSection": 1116,
"text": "transgenic animals can be readily created to express fluorescently tagged proteins or reporters"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21406720",
"endSection": "abstract",
"offsetInBeginSection": 1342,
"offsetInEndSection": 1487,
"text": "These findings suggest that mhc2dab:GFP and cd45:DsRed transgenic lines will be instrumental in elucidating the immune response in the zebrafish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21316751",
"endSection": "abstract",
"offsetInBeginSection": 912,
"offsetInEndSection": 996,
"text": "f 33 mice born, 28 (81%) carried the transgene DNA and 15 (55.5%) were GFP-positive."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21316751",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Lentiviral vectors containing the green fluorescent protein gene have been successfully used to select transgenic embryos before transfer to a surrogate mother"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21248708",
"endSection": "abstract",
"offsetInBeginSection": 306,
"offsetInEndSection": 476,
"text": "Typically transgenes are generated by placing a promoter upstream of a GFP reporter gene or cDNA of interest, and this often produces a representative expression pattern."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20378924",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Survival and immunogenicity of mesenchymal stem cells from the green fluorescent protein transgenic rat in the adult rat brain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20378924",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 309,
"text": "This problem has been lessened by the availability of transgenic animals that express \"reporter\" genes, such as green fluorescent protein (GFP)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20226563",
"endSection": "abstract",
"offsetInBeginSection": 133,
"offsetInEndSection": 203,
"text": " full-length GFP fusion proteins was examined, in transgenic animals, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20085825",
"endSection": "abstract",
"offsetInBeginSection": 664,
"offsetInEndSection": 734,
"text": "Two stable transgenic lines express GFP prior to hair-bundle formation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19688097",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 579,
"text": "we generated two transgenic pigs by somatic cell nuclear transfer (SCNT) that express green fluorescent protein (GFP) driven by cytomegalovirus (CMV)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19549299",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 140,
"text": "Fluorescent proteins such as the green fluorescent protein (GFP) have widely been used in transgenic animals as reporter genes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19087237",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 137,
"text": "Green Fluorescent Protein (GFP) is used extensively as a reporter for transgene expression in Drosophila and other organisms."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D030801",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019076",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000818",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D030781",
"http://www.uniprot.org/uniprot/GFP_AEQVI"
] |
[] |
5523e8cc7b523f2123000007
|
bioasq_yesno
|
yesno
|
Is ABCE1 involved in ribosomal recycling?
|
['yes']
|
[
"yes"
] |
['Yes, recent studies have identified ABCE1 as a ribosome-recycling factor important for translation termination in mammalian cells, yeast and also archaea']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27824037",
"http://www.ncbi.nlm.nih.gov/pubmed/26276635",
"http://www.ncbi.nlm.nih.gov/pubmed/25001285",
"http://www.ncbi.nlm.nih.gov/pubmed/25659154",
"http://www.ncbi.nlm.nih.gov/pubmed/25128630"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27824037",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Ribosome recycling orchestrated by the ATP binding cassette (ABC) protein ABCE1 can be considered as the final-or the first-step within the cyclic process of protein synthesis, connecting translation termination and mRNA surveillance with re-initiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25659154",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 260,
"text": " Recent studies have identified ABCE1 as a ribosome-recycling factor important for translation termination in mammalian cells, yeast and also archaea."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25001285",
"endSection": "abstract",
"offsetInBeginSection": 502,
"offsetInEndSection": 560,
"text": "d a termination/prerecycling complex containing eRF1-ABCE1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25128630",
"endSection": "abstract",
"offsetInBeginSection": 653,
"offsetInEndSection": 698,
"text": "ABCE1, a eukaryotic ribosome recycling factor"
}
] | 6
|
BioASQ-training6b
| null | null |
58ce5a1602b8c60953000049
|
bioasq_yesno
|
factoid
|
What is the suggested therapy for Mycobacterium avium infection?
|
[['Rifampin 10 mg/kg daily, ciprofloxacin 500 mg twice daily, clofazimine 100 mg every day, and ethambutol 15 mg/kg orally daily for 24 weeks, with or without amikacin 10 mg/kg intravenously or intramuscularly 5 days weekly for the first 4 weeks']]
|
[
"Rifampin",
"Rifampicin",
"Ciprofloxacin",
"Clofazimine",
"Ethambutol",
"Amikacin"
] |
['The activity of TLC G-65 (a liposomal gentamicin preparation), alone and in combination with rifapentine, clarithromycin, clofazimine and ethambutol, was evaluated in the beige mouse (C57BL/6J--bgj/bgj) model of disseminated Mycobacterium avium infection. TLC G-65 in combination with rifapentine appears to be an attractive regimen for the treatment of infections caused by bacteria in the M. avium complex. Rifampin 10 mg/kg daily, ciprofloxacin 500 mg twice daily, clofazimine 100 mg every day, and ethambutol 15 mg/kg orally daily for 24 weeks, with or without amikacin 10 mg/kg intravenously or intramuscularly 5 days weekly for the first 4 weeks. In vivo phage treatment may also be used in some cases.', 'The activity of TLC G-65 (a liposomal gentamicin preparation), alone and in combination with rifapentine, clarithromycin, clofazimine and ethambutol, was evaluated in the beige mouse (C57BL/6J--bgj/bgj) model of disseminated Mycobacterium avium infection', 'The activity of TLC G-65 (a liposomal gentamicin preparation), alone and in combination with rifapentine, clarithromycin, clofazimine and ethambutol, was evaluated in the beige mouse (C57BL/6J--bgj/bgj) model of disseminated Mycobacterium avium infection', 'The activity of TLC G-65 (a liposomal gentamicin preparation), alone and in combination with rifapentine, clarithromycin, clofazimine and ethambutol, was evaluated in the beige mouse (C57BL/6J--bgj/bgj) model of disseminated Mycobacterium avium infection', 'The activity of TLC G-65 (a liposomal gentamicin preparation), alone and in combination with rifapentine, clarithromycin, clofazimine and ethambutol, was evaluated in the beige mouse (C57BL/6J--bgj/bgj) model of disseminated Mycobacterium avium infection', 'The activity of TLC G-65 (a liposomal gentamicin preparation), alone and in combination with rifapentine, clarithromycin, clofazimine and ethambutol, was evaluated in the beige mouse (C57BL/6J--bgj/bgj) model of disseminated Mycobacterium avium infection']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/16584300",
"http://www.ncbi.nlm.nih.gov/pubmed/9875582",
"http://www.ncbi.nlm.nih.gov/pubmed/1387133",
"http://www.ncbi.nlm.nih.gov/pubmed/1832527",
"http://www.ncbi.nlm.nih.gov/pubmed/10714126",
"http://www.ncbi.nlm.nih.gov/pubmed/11073759",
"http://www.ncbi.nlm.nih.gov/pubmed/19929882",
"http://www.ncbi.nlm.nih.gov/pubmed/8733409"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1387133",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "The activity of TLC G-65 (a liposomal gentamicin preparation), alone and in combination with rifapentine, clarithromycin, clofazimine and ethambutol, was evaluated in the beige mouse (C57BL/6J--bgj/bgj) model of disseminated Mycobacterium avium infection"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1387133",
"endSection": "abstract",
"offsetInBeginSection": 728,
"offsetInEndSection": 880,
"text": "TLC G-65 in combination with rifapentine appears to be an attractive regimen for the treatment of infections caused by bacteria in the M. avium complex."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9875582",
"endSection": "abstract",
"offsetInBeginSection": 379,
"offsetInEndSection": 621,
"text": "Rifampin 10 mg/kg daily, ciprofloxacin 500 mg twice daily, clofazimine 100 mg every day, and ethambutol 15 mg/kg orally daily for 24 weeks, with or without amikacin 10 mg/kg intravenously or intramuscularly 5 days weekly for the first 4 weeks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16584300",
"endSection": "abstract",
"offsetInBeginSection": 266,
"offsetInEndSection": 493,
"text": "TM4 is a lytic mycobacteriophage that kills both extracellular M. avium and M. tuberculosis. When delivered by M. smegmatis transiently infected with TM4, it kills both M. avium and M. tuberculosis within RAW 264.7 macrophages."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714126",
"endSection": "abstract",
"offsetInBeginSection": 753,
"offsetInEndSection": 898,
"text": "The patient was commenced on a 3-drug regimen with rifabutin, ethambutol and clarithromycin and has remained asymptomatic now for over 9 months. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714126",
"endSection": "abstract",
"offsetInBeginSection": 753,
"offsetInEndSection": 898,
"text": "The patient was commenced on a 3-drug regimen with rifabutin, ethambutol and clarithromycin and has remained asymptomatic now for over 9 months. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714126",
"endSection": "abstract",
"offsetInBeginSection": 753,
"offsetInEndSection": 898,
"text": "The patient was commenced on a 3-drug regimen with rifabutin, ethambutol and clarithromycin and has remained asymptomatic now for over 9 months. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11073759",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "A randomized, double-blind trial comparing azithromycin and clarithromycin in the treatment of disseminated Mycobacterium avium infection in patients with human immunodeficiency virus."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1832527",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Activity of clarithromycin against Mycobacterium avium infection in patients with the acquired immune deficiency syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714126",
"endSection": "abstract",
"offsetInBeginSection": 753,
"offsetInEndSection": 898,
"text": "The patient was commenced on a 3-drug regimen with rifabutin, ethambutol and clarithromycin and has remained asymptomatic now for over 9 months. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19929882",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Evolution was favorable with multiple-drug therapy including rifampicin, ethambutol, and clarithromycin, along with a slight reduction in immunosuppression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8733409",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "The turning point in antimicrobial therapy of Mycobacterium avium infections came with the development of two new macrolides, clarithromycin and azithromycin."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8733409",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Clarithromycin against Mycobacterium avium complex infections."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8733409",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "The turning point in antimicrobial therapy of Mycobacterium avium infections came with the development of two new macrolides, clarithromycin and azithromycin."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8733409",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Clarithromycin against Mycobacterium avium complex infections."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8733409",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "The turning point in antimicrobial therapy of Mycobacterium avium infections came with the development of two new macrolides, clarithromycin and azithromycin."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8733409",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Clarithromycin against Mycobacterium avium complex infections."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8733409",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "The turning point in antimicrobial therapy of Mycobacterium avium infections came with the development of two new macrolides, clarithromycin and azithromycin."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
5710ade4cf1c32585100002c
|
bioasq_factoid
|
yesno
|
Is tebentafusp effective for uveal melanoma?
|
['yes']
|
[
"yes"
] |
['Yes. Tebentafusp effective for uveal melanoma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34999237",
"http://www.ncbi.nlm.nih.gov/pubmed/35364557",
"http://www.ncbi.nlm.nih.gov/pubmed/35364798"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35364798",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Tebentafusp (tebentafusp-tebn; Kimmtrak®) is a first-in-class, bispecific gp100 peptide-HLA-A*02:01 directed T cell receptor (TCR) CD3 T cell engager being developed by Immunocore for the treatment of uveal melanoma and malignant melanoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35364798",
"endSection": "abstract",
"offsetInBeginSection": 1018,
"offsetInEndSection": 1168,
"text": "This article summarizes the milestones in the development of tebentafusp leading to this first approval for unresectable or metastatic uveal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35364557",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 425,
"text": "Tebentafusp was granted full approval on January 25th 2022 in the setting of HLA-A*02:01-positive adult patients with unresectable or metastatic uveal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34999237",
"endSection": "abstract",
"offsetInBeginSection": 1757,
"offsetInEndSection": 2188,
"text": "In a large meta-analysis, surgical treatment was associated with 6 months longer median overall survival as compared to conventional chemotherapy and, recently, tebentafusp as first-line treatment at the first interim analysis of a randomized phase III trial likewise provided a 6 months longer median overall survival compared to investigator's choice, mostly pembrolizumab; these treatments currently apply to selected patients. "
}
] | 12
|
BioASQ-training12b
| null | null |
64041f38201352f04a00001f
|
bioasq_yesno
|
yesno
|
Is c-met involved in the activation of the Akt pathway?
|
['yes']
|
[
"yes"
] |
HGF-induced activation of c-Met is playing a pivotal role in the stimulation of c-Src activation, resulting in induction of phosphatidylinositol 3-kinase complexes p85α/p110α and p85α/p110δ, which is required for Akt-mediated activation of mammalian target of rapamycin, with consequent inhibition of IκB kinase and nuclear factor-κB activation, resulting in enhanced cell survival.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23345546",
"http://www.ncbi.nlm.nih.gov/pubmed/23229794",
"http://www.ncbi.nlm.nih.gov/pubmed/22820099",
"http://www.ncbi.nlm.nih.gov/pubmed/22789825",
"http://www.ncbi.nlm.nih.gov/pubmed/21687953",
"http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"http://www.ncbi.nlm.nih.gov/pubmed/20233866",
"http://www.ncbi.nlm.nih.gov/pubmed/19850646",
"http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"http://www.ncbi.nlm.nih.gov/pubmed/18234991",
"http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"http://www.ncbi.nlm.nih.gov/pubmed/17464994",
"http://www.ncbi.nlm.nih.gov/pubmed/17258200",
"http://www.ncbi.nlm.nih.gov/pubmed/16278380",
"http://www.ncbi.nlm.nih.gov/pubmed/15522281",
"http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"http://www.ncbi.nlm.nih.gov/pubmed/11821397",
"http://www.ncbi.nlm.nih.gov/pubmed/10714768"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23345546",
"endSection": "abstract",
"offsetInBeginSection": 421,
"offsetInEndSection": 726,
"text": "Amplification of MET has been reported in approximately 5%-22% of lung tumors with acquired resistance to small-molecule inhibitors of the epidermal growth factor receptor (EGFR). Resistance to EGFR inhibitors is likely mediated through downstream activation of the phosphoinositide 3-kinase /AKT pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23345546",
"endSection": "abstract",
"offsetInBeginSection": 727,
"offsetInEndSection": 965,
"text": "Simultaneous treatment of resistant tumors with a MET inhibitor plus an EGFR inhibitor can abrogate activation of downstream effectors of cell growth, proliferation, and survival, thereby overcoming acquired resistance to EGFR inhibitors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23229794",
"endSection": "abstract",
"offsetInBeginSection": 839,
"offsetInEndSection": 885,
"text": "HGF mediated both ERK and Akt phosphorylation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23229794",
"endSection": "abstract",
"offsetInBeginSection": 1263,
"offsetInEndSection": 1360,
"text": "ERK/Akt signaling, but not the Smad pathway, may be one of the main processes in HGF-induced EMT,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23229794",
"endSection": "abstract",
"offsetInBeginSection": 1442,
"offsetInEndSection": 1503,
"text": "The MAPK/Akt pathway is indispensable in HGF/c-Met signaling."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820099",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Inhibition of c-Met activation sensitizes osteosarcoma cells to cisplatin via suppression of the PI3K-Akt signaling"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820099",
"endSection": "abstract",
"offsetInBeginSection": 933,
"offsetInEndSection": 1083,
"text": "Specifically, we demonstrated that inhibition of c-Met activity led to suppression of the PI3K-Akt pathway, thus enhancing cisplatin chemosensitivity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820099",
"endSection": "abstract",
"offsetInBeginSection": 1084,
"offsetInEndSection": 1245,
"text": "Our study clearly suggests that inhibition of c-Met activity can effectively sensitize osteosarcoma cells to cisplatin via suppression of the PI3K-Akt signaling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22789825",
"endSection": "abstract",
"offsetInBeginSection": 604,
"offsetInEndSection": 806,
"text": "We found that a dual Met/VEGF receptor 2 kinase inhibitor, E7050, circumvented HGF-induced EGFR-TKI resistance in EGFR mutant lung cancer cell lines by inhibiting the Met/Gab1/PI3K/Akt pathway in vitro."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21687953",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 728,
"text": "Here, we report that i) treatment of RL95-2 cells with HGF resulted in phosphorylation of the HGF receptor c-Met, activation of Akt and IκB, translocation of NF-κB into the nucleus, and up-regulation of COX-2 mRNA;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21687953",
"endSection": "abstract",
"offsetInBeginSection": 1062,
"offsetInEndSection": 1205,
"text": "Our data suggest that HGF possesses chemotactic ability, has anti-apoptosis action, and induces cellular infiltration via the PI3K/Akt pathway;"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Hepatocyte growth factor-induced c-Src-phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin pathway inhibits dendritic cell activation by blocking IκB kinase activity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"endSection": "abstract",
"offsetInBeginSection": 715,
"offsetInEndSection": 938,
"text": "Activation of c-Src in turn establishes a complex consisting of phosphatidylinositol 3-kinase and c-MET, and promotes downstream activation of the phosphatidylinositol 3-kinase/AKT pathway and mammalian target of rapamycin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"endSection": "abstract",
"offsetInBeginSection": 1150,
"offsetInEndSection": 1443,
"text": "Notably, hepatocyte growth factor-stimulated c-Src activation results in induction of phosphatidylinositol 3-kinase complexes p85α/p110α and p85α/p110δ, which is required for activation of mammalian target of rapamycin, and consequent inhibition of IκB kinase and nuclear factor-κB activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"endSection": "abstract",
"offsetInBeginSection": 1444,
"offsetInEndSection": 1735,
"text": "Our findings, for the first time, have identified the c-Src-phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin pathway that plays a pivotal role in mediating the inhibitory effects of hepatocyte growth factor on dendritic cell activation by blocking nuclear factor-κB signaling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20233866",
"endSection": "abstract",
"offsetInBeginSection": 1280,
"offsetInEndSection": 1487,
"text": "Cyr61 siRNA inhibited a second phase of Akt phosphorylation measured 12 hours after cell stimulation with HGF and also inhibited HGF-induced phosphorylation of the Akt target glycogen synthase kinase 3alpha."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19850646",
"endSection": "abstract",
"offsetInBeginSection": 1342,
"offsetInEndSection": 1594,
"text": "HGF+EGF treatment increased the duration of ERK1/2 and AKT activation compared to HGF or EGF alone. All these data indicate that a crosstalk between the EGF and HGF pathways in mammary epithelial cells may modulate the development of the mammary gland."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Hepatocyte growth factor and c-Met promote dendritic maturation during hippocampal neuron differentiation via the Akt pathway"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "abstract",
"offsetInBeginSection": 758,
"offsetInEndSection": 1053,
"text": "Consistent with these results, HGF activated Akt, which phosphorylates glycogen synthase kinase-3beta (GSK-3beta) to inactivate it, and reduced phosphorylation of microtubule-associated protein 2 (MAP2), which can promote microtubule polymerization and dendrite elongation when dephosphorylated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "abstract",
"offsetInBeginSection": 1054,
"offsetInEndSection": 1374,
"text": "Conversely, pharmacological inhibition of c-Met with its specific inhibitor, PHA-665752, or genetic knock-down of c-Met with short hairpin RNAs (shRNAs) suppressed HGF-induced phosphorylation of Akt and GSK-3beta, increased phosphorylation of MAP2, and reduced dendrite number and length in cultured hippocampal neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "abstract",
"offsetInBeginSection": 1458,
"offsetInEndSection": 1699,
"text": "Inhibiting Akt activity with the phosphoinositide-3-kinase inhibitor LY294002 or Akt inhibitor X suppressed HGF-induced phosphorylation of GSK-3beta, increased MAP2 phosphorylation, and blocked the ability of HGF to enhance dendritic length."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "abstract",
"offsetInBeginSection": 1700,
"offsetInEndSection": 1844,
"text": "These observations indicate that HGF and c-Met can regulate the early stages of dendrite maturation via activation of the Akt/GSK-3beta pathway."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18234991",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Involvement of PI3K/Akt signaling pathway in hepatocyte growth factor-induced migration of uveal melanoma cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18234991",
"endSection": "abstract",
"offsetInBeginSection": 1031,
"offsetInEndSection": 1415,
"text": "HGF was found to enhance cell migration, and that HGF-induced migration depends on PI3K/Akt pathway. The activation of PI3K/Akt pathway induced by the HGF/c-Met axis is involved in the downregulation of cell adhesion molecules E-cadherin and beta-catenin, contributing to the attenuation of cell-cell adhesion and promoting the enhanced motility and migration of uveal melanoma cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "HGF protects cultured cortical neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and PI-3K/Akt pathways"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"endSection": "abstract",
"offsetInBeginSection": 462,
"offsetInEndSection": 528,
"text": "HGF stimulated both ERK1/2 and Akt activities in cortical neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"endSection": "abstract",
"offsetInBeginSection": 529,
"offsetInEndSection": 718,
"text": "Inhibition of ERK activation completely abolished the protective effects of HGF, and inhibition of Akt activation reduced, but did not completely eliminate the HGF mediated neuroprotection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"endSection": "abstract",
"offsetInBeginSection": 719,
"offsetInEndSection": 837,
"text": "It is suggested that the neuroprotection of HGF depend on ERK1/2 pathway, and, to a lesser extent, PI-3K/Akt pathway. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17464994",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Met signals hepatocyte survival by preventing Fas-triggered FLIP degradation in a PI3k-Akt-dependent manner"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17464994",
"endSection": "abstract",
"offsetInBeginSection": 1318,
"offsetInEndSection": 1488,
"text": "Thus, Met acting on PI3K and Akt ensures high levels of FLIPL, and disruption of this pathway contributes to hepatic apoptosis and possibly to Fas-related liver diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17258200",
"endSection": "abstract",
"offsetInBeginSection": 744,
"offsetInEndSection": 990,
"text": "The HGF-induced increase in Nkx 2.5 expression was inhibited by co-treatment with the PI3 kinase inhibitors Wortmannin and LY294002, but not by its inactive homolog LY303511, suggesting an involvement of the PI3 kinase/Akt pathway in this effect."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16278380",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "X-Linked inhibitor of apoptosis protein expression level in colorectal cancer is regulated by hepatocyte growth factor/C-met pathway via Akt signaling"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16278380",
"endSection": "abstract",
"offsetInBeginSection": 1263,
"offsetInEndSection": 1347,
"text": "Activation of XIAP expression by HGF was inhibited by siRNA targeting Akt1 and Akt2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16278380",
"endSection": "abstract",
"offsetInBeginSection": 1361,
"offsetInEndSection": 1419,
"text": "Activation of C-MET enhances XIAP through the Akt pathway."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15522281",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Hepatocyte growth factor prevents ventricular remodeling and dysfunction in mice via Akt pathway and angiogenesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15522281",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1331,
"text": "A significant reduction in apoptosis in the HGF-treated hearts was observed compared with control hearts, and was strongly associated with increased Akt activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15522281",
"endSection": "abstract",
"offsetInBeginSection": 1461,
"offsetInEndSection": 1546,
"text": "The antiapoptotic effect of HGF was mediated by activation of PI3-kinase/Akt pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 874,
"text": "The protective effect of HGF/SF against the ADR-induced apoptosis was abolished in the presence of either LY294002, an inhibitor of phosphatidylinositol-3'-OH kinase (PI3-K) or 1L-6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate, an inhibitor of Akt, thus implicating the activation of PI3-K-Akt signaling in the antiapoptotic action of HGF/SF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"endSection": "abstract",
"offsetInBeginSection": 875,
"offsetInEndSection": 985,
"text": "Immunoblotting analysis revealed that HGF/SF stimulated the sustained phosphorylation of Akt for several hours"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"endSection": "abstract",
"offsetInBeginSection": 1048,
"offsetInEndSection": 1185,
"text": "Furthermore, ADR-induced activation of caspase-9, a downstream molecule of Akt, was inhibited for at least 24 h after HGF/SF stimulation,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"endSection": "abstract",
"offsetInBeginSection": 1479,
"offsetInEndSection": 1656,
"text": "These results indicate that HGF/SF, but not EGF, transmitted protective signals against ADR-induced apoptosis by causing sustained activation of the PI3-K-Akt signaling pathway."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11821397",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Hepatocyte growth factor/scatter factor inhibits UVB-induced apoptosis of human keratinocytes but not of keratinocyte-derived cell lines via the phosphatidylinositol 3-kinase/AKT pathway"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11821397",
"endSection": "abstract",
"offsetInBeginSection": 349,
"offsetInEndSection": 575,
"text": "When we analyzed the signaling pathways initiated by the HGF/SF receptor c-met, we found that the phosphatidylinositol (PI) 3-kinase and its downstream-element AKT and the mitogen-activated protein (MAP) kinase were activated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11821397",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 728,
"text": "Inhibition of PI 3-kinase led to a complete abrogation of the anti-apoptotic effect of HGF/SF, whereas blockade of the MAP kinase pathway had no effect."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714768",
"endSection": "abstract",
"offsetInBeginSection": 1261,
"offsetInEndSection": 1411,
"text": "We now show in detached cells a cooperative effect of HGF and FN in the activation of PI 3-kinase and on the phosphorylation of PKB/Akt at serine 473."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714768",
"endSection": "abstract",
"offsetInBeginSection": 1412,
"offsetInEndSection": 1554,
"text": "PI 3-kinase activity is also required for the HGF- and fibronectin-induced survival responses, as well as anchorage-independent colony growth."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714768",
"endSection": "abstract",
"offsetInBeginSection": 1645,
"offsetInEndSection": 1964,
"text": "Together, these results demonstrate that the PI 3-kinase/Akt pathway is a key effector of the HGF- and fibronectin-induced survival response of breast carcinoma cells under detached conditions and corroborate an interaction between integrin and HGF/ Met signalling pathways in the development of invasive breast cancer."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051057",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019859",
"http://www.uniprot.org/uniprot/SLTM_HUMAN",
"http://www.uniprot.org/uniprot/AKT1_HUMAN",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0043491",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0048012",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0051896"
] |
[] |
5318a955b166e2b806000020
|
bioasq_yesno
|
factoid
|
Where in the cell do we find the protein Cep135?
|
['centrosome']
|
[
"centrosome",
"microtubule organizing center",
"MTOC",
"centrosomal complex"
] |
['centrosome']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23456457",
"http://www.ncbi.nlm.nih.gov/pubmed/23213374",
"http://www.ncbi.nlm.nih.gov/pubmed/23115304",
"http://www.ncbi.nlm.nih.gov/pubmed/22976301",
"http://www.ncbi.nlm.nih.gov/pubmed/22898782",
"http://www.ncbi.nlm.nih.gov/pubmed/22521416",
"http://www.ncbi.nlm.nih.gov/pubmed/22261722",
"http://www.ncbi.nlm.nih.gov/pubmed/21766470",
"http://www.ncbi.nlm.nih.gov/pubmed/20392737",
"http://www.ncbi.nlm.nih.gov/pubmed/19454482",
"http://www.ncbi.nlm.nih.gov/pubmed/19321663",
"http://www.ncbi.nlm.nih.gov/pubmed/19293139",
"http://www.ncbi.nlm.nih.gov/pubmed/18851962",
"http://www.ncbi.nlm.nih.gov/pubmed/17681131",
"http://www.ncbi.nlm.nih.gov/pubmed/16240430",
"http://www.ncbi.nlm.nih.gov/pubmed/14983524",
"http://www.ncbi.nlm.nih.gov/pubmed/11781336",
"http://www.ncbi.nlm.nih.gov/pubmed/10842375"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23456457",
"endSection": "sections.0",
"offsetInBeginSection": 163,
"offsetInEndSection": 219,
"text": "CEP family protein is the active component of centrosome"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22976301",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "Cep135/Bld10 is a conserved centriolar protein required for the formation of the central cartwheel, an early intermediate in centriole assembly."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22976301",
"endSection": "sections.0",
"offsetInBeginSection": 939,
"offsetInEndSection": 1157,
"text": "Thus, in flies, Cep135/Bld10 is not essential for cartwheel assembly or for establishing the ninefold symmetry of centrioles; rather, it appears to stabilize the connection between inner and outer centriole components."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14983524",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Cep135 is a 135-kDa, coiled-coil centrosome protein important for microtubule organization in mammalian cells"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22521416",
"endSection": "sections.0",
"offsetInBeginSection": 634,
"offsetInEndSection": 670,
"text": "135 kDa centrosomal protein (CEP135)"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18851962",
"endSection": "sections.0",
"offsetInBeginSection": 301,
"offsetInEndSection": 415,
"text": "In the present study, we investigated a novel interaction between CEP135 and C-NAP1, two core centriolar proteins."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19321663",
"endSection": "sections.0",
"offsetInBeginSection": 350,
"offsetInEndSection": 520,
"text": "Drosophila Bld10, the ortholog of Chlamydomonas reinhardtii Bld10p and human Cep135, is a ubiquitous centriolar protein that also localizes to the spermatid basal body. M"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22898782",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "BLD10/CEP135 is a microtubule-associated protein that controls the formation of the flagellum central microtubule pair."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20392737",
"endSection": "sections.0",
"offsetInBeginSection": 683,
"offsetInEndSection": 877,
"text": "We found an evolutionarily cohesive and ancestral module, which we term UNIMOD and is defined by three components (SAS6, SAS4/CPAP and BLD10/CEP135), that correlates with the occurrence of CBBs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22261722",
"endSection": "sections.0",
"offsetInBeginSection": 717,
"offsetInEndSection": 783,
"text": "pericentriolar material proteins including pericentrin and CEP135."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17681131",
"endSection": "sections.0",
"offsetInBeginSection": 690,
"offsetInEndSection": 802,
"text": "hereas Cep135 and CPAP formed a core structure within the proximal lumen of both parental and nascent centrioles"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21766470",
"endSection": "sections.0",
"offsetInBeginSection": 960,
"offsetInEndSection": 1016,
"text": ". Centrosome components, including γ-tubulin and Cep135,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10842375",
"endSection": "sections.0",
"offsetInBeginSection": 257,
"offsetInEndSection": 324,
"text": "suggesting that Cep135 is a structural component of the centrosome."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/CP135_HUMAN"
] | null |
51596a8ad24251bc0500009e
|
bioasq_factoid
|
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