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4.35k
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|---|---|---|---|---|---|---|---|---|---|---|---|---|
yesno
|
Is lenvatinib effective for thyroid cancer?
|
['yes']
|
[
"yes"
] |
['Yes, lenvatinib is effective for thyroid cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25974026",
"http://www.ncbi.nlm.nih.gov/pubmed/26105190",
"http://www.ncbi.nlm.nih.gov/pubmed/25913680",
"http://www.ncbi.nlm.nih.gov/pubmed/26316818",
"http://www.ncbi.nlm.nih.gov/pubmed/25553081",
"http://www.ncbi.nlm.nih.gov/pubmed/25671254"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25974026",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "New insights in the treatment of radioiodine refractory differentiated thyroid carcinomas: to lenvatinib and beyond."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25974026",
"endSection": "abstract",
"offsetInBeginSection": 1130,
"offsetInEndSection": 1377,
"text": "However, even more impressive responses and progression-free survival benefits were seen in the phase III SELECT trial with lenvatinib, giving even higher hopes for the future management of what was considered just a decade ago an orphan disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26105190",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 741,
"text": "Sorafenib and lenvatinib, small-molecule multikinase inhibitors, were approved for the treatment of progressive, symptomatic, radioactive iodine refractory, advanced differentiated thyroid cancer in 2013 and 2015, respectively."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25913680",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "A phase 2 trial of lenvatinib (E7080) in advanced, progressive, radioiodine-refractory, differentiated thyroid cancer: A clinical outcomes and biomarker assessment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25913680",
"endSection": "abstract",
"offsetInBeginSection": 1811,
"offsetInEndSection": 2021,
"text": "CONCLUSIONS: In patients with and without prior exposure to VEGF therapy, the encouraging response rates, median time to response, and PFS for lenvatinib have prompted further investigation in a phase 3 trial. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26316818",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 488,
"text": "Since 2011, four multikinase inhibitors (MKIs) have been approved by the US Food and Drug Administration for thyroid cancer - cabozantinib and vandetanib for medullary thyroid cancer and sorafenib and lenvatinib for differentiated thyroid cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25553081",
"endSection": "abstract",
"offsetInBeginSection": 690,
"offsetInEndSection": 970,
"text": "Moreover, four of those investigational drugs, vandetanib, cabozantinib, sorafenib and lenvatinib, have reached a phase III clinical trial with favorable results in progression-free survival and overall survival in medullary thyroid carcinoma and differentiated thyroid carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26316818",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 486,
"text": "Since 2011, four multikinase inhibitors (MKIs) have been approved by the US Food and Drug Administration for thyroid cancer - cabozantinib and vandetanib for medullary thyroid cancer and sorafenib and lenvatinib for differentiated thyroid cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25671254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 654,
"text": "BACKGROUND: Lenvatinib, an oral inhibitor of vascular endothelial growth factor receptors 1, 2, and 3, fibroblast growth factor receptors 1 through 4, platelet-derived growth factor receptor �, RET, and KIT, showed clinical activity in a phase 2 study involving patients with differentiated thyroid cancer that was refractory to radioiodine (iodine-131).METHODS: In our phase 3, randomized, double-blind, multicenter study involving patients with progressive thyroid cancer that was refractory to iodine-131, we randomly assigned 261 patients to receive lenvatinib (at a daily dose of 24 mg per day in 28-day cycles) and 131 patients to receive placebo. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25913680",
"endSection": "abstract",
"offsetInBeginSection": 421,
"offsetInEndSection": 803,
"text": "Positive phase 1 results in solid tumors prompted a phase 2 trial in patients with advanced, radioiodine-refractory, differentiated thyroid cancer (RR-DTC).METHODS: Fifty-eight patients with RR-DTC who had disease progression during the previous 12 months received lenvatinib 24 mg once daily in 28-day cycles until disease progression, unmanageable toxicity, withdrawal, or death. "
}
] | 5
|
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:1781",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013964",
"http://www.disease-ontology.org/api/metadata/DOID:3963"
] |
[] |
56c1f002ef6e394741000038
|
bioasq_yesno
|
yesno
|
Are genomic regulatory blocks (GRBs) any different than TADs?
|
['no']
|
[
"no"
] |
['No, clusters of CNEs (GRBs) strongly coincide with topological organisation, predicting the boundaries of hundreds of topologically associating domains (TADs) in human and Drosophila. The set of TADs that are associated with high levels of noncoding conservation exhibit distinct properties compared to TADs devoid of extreme noncoding conservation. The close correspondence between extreme noncoding conservation and TADs suggests that these TADs are ancient, revealing a regulatory architecture conserved over hundreds of millions of years.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28874668"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28874668",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Topologically associating domains are ancient features that coincide with Metazoan clusters of extreme noncoding conservation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28874668",
"endSection": "abstract",
"offsetInBeginSection": 235,
"offsetInEndSection": 1358,
"text": "Clusters of CNEs define the span of regulatory inputs for many important developmental regulators and have been described previously as genomic regulatory blocks (GRBs). Their function and distribution around important regulatory genes raises the question of how they relate to 3D conformation of these loci. Here, we show that clusters of CNEs strongly coincide with topological organisation, predicting the boundaries of hundreds of topologically associating domains (TADs) in human and Drosophila. The set of TADs that are associated with high levels of noncoding conservation exhibit distinct properties compared to TADs devoid of extreme noncoding conservation. The close correspondence between extreme noncoding conservation and TADs suggests that these TADs are ancient, revealing a regulatory architecture conserved over hundreds of millions of years.Metazoan genomes contain many clusters of conserved noncoding elements. Here, the authors provide evidence that these clusters coincide with distinct topologically associating domains in humans and Drosophila, revealing a conserved regulatory genomic architecture."
}
] | 11
|
BioASQ-training11b
| null | null |
5e4946bf6d0a277941000005
|
bioasq_yesno
|
yesno
|
Is Annexin V an apoptotic marker?
|
['yes']
|
[
"yes"
] |
['Yes, annexin V is an early apoptotic marker.', 'Yes, Annexin V is an apoptotic marker.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24412631",
"http://www.ncbi.nlm.nih.gov/pubmed/16046522",
"http://www.ncbi.nlm.nih.gov/pubmed/23000925",
"http://www.ncbi.nlm.nih.gov/pubmed/20122665",
"http://www.ncbi.nlm.nih.gov/pubmed/26582221",
"http://www.ncbi.nlm.nih.gov/pubmed/27619241",
"http://www.ncbi.nlm.nih.gov/pubmed/9776585",
"http://www.ncbi.nlm.nih.gov/pubmed/26734508",
"http://www.ncbi.nlm.nih.gov/pubmed/24021657",
"http://www.ncbi.nlm.nih.gov/pubmed/7812008",
"http://www.ncbi.nlm.nih.gov/pubmed/16740972",
"http://www.ncbi.nlm.nih.gov/pubmed/20444920",
"http://www.ncbi.nlm.nih.gov/pubmed/16331047",
"http://www.ncbi.nlm.nih.gov/pubmed/22913657",
"http://www.ncbi.nlm.nih.gov/pubmed/9461328",
"http://www.ncbi.nlm.nih.gov/pubmed/11585299",
"http://www.ncbi.nlm.nih.gov/pubmed/14676140",
"http://www.ncbi.nlm.nih.gov/pubmed/25339644",
"http://www.ncbi.nlm.nih.gov/pubmed/12573319",
"http://www.ncbi.nlm.nih.gov/pubmed/25591763",
"http://www.ncbi.nlm.nih.gov/pubmed/26935620",
"http://www.ncbi.nlm.nih.gov/pubmed/9359032",
"http://www.ncbi.nlm.nih.gov/pubmed/21340828",
"http://www.ncbi.nlm.nih.gov/pubmed/25116573",
"http://www.ncbi.nlm.nih.gov/pubmed/16737615",
"http://www.ncbi.nlm.nih.gov/pubmed/21203987",
"http://www.ncbi.nlm.nih.gov/pubmed/22960471",
"http://www.ncbi.nlm.nih.gov/pubmed/16253964",
"http://www.ncbi.nlm.nih.gov/pubmed/12552341",
"http://www.ncbi.nlm.nih.gov/pubmed/14666384",
"http://www.ncbi.nlm.nih.gov/pubmed/18441250",
"http://www.ncbi.nlm.nih.gov/pubmed/16813956",
"http://www.ncbi.nlm.nih.gov/pubmed/20520578",
"http://www.ncbi.nlm.nih.gov/pubmed/7622868",
"http://www.ncbi.nlm.nih.gov/pubmed/9462458",
"http://www.ncbi.nlm.nih.gov/pubmed/14734682",
"http://www.ncbi.nlm.nih.gov/pubmed/18554742",
"http://www.ncbi.nlm.nih.gov/pubmed/16239600",
"http://www.ncbi.nlm.nih.gov/pubmed/11708469",
"http://www.ncbi.nlm.nih.gov/pubmed/20430734",
"http://www.ncbi.nlm.nih.gov/pubmed/10541822",
"http://www.ncbi.nlm.nih.gov/pubmed/16306419",
"http://www.ncbi.nlm.nih.gov/pubmed/26112094"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26935620",
"endSection": "abstract",
"offsetInBeginSection": 430,
"offsetInEndSection": 579,
"text": "The apoptosis of the MSCs was induced by subjecting the cells to OGD conditions for 4 h and was detected by Annexin V/PI and Hoechst 33258 staining. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26734508",
"endSection": "abstract",
"offsetInBeginSection": 969,
"offsetInEndSection": 1304,
"text": "In addition to the antimicrobial activity, we found that treatment of the cancer cell lines, Jurkat T-cells, Granta cells, and melanoma cells, with the Pseudomonas sp. In5 crude extract increased staining with the apoptotic marker Annexin V while no staining of healthy normal cells, i.e., naïve or activated CD4 T-cells, was observed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26582221",
"endSection": "abstract",
"offsetInBeginSection": 1175,
"offsetInEndSection": 1402,
"text": "At the same time, the expressions of CD105, CD31, and the apoptotic marker of Annexin V were detected through flow cytometry for analyzing the relationship between the expression of cell surface markers and biological behavior."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24412631",
"endSection": "abstract",
"offsetInBeginSection": 354,
"offsetInEndSection": 505,
"text": "However, we found decreased sperm concentration, increase of morphologically abnormal spermatozoa and increased binding of apoptotic marker annexin V. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20444920",
"endSection": "abstract",
"offsetInBeginSection": 648,
"offsetInEndSection": 895,
"text": "hCG enhanced viability of granulosa-lutein cells through antiapoptosis but not proliferation, because the apoptotic marker of annexin V was decreased, but the proliferative markers of Ki67 and proliferating cell nuclear antigen were not increased."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18554742",
"endSection": "abstract",
"offsetInBeginSection": 650,
"offsetInEndSection": 863,
"text": "However, as the DOTAP concentration increased from 50 to 800 microM, the apoptotic marker Annexin V and ROS double positive cells increased, suggesting that high dose of DOTAP-generated ROS causes cell apoptosis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16331047",
"endSection": "abstract",
"offsetInBeginSection": 1093,
"offsetInEndSection": 1326,
"text": "Expression of the apoptotic marker annexin V was unaffected by antibiotic exposure, whereas the uptake of the necrotic marker PI was increased by ofloxacin (5 mg/mL) but not by netilmicin (ofloxacin versus netilmicin, ANOVA, P<0.05)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20444920",
"endSection": "abstract",
"offsetInBeginSection": 751,
"offsetInEndSection": 797,
"text": "he apoptotic marker of annexin V was decreased"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18554742",
"endSection": "abstract",
"offsetInBeginSection": 719,
"offsetInEndSection": 749,
"text": "the apoptotic marker Annexin V"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9462458",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "Annexin V labels apoptotic neurons following hypoxia-ischemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11708469",
"endSection": "abstract",
"offsetInBeginSection": 430,
"offsetInEndSection": 584,
"text": "In the present study, the apoptotic cell population was identified immunocytochemically using Annexin V, a marker of cells in an early stage of apoptosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11708469",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Use of annexin V antibody to identify apoptotic cells during pregnancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25339644",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 726,
"text": "Only few SF Treg cells were apoptotic, as indicated by limited annexin V staining of these cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9776585",
"endSection": "abstract",
"offsetInBeginSection": 470,
"offsetInEndSection": 697,
"text": "Eosinophils 'aged' in vitro for 48 h exhibited endonuclease DNA degradation, apoptotic morphology, increased red autofluorescence and externalisation of phosphatidylserine (PS) as assessed by binding of FITC-labelled annexin V."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16813956",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 672,
"text": "In vivo detection of apoptotic cells with fluorescently labeled annexin V is an emerging technique that we evaluated for detecting apoptotic germ cells in a mouse model of testicular torsion.Annexin V labeled with an indocyanine fluorophore (bisfunctional succinimidyl ester of cyanine 5.5) (Amersham, Little Chalfont, United Kingdom) was injected intravenously in mice 18 hours after the repair of unilateral 720-degree testicular torsion for 2 hours"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20520578",
"endSection": "abstract",
"offsetInBeginSection": 238,
"offsetInEndSection": 1091,
"text": "Here, we tested the hypothesis that enhanced endothelial apoptotic microparticles and decreased endothelial progenitor cell (EPC) levels might contribute to the pathophysiology of microalbuminuria or macroalbuminuria in cardiovascular disease.Flow cytometry was used to assess endothelial cell apoptosis and circulating EPC levels by quantification of circulating CD31/annexin V apoptotic microparticles and EPC markers (defined as KDRCD133, CD34CD133, CD34KDR) in peripheral blood.In total, 125 patients with hypertension were enrolled in the study, of whom 80 patients (64%) were with normoalbuminuria (albumin excretion rate of <20 microg/min, overnight urine samples), 35 patients (28%) with microalbuminuria (an albumin excretion rate of 20-200 microg/min), and 10 patients (8%) with macroalbuminuria (an albumin excretion rate >200 microg/min)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21203987",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Surfactant protein A (SP-A) binds to phosphatidylserine and competes with annexin V binding on late apoptotic cells"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14676140",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Targeting of apoptotic macrophages and experimental atheroma with radiolabeled annexin V: a technique with potential for noninvasive imaging of vulnerable plaque"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14676140",
"endSection": "abstract",
"offsetInBeginSection": 86,
"offsetInEndSection": 469,
"text": "Because annexin V has a high affinity for exposed phosphatidylserine on apoptotic cells, radiolabeled annexin V may be used for noninvasive detection of apoptosis in atherosclerotic lesions.Atherosclerotic plaques were produced in 5 rabbits by deendothelialization of the infradiaphragmatic aorta followed by 12 weeks of cholesterol diet; 5 controls were studied without manipulation"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20122665",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Apoptotic abscess imaging with 99mTc-HYNIC-rh-Annexin-V."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12573319",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Synthesis and evaluation of a 18F-labelled recombinant annexin-V derivative, for identification and quantification of apoptotic cells with PET."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24021657",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Sensitive and visible detection of apoptotic cells on Annexin-V modified substrate using aminophenylboronic acid modified gold nanoparticles (APBA-GNPs) labeling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960471",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1148,
"text": "Fluorescence-activated cell sorting (FACS) for expression of the early apoptosis marker Annexin V and for nuclear staining by 7-aminoactinomycin (7-AAD) revealed different extents of apoptosis versus non-apoptotic cell death for the three agents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26112094",
"endSection": "abstract",
"offsetInBeginSection": 680,
"offsetInEndSection": 876,
"text": "At immunofluorescence these cells contained lipid vesicles positive for the apoptotic cell marker Annexin V suggesting the phagocytosis of apoptotic bodies derived from dead fat-laden hepatocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7812008",
"endSection": "abstract",
"offsetInBeginSection": 1612,
"offsetInEndSection": 1708,
"text": "In this respect, we identified binding of Annexin V as an convenient marker for apoptotic cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16046522",
"endSection": "abstract",
"offsetInBeginSection": 540,
"offsetInEndSection": 697,
"text": "DR5 expression was elevated and associated with the apoptotic marker annexin V. Apoptosis was reduced in CD4(+) T cells when cultured with anti-DR5 antibody."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25116573",
"endSection": "abstract",
"offsetInBeginSection": 924,
"offsetInEndSection": 1080,
"text": "Flow cytometric analysis using the apoptotic marker, Annexin V, shows that this endogenous re-expression is sufficient to drive the SCLC cells to apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16253964",
"endSection": "abstract",
"offsetInBeginSection": 664,
"offsetInEndSection": 853,
"text": "Apoptotic cell death was evaluated by staining nuclei with propidium iodide and phosphatidylserine (a marker of early apoptotic events) with Annexin V as well as by DNA fragmentation assay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18441250",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 638,
"text": "Decreased cell growth was not caused by cell death as BEL exposure did not alter nuclear morphology or increase annexin V (apoptotic cell marker) or propidium iodide (necrotic cell marker) staining after 48 h."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21340828",
"endSection": "abstract",
"offsetInBeginSection": 2979,
"offsetInEndSection": 3261,
"text": "Four populations of cells can be identified: region R1: vital cells (annexin V negative/PI negative), region R2: apoptotic cells (annexin V positive/PI negative), region R3: dead cells (annexin V positive/ PI positive); and region R4: damaged cells (annexin V negative/PI positive)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14734682",
"endSection": "abstract",
"offsetInBeginSection": 2109,
"offsetInEndSection": 2222,
"text": "Furthermore, uptake of (111)In-DTPA-PEG-annexin V by tumors correlated with apoptotic index (r = 0.87, P = 0.02)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20430734",
"endSection": "abstract",
"offsetInBeginSection": 1177,
"offsetInEndSection": 1309,
"text": "Annexin V(+)/PI(-) cells were characterized as early apoptotic, Annexin V(+)/PI(+) as late apoptotic and Annexin V(-)/PI(+) as dead."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27619241",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 580,
"text": "Targeting ability of Annexin V for apoptotic macrophages was kept and enhanced."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14666384",
"endSection": "abstract",
"offsetInBeginSection": 817,
"offsetInEndSection": 923,
"text": "[18F]annexin V accumulated in the infarct area of the left ventricle, where apoptotic cells were observed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22913657",
"endSection": "abstract",
"offsetInBeginSection": 405,
"offsetInEndSection": 714,
"text": "The viability of SiHa cells was evaluated using the MTT assay, apoptosis by acridine orange/ethidium bromide, propidium iodide, TUNEL assay, and Annexin V-Cy3, cell cycle distribution and mitochondrial transmembrane potential using flow cytometry, and apoptotic marker genes using quantitative real-time PCR. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22913657",
"endSection": "abstract",
"offsetInBeginSection": 1242,
"offsetInEndSection": 1325,
"text": "Furthermore, hesperetin-induced apoptosis was confirmed by TUNEL and Annexin V-Cy3."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16306419",
"endSection": "abstract",
"offsetInBeginSection": 161,
"offsetInEndSection": 274,
"text": "The procedure delivers two sperm fractions: annexin V-negative (nonapoptotic) and annexin V-positive (apoptotic)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16740972",
"endSection": "abstract",
"offsetInBeginSection": 603,
"offsetInEndSection": 811,
"text": "The percentage of cells stained with annexin V, an early apoptotic marker, increased dramatically after cytoskeletal disruption with cytochalasin D compared with non-cytochalasin-D-treated controls (P<0.05). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16737615",
"endSection": "abstract",
"offsetInBeginSection": 373,
"offsetInEndSection": 498,
"text": "Apoptotic marker Annexin V analysis showed that the apoptotic rate of NB4 cells was increased after treatment with quercetin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16737615",
"endSection": "abstract",
"offsetInBeginSection": 149,
"offsetInEndSection": 291,
"text": "The cytomorphology of NB4 cells was assessed by Wright-stain, apoptosis rate by apoptotic marker Annexin V, and VEGF secretion level by ELISA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10541822",
"endSection": "abstract",
"offsetInBeginSection": 707,
"offsetInEndSection": 923,
"text": " We have coupled annexin V with the bifunctional hydrazinonicotinamide reagent (HYNIC) to prepare technetium-99m HYNIC-annexin V and demonstrated localization of radioactivity in tissues undergoing apoptosis in vivo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10541822",
"endSection": "abstract",
"offsetInBeginSection": 2914,
"offsetInEndSection": 3070,
"text": "In conlusion, these studies confirm the value of (99m)Tc-HYNIC-annexin V uptake as a marker for the detection and quantification of apoptotic cells in vivo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9359032",
"endSection": "abstract",
"offsetInBeginSection": 1111,
"offsetInEndSection": 1265,
"text": "The application of Annexin V labeling at electron microscopy will allow a more refined description of the morphological events occurring during apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25591763",
"endSection": "abstract",
"offsetInBeginSection": 690,
"offsetInEndSection": 753,
"text": "Apoptotic cells were identified by Annexin V-FITC/PI staining. "
}
] | 6
|
BioASQ-training6b
|
[
"http://www.uniprot.org/uniprot/ANXA5_CYNPY",
"http://www.uniprot.org/uniprot/ANXA5_MOUSE",
"http://www.uniprot.org/uniprot/ANXA5_HUMAN",
"http://www.uniprot.org/uniprot/ANXA5_MACFA",
"http://www.uniprot.org/uniprot/ANXA5_BOVIN",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017304",
"http://www.uniprot.org/uniprot/ANXA5_CHICK",
"http://www.uniprot.org/uniprot/ANXA5_PANTR",
"http://www.uniprot.org/uniprot/ANXA5_RAT"
] | null |
5894597e7d9090f353000004
|
bioasq_yesno
|
factoid
|
Which protein is the main marker of Cajal bodies?
|
['coilin']
|
[
"coilin",
"Coilin protein",
"coilin protein",
"coilin (human)",
"coilin (mouse)",
"coilin (rat)"
] |
['Coilin is widely known as the protein marker of the Cajal body, a subnuclear domain important to the biogenesis of small nuclear ribonucleoproteins and telomerase, complexes that are crucial to pre-messenger RNA splicing and telomere maintenance, respectively The Cajal body has now regained the interest of biologists, due to the isolation of a protein marker, coilin.', 'Coilin is widely known as the protein marker of the Cajal body, a subnuclear domain important to the biogenesis of small nuclear ribonucleoproteins and telomerase, complexes that are crucial to pre-messenger RNA splicing and telomere maintenance, respectively Extensive studies have characterized the interaction between coilin and the various other protein components of CBs and related subnuclear domains; however, only a few have examined interactions between coilin and nucleic acid.', 'Coilin is widely known as the protein marker of the Cajal body, a subnuclear domain important to the biogenesis of small nuclear ribonucleoproteins and telomerase, complexes that are crucial to pre-messenger RNA splicing and telomere maintenance, respectively. The Cajal (coiled) body is a discrete nuclear organelle that was first described in mammalian neurons in 1903.', 'coilin', 'Coilin is widely known as the protein marker of the Cajal body, a subnuclear domain important to the biogenesis of small nuclear ribonucleoproteins and telomerase, complexes that are crucial to pre-messenger RNA splicing and telomere maintenance, respectively', 'Coilin, more than a molecular marker of the cajal (coiled) body The Cajal body has now regained the interest of biologists, due to the isolation of a protein marker, coilin.', 'Coilin is widely known as the protein marker of the Cajal body, a subnuclear domain important to the biogenesis of small nuclear ribonucleoproteins and telomerase, complexes that are crucial to pre-messenger RNA splicing and telomere maintenance, respectively.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22558428",
"http://www.ncbi.nlm.nih.gov/pubmed/11302690",
"http://www.ncbi.nlm.nih.gov/pubmed/10806077",
"http://www.ncbi.nlm.nih.gov/pubmed/14989147",
"http://www.ncbi.nlm.nih.gov/pubmed/10944589",
"http://www.ncbi.nlm.nih.gov/pubmed/16079131",
"http://www.ncbi.nlm.nih.gov/pubmed/23274112",
"http://www.ncbi.nlm.nih.gov/pubmed/24358231",
"http://www.ncbi.nlm.nih.gov/pubmed/23064547",
"http://www.ncbi.nlm.nih.gov/pubmed/27317682",
"http://www.ncbi.nlm.nih.gov/pubmed/24569877",
"http://www.ncbi.nlm.nih.gov/pubmed/21920476"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23274112",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 259,
"text": "Coilin is widely known as the protein marker of the Cajal body, a subnuclear domain important to the biogenesis of small nuclear ribonucleoproteins and telomerase, complexes that are crucial to pre-messenger RNA splicing and telomere maintenance, respectively"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23274112",
"endSection": "abstract",
"offsetInBeginSection": 261,
"offsetInEndSection": 488,
"text": "Extensive studies have characterized the interaction between coilin and the various other protein components of CBs and related subnuclear domains; however, only a few have examined interactions between coilin and nucleic acid."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23274112",
"endSection": "abstract",
"offsetInBeginSection": 521,
"offsetInEndSection": 735,
"text": "coilin is tightly associated with nucleic acid, displays RNase activity in vitro, and is redistributed to the ribosomal RNA (rRNA)-rich nucleoli in cells treated with the DNA-damaging agents cisplatin and etoposide"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23274112",
"endSection": "abstract",
"offsetInBeginSection": 737,
"offsetInEndSection": 1044,
"text": "Here, we report a specific in vivo association between coilin and rRNA, U small nuclear RNA (snRNA), and human telomerase RNA, which is altered upon treatment with DNA-damaging agents. Using chromatin immunoprecipitation, we provide evidence of coilin interaction with specific regions of U snRNA gene loci."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23274112",
"endSection": "abstract",
"offsetInBeginSection": 1191,
"offsetInEndSection": 1315,
"text": "Additionally, we provide evidence of coilin involvement in the processing of human telomerase RNA both in vitro and in vivo."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10944589",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Coilin, more than a molecular marker of the cajal (coiled) body"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10944589",
"endSection": "abstract",
"offsetInBeginSection": 278,
"offsetInEndSection": 387,
"text": "The Cajal body has now regained the interest of biologists, due to the isolation of a protein marker, coilin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10944589",
"endSection": "abstract",
"offsetInBeginSection": 533,
"offsetInEndSection": 733,
"text": "Here, I would like to discuss what we have learned about coilin and suggest a possible role for coilin in RNA processing and cellular trafficking, especially in relation to Cajal bodies and nucleoli. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11302690",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 317,
"text": "Coilin-p80 is a marker protein for nuclear Cajal bodies (coiled bodies; CBs) which are also involved in snRNP maturation, storage or transport."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24358231",
"endSection": "abstract",
"offsetInBeginSection": 1075,
"offsetInEndSection": 1165,
"text": "Coilin is another nuclear SMN binding partner and a marker protein for Cajal bodies (CBs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14989147",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 372,
"text": "A limited set of NBs also contained coilin, a marker protein for Cajal bodies (CBs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24569877",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 430,
"text": "We performed a genome-wide screen to identify proteins that colocalize with coilin, the marker protein of Cajal bodies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27317682",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "Coilin is a marker protein for subnuclear organelles known as Cajal bodies, which are sites of various RNA metabolic processes including the biogenesis of spliceosomal small nuclear ribonucleoprotein particles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16079131",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Coilin is a marker protein for the Cajal body, a subnuclear domain acting as a site for assembly and maturation of nuclear RNA-protein complexes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24569877",
"endSection": "abstract",
"offsetInBeginSection": 313,
"offsetInEndSection": 431,
"text": "We performed a genome-wide screen to identify proteins that colocalize with coilin, the marker protein of Cajal bodies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23064547",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Cajal bodies (CB) are subnuclear domains that contain various proteins with diverse functions including the CB marker protein coilin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24358231",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1172,
"text": "Coilin is another nuclear SMN binding partner and a marker protein for Cajal bodies (CBs)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21920476",
"endSection": "abstract",
"offsetInBeginSection": 1088,
"offsetInEndSection": 1175,
"text": "One of these target proteins is coilin; a basic protein located in nuclear Cajal bodies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22558428",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 191,
"text": "Coilin is known as the marker protein for Cajal bodies (CBs), subnuclear domains important for the biogenesis of small nuclear ribonucleoproteins (snRNPs) which function in pre-mRNA splicing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10806077",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 363,
"text": "Cajal bodies (coiled bodies, CBs) are nuclear organelles of unknown function and are characterized by a wide variety of components including various basal transcription and cell cycle proteins, the nucleolar proteins fibrillarin and Nopp140, numerous small nuclear ribonucleoproteins, the survival motor neuron protein complex, and the marker protein, p80 coilin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16301532",
"endSection": "abstract",
"offsetInBeginSection": 1182,
"offsetInEndSection": 1312,
"text": "Perturbation of SMN function results in disassembly of Cajal bodies and relocalization of the marker protein, coilin, to nucleoli."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22038794",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 495,
"text": "Human coilin interacting nuclear ATPase protein (hCINAP) directly interacts with coilin, a marker protein of Cajal Bodies (CBs), nuclear organelles involved in the maturation of small nuclear ribonucleoproteins UsnRNPs and snoRNPs. hCINAP has previously been designated as an adenylate kinase (AK6), but is very atypical as it exhibits unusually broad substrate specificity, structural features characteristic of ATPase/GTPase proteins (Walker motifs A and B) and also intrinsic ATPase activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24358231",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1173,
"text": "Coilin is another nuclear SMN binding partner and a marker protein for Cajal bodies (CBs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23064547",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Cajal bodies (CB) are subnuclear domains that contain various proteins with diverse functions including the CB marker protein coilin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11102515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "We have found that coilin, the marker protein for Cajal bodies (coiled bodies, CBs), is a self-interacting protein, and we have mapped the domain responsible for this activity to the amino-terminus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11031238",
"endSection": "abstract",
"offsetInBeginSection": 257,
"offsetInEndSection": 405,
"text": "Cajal bodies contain a marker protein of unknown function, p80-coilin, and many components involved in transcription and processing of nuclear RNAs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24569877",
"endSection": "abstract",
"offsetInBeginSection": 313,
"offsetInEndSection": 432,
"text": "We performed a genome-wide screen to identify proteins that colocalize with coilin, the marker protein of Cajal bodies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22250197",
"endSection": "abstract",
"offsetInBeginSection": 592,
"offsetInEndSection": 704,
"text": "A defect in this activity caused a significant accumulation of the Cajal body marker protein coilin in nucleoli."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10944589",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Coilin, more than a molecular marker of the cajal (coiled) body."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11134083",
"endSection": "abstract",
"offsetInBeginSection": 300,
"offsetInEndSection": 473,
"text": "We have constructed a stable HeLa cell line, HeLa(GFP-coilin), that expresses the Cajal body marker protein, p80 coilin, fused to the green fluorescent protein (GFP-coilin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18755223",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "The Cajal body, originally identified over 100 years ago as a nucleolar accessory body in neurons, has come to be identified with nucleoplasmic structures, often quite tiny, that contain coiled threads of the marker protein, coilin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21072240",
"endSection": "abstract",
"offsetInBeginSection": 600,
"offsetInEndSection": 857,
"text": "By immunoprecipitation we find that WRAP53 associates with the Cajal body marker coilin, the splicing regulatory protein SMN, and the nuclear import receptor importinβ, and that WRAP53 is essential for complex formation between SMN-coilin and SMN-importinβ."
}
] | 6
|
BioASQ-training6b
| null | null |
58eb9542eda5a57672000007
|
bioasq_factoid
|
factoid
|
Do A-type lamins bind euchromatin or heterochromatin?
|
[['Both euchromatin and heterochromatin']]
|
[
"euchromatin",
"heterochromatin",
"euchromatin and heterochromatin",
"euchromatin (light-staining chromatin)",
"heterochromatin (dark-staining chromatin)"
] |
['Comparative genomic hybridization (CGH) analyses of microdissected blebs, fluorescence in situ hybridization (FISH), and immunofluorescence localization of modified histones demonstrate that gene-rich euchromatin associates with the LA/C blebs. On the other hand, the domain encoded by exon 9 is important to maintain telomere homeostasis and heterochromatin structure but does not play a role in DNA repair, thus pointing to other exons in the lamin A tail as responsible for the genomic instability phenotype in Lmna(Δ8-11/Δ8-11) mice', 'These data reveal that the domain encoded by exon 9 is important to maintain telomere homeostasis and heterochromatin structure but does not play a role in DNA repair, thus pointing to other exons in the lamin A tail as responsible for the genomic instability phenotype in Lmna(Δ8-11/Δ8-11) mice', 'These data reveal that the domain encoded by exon 9 is important to maintain telomere homeostasis and heterochromatin structure but does not play a role in DNA repair, thus pointing to other exons in the lamin A tail as responsible for the genomic instability phenotype in Lmna(Δ8-11/Δ8-11) mice', 'These data reveal that the domain encoded by exon 9 is important to maintain telomere homeostasis and heterochromatin structure but does not play a role in DNA repair, thus pointing to other exons in the lamin A tail as responsible for the genomic instability phenotype in Lmna(Δ8-11/Δ8-11) mice']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22713752",
"http://www.ncbi.nlm.nih.gov/pubmed/20130288",
"http://www.ncbi.nlm.nih.gov/pubmed/19141474",
"http://www.ncbi.nlm.nih.gov/pubmed/11953316",
"http://www.ncbi.nlm.nih.gov/pubmed/24153156",
"http://www.ncbi.nlm.nih.gov/pubmed/18497856",
"http://www.ncbi.nlm.nih.gov/pubmed/3497271",
"http://www.ncbi.nlm.nih.gov/pubmed/7172763"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24153156",
"endSection": "abstract",
"offsetInBeginSection": 1243,
"offsetInEndSection": 1538,
"text": "These data reveal that the domain encoded by exon 9 is important to maintain telomere homeostasis and heterochromatin structure but does not play a role in DNA repair, thus pointing to other exons in the lamin A tail as responsible for the genomic instability phenotype in Lmna(Δ8-11/Δ8-11) mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24153156",
"endSection": "abstract",
"offsetInBeginSection": 850,
"offsetInEndSection": 1031,
"text": "Lmna(Δ9/Δ9) MEFs exhibit telomere shortening and heterochromatin alterations but do not activate cathepsin L-mediated degradation of 53BP1 and maintain expression of BRCA1 and RAD51"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24153156",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Lamin A Δexon9 mutation leads to telomere and chromatin defects but not genomic instability"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11953316",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Caspase-6 gene disruption reveals a requirement for lamin A cleavage in apoptotic chromatin condensation"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19141474",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "The A- and B-type nuclear lamin networks: microdomains involved in chromatin organization and transcription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19141474",
"endSection": "abstract",
"offsetInBeginSection": 667,
"offsetInEndSection": 910,
"text": "Comparative genomic hybridization (CGH) analyses of microdissected blebs, fluorescence in situ hybridization (FISH), and immunofluorescence localization of modified histones demonstrate that gene-rich euchromatin associates with the LA/C blebs"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20130288",
"endSection": "title",
"offsetInBeginSection": 8,
"offsetInEndSection": 103,
"text": "Lamin A/C, caspase-6, and chromatin configuration during meiosis resumption in the mouse oocyte"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20130288",
"endSection": "abstract",
"offsetInBeginSection": 678,
"offsetInEndSection": 862,
"text": "Our results demonstrated that these proteins were always present and that their distributions were related to oocyte maturity, determined by chromatin configuration and oocyte diameter"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22713752",
"endSection": "abstract",
"offsetInBeginSection": 513,
"offsetInEndSection": 728,
"text": "Histone acetylation controls, almost exclusively, euchromatin protein dynamics; lamin A expression regulates heterochromatin protein dynamics, and G9a regulates both euchromatin and heterochromatin protein dynamics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22713752",
"endSection": "abstract",
"offsetInBeginSection": 725,
"offsetInEndSection": 940,
"text": "Histone acetylation controls, almost exclusively, euchromatin protein dynamics; lamin A expression regulates heterochromatin protein dynamics, and G9a regulates both euchromatin and heterochromatin protein dynamics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3497271",
"endSection": "abstract",
"offsetInBeginSection": 1215,
"offsetInEndSection": 1414,
"text": "Other proteins that reversibly interact with DNA, such as the lamins and nuclear pores, may have a role in the organization of DNA into transcribable euchromatin and nontranscribable heterochromatin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3497271",
"endSection": "abstract",
"offsetInBeginSection": 1215,
"offsetInEndSection": 1414,
"text": "Other proteins that reversibly interact with DNA, such as the lamins and nuclear pores, may have a role in the organization of DNA into transcribable euchromatin and nontranscribable heterochromatin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22713752",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 729,
"text": "Histone acetylation controls, almost exclusively, euchromatin protein dynamics; lamin A expression regulates heterochromatin protein dynamics, and G9a regulates both euchromatin and heterochromatin protein dynamics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3497271",
"endSection": "abstract",
"offsetInBeginSection": 1024,
"offsetInEndSection": 1223,
"text": "Other proteins that reversibly interact with DNA, such as the lamins and nuclear pores, may have a role in the organization of DNA into transcribable euchromatin and nontranscribable heterochromatin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22713752",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 729,
"text": "Histone acetylation controls, almost exclusively, euchromatin protein dynamics; lamin A expression regulates heterochromatin protein dynamics, and G9a regulates both euchromatin and heterochromatin protein dynamics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22713752",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 729,
"text": "Histone acetylation controls, almost exclusively, euchromatin protein dynamics; lamin A expression regulates heterochromatin protein dynamics, and G9a regulates both euchromatin and heterochromatin protein dynamics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22713752",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 729,
"text": "Histone acetylation controls, almost exclusively, euchromatin protein dynamics; lamin A expression regulates heterochromatin protein dynamics, and G9a regulates both euchromatin and heterochromatin protein dynamics."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18497856",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Role for A-type lamins in herpesviral DNA targeting and heterochromatin modulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3497271",
"endSection": "abstract",
"offsetInBeginSection": 1024,
"offsetInEndSection": 1223,
"text": "Other proteins that reversibly interact with DNA, such as the lamins and nuclear pores, may have a role in the organization of DNA into transcribable euchromatin and nontranscribable heterochromatin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22713752",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 729,
"text": "Histone acetylation controls, almost exclusively, euchromatin protein dynamics; lamin A expression regulates heterochromatin protein dynamics, and G9a regulates both euchromatin and heterochromatin protein dynamics."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18497856",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Role for A-type lamins in herpesviral DNA targeting and heterochromatin modulation."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D034904",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D034882",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D022041",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006570",
"http://amigo.geneontology.org/amigo/term/GO:0000791",
"http://amigo.geneontology.org/amigo/term/GO:0000792",
"http://amigo.geneontology.org/amigo/term/GO:0005521"
] |
[] |
570917bccf1c325851000015
|
bioasq_factoid
|
factoid
|
Where are Goblet cells localized?
|
['Epithelium']
|
[
"Epithelium",
"Epithelial tissue",
"Epithelial cells",
"Epithelia"
] |
['Goblet cells are found in the intestine, in the lungs, in the eyes etc. Goblet cells are localized in the epithelium.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31751647",
"http://www.ncbi.nlm.nih.gov/pubmed/31819932",
"http://www.ncbi.nlm.nih.gov/pubmed/31734511",
"http://www.ncbi.nlm.nih.gov/pubmed/31782555",
"http://www.ncbi.nlm.nih.gov/pubmed/31762020",
"http://www.ncbi.nlm.nih.gov/pubmed/31922915"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31782555",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Goblet cells (GCs) and endocrine cells (ECs) play an important role in intestine physiology,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31734511",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Conjunctival goblet cells (CGCs) are specialized cells that produce and secrete soluble mucins to the tear film that bathes the ocular surface."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31751647",
"endSection": "abstract",
"offsetInBeginSection": 1853,
"offsetInEndSection": 1878,
"text": "goblet cells in the lungs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31819932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "The epithelial lining of the small intestine consists of multiple cell types, including Paneth cells and goblet cells, that work in cohort to maintain gut health. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31922915",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 73,
"text": "goblet cell numbers are increased within the airway epithelium"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31762020",
"endSection": "abstract",
"offsetInBeginSection": 319,
"offsetInEndSection": 438,
"text": " The mucosa is lined with a stratified secretory epithelium rich in goblet cells that secrete neutral and acid mucins. "
}
] | 11
|
BioASQ-training11b
| null | null |
6049080c1cb411341a000164
|
bioasq_factoid
|
factoid
|
What is the function of the stard10 protein?
|
['STARD10 is a lipid transfer protein']
|
[
"STARD10",
"StARD10",
"StAR-related lipid transfer protein 10",
"Steroidogenic acute regulatory protein 10"
] |
['STARD10, a member of the steroidogenic acute regulatory protein (StAR)-related lipid transfer (START) protein family, is highly expressed in the liver and has been shown to transfer phosphatidylcholine.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23200860",
"http://www.ncbi.nlm.nih.gov/pubmed/15976441",
"http://www.ncbi.nlm.nih.gov/pubmed/15911624"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23200860",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "STARD10, a member of the steroidogenic acute regulatory protein (StAR)-related lipid transfer (START) protein family, is highly expressed in the liver and has been shown to transfer phosphatidylcholine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15911624",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 327,
"text": "StarD10 contains a steroidogenic acute regulatory protein (StAR/StarD1)-related lipid transfer (START) domain that is thought to mediate binding of lipids. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15976441",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "The steroidogenic acute regulatory protein (StAR)-related lipid transfer (START) domain is a protein module of approximately 210 residues that binds lipids, including sterols"
}
] | 11
|
BioASQ-training11b
| null | null |
608069984e6a4cf630000006
|
bioasq_factoid
|
factoid
|
In what phase of clinical trials is crenezumab? (November 2017)
|
['Phase III']
|
[
"Phase III",
"Phase 3",
"Phase 3 clinical trial",
"Phase III clinical trial"
] |
['Crenezumab is undergoing phase III clinical trials.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28720101"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28720101",
"endSection": "abstract",
"offsetInBeginSection": 1424,
"offsetInEndSection": 1569,
"text": "Ongoing Phase III clinical trials via passive immunotherapy against Aβ peptides (crenezumab, gantenerumab, and aducanumab) seem to be promising. "
}
] | 11
|
BioASQ-training11b
| null | null |
5a9acd921d1251d03b000016
|
bioasq_factoid
|
yesno
|
Should PDYD polymorphism determination be routinely performed in patients with colorectal cancer patients?
|
['yes']
|
[
"yes"
] |
['Yes, determining DPYD polymorphism should be routinely performed in colorectal cancer patients to improve patient safety by allowing for dose adjustments of fluoropyrimidine treatment based on genetic predisposition to toxicity.', 'Yes, prospective DPYD genotyping should be routinely performed in colorectal cancer patients treated with fluoropyrimidines (FP). DPYD genetic variants are associated with extremely severe, early-onset FP toxicity. Prospective DPYD genotyping is feasible in routine clinical practice, and DPYD genotype-based FP dose reductions improve patient safety.', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer patients.', 'Yes, DPYD polymorphism determination should be considered for routine performance in patients with colorectal cancer who are candidates for fluoropyrimidine treatment such as 5-fluorouracil or capecitabine. This is because genetic variants in the dihydropyrimidine dehydrogenase (DPYD) gene have been associated with an increased risk of severe and potentially life-threatening toxicity, particularly when patients carry certain DPYD alleles that result in reduced enzyme activity. By identifying these polymorphisms before initiating treatment, clinicians can adjust the fluoropyrimidine dose to reduce the likelihood of severe toxic effects, thereby improving patient safety and outcomes.', "There is currently no consensus on the routine determination of PDYD polymorphism in colorectal cancer patients. The clinical utility of this test is still under investigation and its use should be based on individual patient's needs and the availability of resources. It is recommended to consult with a healthcare provider to determine the most appropriate course of action.", 'The question of whether PDYD polymorphism determination should be routinely performed in patients with colorectal cancer is a complex one. The literature suggests that DPD deficiency, which is caused by genetic variations in the DPYD gene, is a significant risk factor for severe toxicities associated with 5-fluorouracil (5-FU) therapy. However, the current methods for determining DPD status are not yet suitable for routine clinical practice. While complete genotyping of the DPYD gene would be ideal, it is not currently feasible for routine use. Prospective genotyping for specific polymorphisms, such as the exon 14-skipping and 2846A>T-polymorphisms, may reduce the risk of serious toxic events by about 25%. However, the cost-effectiveness of such screening methods would need to be evaluated before they could be widely implemented in', 'Yes, DPYD genotyping is feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment.', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer. Host genetic variants in the DPYD gene have been found to be associated with severe toxicity in patients treated with fluoropyrimidine drugs. Prospective DPYD genotyping has been shown to be feasible in routine clinical practice and has led to improved patient safety by allowing for genotype-based dose reductions. Therefore, routine DPYD polymorphism determination can help identify patients who are at higher risk of toxicity and guide personalized treatment strategies.', 'The determination of the PDYD polymorphism should not be routinely performed in patients with colorectal cancer. Although polymorphisms in certain genes, such as p53 and hMLH1, have been shown to play a role in the pathogenesis of colorectal cancer, there is currently insufficient evidence to support the routine use of PDYD polymorphism determination in clinical practice. Further research is needed to establish the clinical significance and prognostic value of PDYD polymorphism in colorectal cancer patients.', 'Yes, prospective DPYD genotyping was feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment.', 'PDYD polymorphism determination should not be routinely performed in patients with colorectal cancer.The PDYD gene encodes a protein involved in the biosynthesis of the amino acid proline. The PDYD polymorphism is associated with altered proline metabolism, which may have implications for cancer development and progression. However, the clinical utility of PDYD polymorphism determination in colorectal cancer patients is not well established.The clinical utility of PDYD polymorphism determination in colorectal cancer patients is not well established.The PDYD polymorphism is associated with altered proline metabolism, which may have implications for cancer development and progression. However, the clinical utility of PDYD polymorphism determination in colorectal cancer patients is not well established.', 'Based on the current evidence, there is no strong recommendation for routine PDYD polymorphism determination in patients with colorectal cancer. The available studies have focused on other gene polymorphisms such as p53 and IRS-2, and there is limited data on the association between PDYD polymorphism and colorectal cancer. Further research is needed to determine the clinical significance and utility of PDYD polymorphism determination in colorectal cancer patients.', 'PDYD polymorphism determination should not be routinely performed in patients with colorectal cancer.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer before they start receiving Fluorouracil (FP) treatment.', 'Prospective DPYD genotyping was feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment.', "Currently, there is no consensus on routine PDYD polymorphism determination in colorectal cancer patients. The decision to perform such testing should be made on a case-by-case basis, taking into account factors such as the patient's medical history, treatment goals, and availability of alternative treatment options. However, it is important for healthcare providers to be aware of the potential for fluoropyrimidine-induced cardiotoxicity and to consider alternative regimens, such as s-MOX, in patients who have experienced this toxicity or who have abnormalities in the DYPD gene.", 'yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer. This is because genetic variants in the DPYD gene can lead to severe toxicity in patients treated with fluoropyrimidine. Prospective DPYD genotyping has been shown to be feasible in routine clinical practice, and using the genotype to guide dose adjustments can significantly improve patient safety.', 'The question of whether PDYD polymorphism determination should be routinely performed in patients with colorectal cancer is a topic of ongoing debate. Some argue that genetic testing for DPYD variants can help identify patients who are at risk of developing severe side effects from fluoropyrimidine chemotherapy, such as 5-FU and capecitabine. This could potentially spare patients from experiencing life-threatening adverse reactions and reduce the need for costly and time-consuming medical interventions. However, others argue that the frequency of DPYD variants is relatively low, and the cost and time required for genetic testing may not be justified for all patients with colorectal cancer. Moreover, there are still concerns about the accuracy and reproducibility of current genotyping methods, and the clinical utility of genetic testing in this setting remains uncertain. Therefore, it is crucial to weigh the potential benefits and', 'The routine determination of PDYD polymorphism in patients with colorectal cancer is not currently a standard practice. However, further research and clinical studies may provide insights into the potential relevance and impact of PDYD polymorphism in the management and treatment of colorectal cancer patients. It is advisable to consult with a healthcare provider or genetic counselor for personalized recommendations regarding genetic testing and its implications in colorectal cancer care.', 'Yes, in summary, polypeptide diversity analysis (PDYD) is a valuable technique for characterizing coloreactal cancer and should be considered for routine use in clinical oncology. It allows for the assessment of genetic, epigenetic, and biological diversity within a tumor population, providing valuable insights into cancer progression and response to treatment. ', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer, particularly those with high-risk stage II resected colorectal cancer enrolled in the TOSCA trial. The presence of the PDYD polymorphism has been associated with improved response to capecitabine and oxaliplatin in these patients.', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer. The XPD Lys751Gln and XRCC1 Arg399Gln polymorphisms have been associated with increased sensitivity to oxaliplatin-based chemotherapy in colorectal cancer patients.', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer. PDYD genetic variants are associated with severe toxicity in patients treated with fluoropyrimidines, which are commonly used in colorectal cancer treatment. Prospective genotyping for PDYD polymorphisms allows for dose individualization and reduces the risk of severe fluoropyrimidine-related toxicity. Implementing PDYD genotype-guided dosing as a standard of care can improve patient safety and treatment outcomes.', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer who are planned to receive fluoropyrimidine treatment. The presence of certain genetic variants in the DPYD gene can result in extremely severe and early onset toxicity in these patients. Prospective DPYD genotyping has been shown to be feasible in routine clinical practice, and DPYD genotype-based dose reductions have been shown to improve patient safety of fluoropyrimidine treatment. By identifying patients who are at risk for severe toxicity, healthcare providers can take steps to minimize the risk of adverse events and optimize treatment outcomes.', 'Yes, PDYD (dihydropyrimidine dehydrogenase) polymorphism determination should be routinely performed in colorectal cancer patients treated with fluoropyrimidines. The abstract describes a prospective study that demonstrated reduced severe toxicity in patients who received genotype-guided dosing of fluoropyrimidines based on PDYD variants. Specifically, DPYD*2A and c.1679T>G carriers benefited from a 50% initial dose reduction, while c.1236G>A and c.2846A>T carriers may require a larger dose reduction of 50%. Given that fluoropyrimidines are commonly used anticancer agents, the implementation of PDYD genotype-guided individualized dosing should be considered a new standard of care to improve patient safety and treatment outcomes.', 'Yes, determining DPYD polymorphism should be routinely performed in patients with colorectal cancer before starting fluoropyrimidine-based chemotherapy. This is because certain genetic variants in the DPYD gene can lead to severe toxicity in patients treated with fluoropyrimidines. Identifying these variants through genotyping can help tailor the treatment dose to improve safety and efficacy for the patient', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer to improve patient safety during fluoropyrimidine treatment.', 'This question is too specific and does not reflect the scope of the study. PDYD polymorphisms are not associated with colorectal cancer in general. The study focuses on a specific subset of colorectal cancer patients, and even for that subset, PDYD polymorphism determination is not routinely recommended, but rather it is suggested as an optional tool to improve clinical management of patients with stage II/III disease.', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer patients to identify those who may be at risk for severe toxicity from fluoropyrimidine-based chemotherapy.', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer to improve patient safety of fluoropyrimidine treatment.', "yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer to improve patient safety by allowing for dose adjustments of fluoropyrimidine treatment based on the patient's genetic profile.", 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer. This is because genetic variants in the DPYD gene can lead to severe toxicity in patients treated with fluoropyrimidine. As mentioned, "Prospective DPYD genotyping was feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment." This indicates that knowing a patient\'s DPYD genotype can help tailor their treatment plan to reduce the risk of severe side effects and enhance treatment safety.', 'Yes, determining dihydropyrimidine dehydrogenase (DPYD) polymorphisms should be considered routine practice for patients with colorectal cancer who are candidates for fluoropyrimidine-based chemotherapy. This is because DPYD plays a crucial role in the metabolism of these drugs and genetic variations can significantly impact both drug efficacy and toxicity. By identifying individuals with variants that may lead to reduced or absent enzyme activity, clinicians can adjust treatment plans accordingly, potentially avoiding severe adverse reactions while optimizing therapeutic outcomes.', 'Yes, complete genotyping of the encoding DPYD gene is desirable, in the interest of drug safety, before treatment is started.', 'No, according to current guidelines from major cancer organizations such as the National Comprehensive Cancer Network (NCCN) and the American Society of Clinical Oncology (ASCO), routine PDYD polymorphism determination is not recommended in patients with colorectal cancer. However, some experts suggest that PDYD genotyping may be considered in certain situations, such as in patients with a history of severe fluoropyrimidine toxicity or in those receiving high-dose fluoropyrimidine therapy. Therefore, the decision to perform PDYD polymorphism determination should be made on a case-by-case basis in consultation with a healthcare provider.', 'Yes, determining DPYD polymorphisms should be routinely performed in patients with colorectal cancer as it can help predict the risk of severe toxicity from fluoropyrimidine treatment and guide personalized dose adjustments to improve patient safety and treatment outcomes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36524458",
"http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"http://www.ncbi.nlm.nih.gov/pubmed/35582139",
"http://www.ncbi.nlm.nih.gov/pubmed/29372689",
"http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"http://www.ncbi.nlm.nih.gov/pubmed/36297556",
"http://www.ncbi.nlm.nih.gov/pubmed/11051215",
"http://www.ncbi.nlm.nih.gov/pubmed/36980706",
"http://www.ncbi.nlm.nih.gov/pubmed/31653159",
"http://www.ncbi.nlm.nih.gov/pubmed/25906475",
"http://www.ncbi.nlm.nih.gov/pubmed/25253112",
"http://www.ncbi.nlm.nih.gov/pubmed/21461655",
"http://www.ncbi.nlm.nih.gov/pubmed/12749725",
"http://www.ncbi.nlm.nih.gov/pubmed/23781135",
"http://www.ncbi.nlm.nih.gov/pubmed/20637356",
"http://www.ncbi.nlm.nih.gov/pubmed/23335937",
"http://www.ncbi.nlm.nih.gov/pubmed/35880438",
"http://www.ncbi.nlm.nih.gov/pubmed/23942539",
"http://www.ncbi.nlm.nih.gov/pubmed/25137161",
"http://www.ncbi.nlm.nih.gov/pubmed/33274825",
"http://www.ncbi.nlm.nih.gov/pubmed/19239324",
"http://www.ncbi.nlm.nih.gov/pubmed/16537192",
"http://www.ncbi.nlm.nih.gov/pubmed/20920994",
"http://www.ncbi.nlm.nih.gov/pubmed/15213713",
"http://www.ncbi.nlm.nih.gov/pubmed/30348537",
"http://www.ncbi.nlm.nih.gov/pubmed/36890284",
"http://www.ncbi.nlm.nih.gov/pubmed/32546132",
"http://www.ncbi.nlm.nih.gov/pubmed/24817302",
"http://www.ncbi.nlm.nih.gov/pubmed/33280607",
"http://www.ncbi.nlm.nih.gov/pubmed/30551678"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35582139",
"endSection": "abstract",
"offsetInBeginSection": 569,
"offsetInEndSection": 759,
"text": "Host genetic variants in the rate limiting enzyme dihydropyrimidine dehydrogenase (DPYD) gene are related to the occurrence of extremely severe, early onset toxicity in FP treated patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30348537",
"endSection": "abstract",
"offsetInBeginSection": 3168,
"offsetInEndSection": 3333,
"text": "Prospective DPYD genotyping was feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20637356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1014,
"text": "Colorectal cancer (CCR), which is one of the most common causes of cancer, has benefited from the major advances in the understanding of the intracellular signaling pathways implicated in the initiation, growing and local and metastasis dissemination of tumor, which have occurred during the 20 past years. The pharmacogenomics approach, especially the determination of the genetic polymorphisms, tries to find prognosis and predictive biomarkers permitting to identify patients who could benefit from a particular treatment or those exhibiting higher risks of toxicity. Among the numerous biomarkers, which have been studied, few are currently in use in clinical practice. The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan. For oxaliplatin, the determination of the polymorphisms of reparases and detoxification systems such as GSTpi seems interesting, but its"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"endSection": "abstract",
"offsetInBeginSection": 22,
"offsetInEndSection": 1708,
"text": "forms the basis for the chemotherapy of advanced colorectal cancer and of other solid tumours. About 9% of patients suffer from serious, sometimes even life-threatening adverse effects of a 5-FU therapy, such as haemotoxicity, which cannot be reliably predicted by conventional clinical and pharmacokinetic criteria. The systemic exposure to 5-FU is fundamentally determined by the genetically polymorphic enzyme dihydropyrimidine dehydrogenase (DPD). This deficiency is closely related to 5-FU-induced toxicity and a variety of non-synonymous variants has been detected in affected patients. The exon14-skipping mutation is the gene defect most frequently associated with serious 5-FU-related adverse effects and it has been reported ten times more often in affected individuals than in the general population. The 2846A>T polymorphism, which leads to an amino acid substitution, appears to be of comparable importance. While the causative role of premature stop codons - presumably resulting from spontaneous mutations - is very likely, the pathophysiological relevance of various other amino acid changes is still unclear. Patients who harbour a high-risk genotype should not be treated with 5-FU if therapeutic alternatives are available. The present data indicate that complete genotyping of the encoding DPYD gene is desirable, in the interest of drug safety, before treatment is started, although only a small number of patients would actually benefit. A method for the quantification of the DPD activity in vivo would have the advantage of reflecting all genetic and non-genetic influences.' However, no such method is currently available for routine use. Prospective genotyping"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "AIMS: Cancer patients with reduced dihydropyrimidine dehydrogenase (DPD) activity are at increased risk of severe fluoropyrimidine (FP)-related adverse events (AE)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"endSection": "abstract",
"offsetInBeginSection": 768,
"offsetInEndSection": 1270,
"text": "For each of the tested polymorphisms, variant allele carriers were matched to respective wild type controls (optimal full matching combined with exact matching, in respect to: age, sex, type of cancer, type of FP, DPYD activity score, use of irinotecan/UGT1A1, adjuvant therapy, radiotherapy, biological therapy and genotype on the remaining two tested polymorphisms).RESULTS: Of the 503 included patients (82.3% colorectal cancer), 283 (56.3%) developed grade ≥3 AEs, mostly diarrhoea and neutropenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"endSection": "abstract",
"offsetInBeginSection": 320,
"offsetInEndSection": 767,
"text": "We evaluated the relationship between three further DPYD polymorphisms: c.496A>G (rs2297595), *6 c.2194G>A (rs1801160) and *9A c.85T>C (rs1801265) and the risk of severe AEs.METHODS: Consecutive FP-treated adult patients were genotyped for \"standard\" and tested DPYD variants, and for UGT1A1*28 if irinotecan was included, and were monitored for the occurrence of grade ≥3 (National Cancer Institute Common Terminology Criteria) vs. grade 0-2 AEs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"endSection": "abstract",
"offsetInBeginSection": 1265,
"offsetInEndSection": 1481,
"text": "The present data indicate that complete genotyping of the encoding DPYD gene is desirable, in the interest of drug safety, before treatment is started, although only a small number of patients would actually benefit."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25906475",
"endSection": "abstract",
"offsetInBeginSection": 1227,
"offsetInEndSection": 1487,
"text": "The studies we reviewed indicate that pharmacogenetic testing is promising to direct personalised dosing of fluoropyrimidines, although further investigations are needed to establish the role of DPD in severe toxicity in patients treated for colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 319,
"text": "Guidelines recommend FP dosing adjusted to genotype-predicted DPD activity based on four DPYD variants (rs3918290, rs55886062, rs67376798 and rs56038477)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25137161",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 847,
"text": "OBJECTIVE: To validate the associations previously found in three cohorts of patients from the General University Hospital Gregorio Marañón, between the polymorphisms rs1128503, rs2032582 and rs1045642 of the ABCB1 gene and the hand-foot syndrome and diarrhea in colorectal cancer patients treated with chemotherapy regimes containing Capecitabine and 5-Fluorouracil, respectively, and between the polymorphisms rs2297595 of the DPYD gene and nausea/vomiting, rs11615 of ERCC1 and neutropenia, and rs28399433 CYP2A6 and neutropenia, in colorectal cancer patients treated with FOLFOX or XELOX as adjuvant therapy.METHOD: Colorectal cancer patients treated with chemotherapy regimes, containing Capecitabine (n = 157), 5-Fluorouracil (n = 99) were included in the study, as well as patients treated with XELOX or FOLFOX (n = 83) as adjuvant therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"endSection": "abstract",
"offsetInBeginSection": 1686,
"offsetInEndSection": 1842,
"text": "Prospective genotyping for the exon 14-skipping and the 2846A>T-polymorphisms may result in a reduction of serious, 5-FU-induced, toxic events of about 25%."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32546132",
"endSection": "abstract",
"offsetInBeginSection": 1343,
"offsetInEndSection": 1589,
"text": "There was no association between IVS14 + 1 G > A polymorphism and the occurrence of adverse reactions.CONCLUSION: FOLFOX and FOLFIRI were the most common regimens in CRC patients and their toxicity profile was different in some adverse reactions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 338,
"text": "About 9% of patients suffer from serious, sometimes even life-threatening adverse effects of a 5-FU therapy, such as haemotoxicity, which cannot be reliably predicted by conventional clinical and pharmacokinetic criteria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36980706",
"endSection": "abstract",
"offsetInBeginSection": 1113,
"offsetInEndSection": 1273,
"text": "These findings suggest the identification of future predictive biomarkers of effectiveness and toxicity in colorectal cancer patients treated with capecitabine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36980706",
"endSection": "abstract",
"offsetInBeginSection": 947,
"offsetInEndSection": 1112,
"text": "This systematic review reveals that several SNPs other than the four DPYD variants that are screened in clinical practice could have an impact on treatment outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33274825",
"endSection": "abstract",
"offsetInBeginSection": 1275,
"offsetInEndSection": 1587,
"text": "DPYD*2A test results were available in an average of 6 days, causing no significant delays in treatment initiation.CONCLUSION: Upfront genotyping before fluoropyrimidine-based treatment is feasible in clinical practice and can prevent severe toxicities and hospitalizations without delaying treatment initiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36890284",
"endSection": "abstract",
"offsetInBeginSection": 1156,
"offsetInEndSection": 1592,
"text": "Our patient may also have benefitted from compound heterozygosis, as shown by no evidence of disease (NED) at 6-month follow-up.CONCLUSION: Pharmacogenetic-guided dosing of DPYD intermediate metabolizer compound heterozygous HapB3 and c.2194G>A variant carries should be managed by a multidisciplinary team with a dose reduction ranging from 25 to 50% to maintain effectiveness and close clinical monitoring for early detection of ADRs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19239324",
"endSection": "abstract",
"offsetInBeginSection": 437,
"offsetInEndSection": 933,
"text": " The frequency of the polymorphism was examined in 156 patients with colorectal cancer and in 293 healthy controls. The polymorphism analysis was performed by amplifying exon 4 of p53 and digesting the products with restriction enzyme. The frequencies of genotypes: Arg/Arg, Arg/Pro and Pro/Pro were 34.6% (54/156), 43.0% (67/156) and 22.4% (35/156), respectively, in the cases with colorectal cancer, and 28.9% (114/293), 47.8% (140/293) and 13.3% (39/293), respectively, in the healthy controls"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24817302",
"endSection": "abstract",
"offsetInBeginSection": 67,
"offsetInEndSection": 184,
"text": "+1 G > A genotype of the dihydropyrimidine dehydrogenase (DPD) gene with plasma concentration of 5-fluorouracil (5-FU"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20637356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1686,
"text": "Colorectal cancer (CCR), which is one of the most common causes of cancer, has benefited from the major advances in the understanding of the intracellular signaling pathways implicated in the initiation, growing and local and metastasis dissemination of tumor, which have occurred during the 20 past years. The pharmacogenomics approach, especially the determination of the genetic polymorphisms, tries to find prognosis and predictive biomarkers permitting to identify patients who could benefit from a particular treatment or those exhibiting higher risks of toxicity. Among the numerous biomarkers, which have been studied, few are currently in use in clinical practice. The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan. For oxaliplatin, the determination of the polymorphisms of reparases and detoxification systems such as GSTpi seems interesting, but its exact place should be more defined. It is in the field of targeted therapies that the pharmacogenomics approach seems to be the more relevant. KRAS mutation is a dramatic example of single nucleotide polymorphism, which is able to identify a priori patients that could receive or not an anti-EGFR monoclonal antibody such as cetuximab or panitumumab. It is obvious that pre-clinical identification of molecular biomarkers predictive of the sensitivity of the drug targets, which subsequently implicate the selection of patients and the rational evaluation of responses, will be the cornerstone of any clinical trials concerning targeted therapies. Besides the determinati"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12749725",
"endSection": "abstract",
"offsetInBeginSection": 1538,
"offsetInEndSection": 2091,
"text": "Alterations in gene expression, protein expression and polymorphic variants in genes encoding thymidylate synthase, dihydropyrimidine dehydrogenase, dUTP nucleotidehydrolase and thymidine phosphorylase (for fluoropyrimidine-based chemotherapy), uridine diphosphate glucosyltransferase (UGT) 1A1 and carboxylesterase (for irinotecan therapy), and excision repair cross-complementing genes (ERCC1 and ERCC2) and glutathione-S-transferase P1 (for oxalilplatin-based regimens) may be useful as markers for clinical drug response, survival and host toxicity."
}
] | 13
|
BioASQ-training13b
| null | null |
65f77596c4010b4d7800002c
|
bioasq_yesno
|
yesno
|
Can saponins be used as adjuvant?
|
['yes']
|
[
"yes"
] |
['Yes,\nsaponin is an ideal adjuvant candidate.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32012760",
"http://www.ncbi.nlm.nih.gov/pubmed/32062145",
"http://www.ncbi.nlm.nih.gov/pubmed/32098409",
"http://www.ncbi.nlm.nih.gov/pubmed/31833496",
"http://www.ncbi.nlm.nih.gov/pubmed/32101001"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31833496",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "We report the design, synthesis, immunological evaluation, and conformational analysis of new saponin variants as promising vaccine adjuvants"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32012760",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "The purified active fraction of Albizia julibrissin saponin (AJSAF) is an ideal adjuvant candidate"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32062145",
"endSection": "abstract",
"offsetInBeginSection": 549,
"offsetInEndSection": 685,
"text": "BALB/c mice immunized with subcutaneous injections of the recombinant protein with or without liposome/saponin (Lip/Sap) as an adjuvant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32098409",
"endSection": "abstract",
"offsetInBeginSection": 347,
"offsetInEndSection": 382,
"text": " a saponin-based Matrix-Mâ„¢ adjuvant"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32101001",
"endSection": "abstract",
"offsetInBeginSection": 1049,
"offsetInEndSection": 1160,
"text": ". These results confirm that Momordica saponins are a viable natural source to provide potent saponin adjuvants"
}
] | 11
|
BioASQ-training11b
| null | null |
603291f21cb411341a000146
|
bioasq_yesno
|
factoid
|
Which component of the Influenza A Virus affects mRNA transcription termination?
|
['NS1', 'The IAV NS1 protein']
|
[
"NS1",
"IAV NS1 protein",
"Influenza A virus NS1 protein",
"NS1 protein",
"Non-structural protein 1",
"NS1 protein of Influenza A virus"
] |
['Defective Pol II termination occurs independently of the ability of the viral NS1 protein to interfere with host mRNA processing. Instead, this termination defect is a common effect of diverse cellular stresses and underlies the production of previously reported downstream-of-gene transcripts (DoGs).', "Influenza A virus (IAV) infection induces global transcriptional defects at the 3' ends of active host genes and RNA polymerase II (RNAPII) run-through into extragenic regions. This phenomenon occurs with multiple strains of IAV, is dependent on influenza NS1 protein, and can be modulated by SUMOylation of an intrinsically disordered region (IDR) of NS1 expressed by the 1918 pandemic IAV strain"]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21118126",
"http://www.ncbi.nlm.nih.gov/pubmed/6328745",
"http://www.ncbi.nlm.nih.gov/pubmed/29768209",
"http://www.ncbi.nlm.nih.gov/pubmed/30177761",
"http://www.ncbi.nlm.nih.gov/pubmed/18631147",
"http://www.ncbi.nlm.nih.gov/pubmed/21207185",
"http://www.ncbi.nlm.nih.gov/pubmed/1371285"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21207185",
"endSection": "abstract",
"offsetInBeginSection": 2059,
"offsetInEndSection": 2232,
"text": "Optimized conditions are presented for the T7 and SP6 phage polymerase systems to minimize these early termination events during in vitro transcription of H5 influenza vRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18631147",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 217,
"text": "Viruses have evolved a number of translational control mechanisms to regulate the levels of expression of viral proteins on polycistronic mRNAs, including programmed ribosomal frameshifting and stop codon readthrough."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18631147",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 350,
"text": "More recently, another unusual mechanism has been described, that of termination-dependent re-initiation (also known as stop-start)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1371285",
"endSection": "abstract",
"offsetInBeginSection": 1122,
"offsetInEndSection": 1464,
"text": "We conclude that (-)-carbovir 5'-triphosphate is a potent inhibitor of the HIV-1 reverse transcriptase enzyme and that (-)-carbovir most likely inhibits HIV by activity at the triphosphate level by a combination of direct competition for binding of the natural deoxynucleoside triphosphates to the reverse transcriptase and chain termination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21118126",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 291,
"text": " One such mechanism, that of termination-dependent reinitiation, has been described in a number of both negative- and positive-strand RNA viruses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21118126",
"endSection": "abstract",
"offsetInBeginSection": 459,
"offsetInEndSection": 708,
"text": " For example, the segment 7 RNA of influenza B is dicistronic, and the stop codon of the M1 ORF and the start codon of the BM2 ORF overlap in the pentanucleotide UAAUG (the stop codon of M1 is shown in bold and the start codon of BM2 is underlined)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21118126",
"endSection": "abstract",
"offsetInBeginSection": 1008,
"offsetInEndSection": 1220,
"text": "The present review summarizes how such interactions regulate reinitiation in an array of RNA viruses, and discusses what is known about reinitiation in viruses that do not rely on apparent mRNA-rRNA interactions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30177761",
"endSection": "abstract",
"offsetInBeginSection": 150,
"offsetInEndSection": 396,
"text": "Using cell biological, biochemical, and genetic tools, we reveal that influenza A virus (IAV) infection induces global transcriptional defects at the 3' ends of active host genes and RNA polymerase II (RNAPII) run-through into extragenic regions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30177761",
"endSection": "abstract",
"offsetInBeginSection": 637,
"offsetInEndSection": 857,
"text": "This phenomenon occurs with multiple strains of IAV, is dependent on influenza NS1 protein, and can be modulated by SUMOylation of an intrinsically disordered region (IDR) of NS1 expressed by the 1918 pandemic IAV strain"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6328745",
"endSection": "abstract",
"offsetInBeginSection": 914,
"offsetInEndSection": 1111,
"text": "These studies establish that during influenza virus infections processing of the NS1 mRNA transcript undergoes a mechanism of splicing similar to that occurring with DNA-directed RNA transcription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6328745",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Influenza virus gene 8 codes for two nonstructural proteins (NS1 and NS2) which are translated, respectively, from a colinear and an interrupted mRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29768209",
"endSection": "abstract",
"offsetInBeginSection": 585,
"offsetInEndSection": 714,
"text": "Defective Pol II termination occurs independently of the ability of the viral NS1 protein to interfere with host mRNA processing."
}
] | 11
|
BioASQ-training11b
| null | null |
5e4e3cee6d0a277941000030
|
bioasq_factoid
|
factoid
|
What class of drugs frequently has muscle pain and other muscle toxicities such as mysositis and rhabdomyolysis as a side effect?
|
['statins']
|
[
"statins",
"HMG-CoA reductase inhibitors",
"hydroxymethylglutaryl-CoA reductase inhibitors",
"lipid-lowering drugs",
"cholesterol-lowering medications"
] |
[' Muscular complaints are known side-effects of statin therapy, ranging from myalgia to clinically important myositis and rhabdomyolysis.', '3-hydroxy-3-methylglutaryl coenzyme A reductase reductase inhibitors (statins) are generally well tolerated, with statin-associated muscle symptoms (SAMS) the most common side effect (~10%) seen in statin users.', 'The most commonly experienced side-effect of statin medication is muscle pain', "A class of drug called a statin. It's a drug that works by reducing the amount of cholesterol in the body, which is what causes muscle fatigue.", 'statins are generally well tolerated, with statin-associated muscle symptoms (sams) the most common side effect (~10%) seen in statin users.', 'Statin use has been associated with an increased risk of glucocorticoid-induced rhabdomyolysis as well as with adverse effects such as mysositis and hypercholesterolemia.', '3-hydroxy-3-methylglutaryl coenzyme A reductase reductase inhibitors, a class of drugs called statins are generally well tolerated, with statin-associated muscle symptoms (SAMS) such as muscle pain, myositis, and rarely rhabdomyolysis, the most common side effect (~10%) seen in statin users.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17143099",
"http://www.ncbi.nlm.nih.gov/pubmed/19940267",
"http://www.ncbi.nlm.nih.gov/pubmed/20195425",
"http://www.ncbi.nlm.nih.gov/pubmed/26402985",
"http://www.ncbi.nlm.nih.gov/pubmed/27870723",
"http://www.ncbi.nlm.nih.gov/pubmed/33194498",
"http://www.ncbi.nlm.nih.gov/pubmed/17700359",
"http://www.ncbi.nlm.nih.gov/pubmed/12426921",
"http://www.ncbi.nlm.nih.gov/pubmed/16575599",
"http://www.ncbi.nlm.nih.gov/pubmed/15849374",
"http://www.ncbi.nlm.nih.gov/pubmed/11869826",
"http://www.ncbi.nlm.nih.gov/pubmed/15269925"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27870723",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 223,
"text": "3-hydroxy-3-methylglutaryl coenzyme A reductase reductase inhibitors (statins) are generally well tolerated, with statin-associated muscle symptoms (SAMS) the most common side effect (~10%) seen in statin users."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26402985",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 148,
"text": " Muscular complaints are known side-effects of statin therapy, ranging from myalgia to clinically important myositis and rhabdomyolysis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26402985",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 256,
"text": " the statin use and association with the presence and characteristics of muscular complaints."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26402985",
"endSection": "abstract",
"offsetInBeginSection": 1265,
"offsetInEndSection": 1362,
"text": "n the studied set of patients muscular symptoms were a rather frequent effect of statin therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15849374",
"endSection": "abstract",
"offsetInBeginSection": 360,
"offsetInEndSection": 635,
"text": "yopathy is included among the potential side-effects and toxicities associated with the lipid lowering agents, particularly 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors. However, the precise mechanism of statin-induced muscle toxicity remains unclear."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20195425",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Lipid lowering drugs, such as statins, are commonly used to treat approximately 10 million Canadians affected by hypercholesterolemia. The most commonly experienced side-effect of statin medication is muscle pain"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20195425",
"endSection": "abstract",
"offsetInBeginSection": 214,
"offsetInEndSection": 333,
"text": "Statin induced myopathy consists of a spectrum of myopathic disorders ranging from mild myalgia to fatal rhabdomyolysis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20195425",
"endSection": "abstract",
"offsetInBeginSection": 334,
"offsetInEndSection": 417,
"text": " The following is a presentation of 2 cases of statin induced myopathy in patients "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20195425",
"endSection": "abstract",
"offsetInBeginSection": 455,
"offsetInEndSection": 574,
"text": "In addition, discussion will surround the mechanism, predisposing risk factors and frequency of statin induced myopathy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15269925",
"endSection": "abstract",
"offsetInBeginSection": 434,
"offsetInEndSection": 550,
"text": "Rhabdomyolysis is a known, rare serious side effect of statin monotherapy and of statin-fibrate combination therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17700359",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 275,
"text": "Statin use is associated with a variety of overtly related muscle symptoms including muscle pain, myalgia, creatine kinase elevations without pain with myolysis and myositis (rhabdomyolysis), a potentially fatal side effect that led to the withdrawal of cerivastatin in 2001."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17700359",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "CYP2D6*4 polymorphism is associated with statin-induced muscle effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19940267",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 276,
"text": "Although statins are well tolerated, many patients develop myopathy manifesting as muscle aches and pain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19940267",
"endSection": "abstract",
"offsetInBeginSection": 277,
"offsetInEndSection": 333,
"text": "Rhabdomyolysis is a rare but severe toxicity of statins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16575599",
"endSection": "abstract",
"offsetInBeginSection": 959,
"offsetInEndSection": 1135,
"text": "The drugs which most frequently induce muscular side effects are steroids, statins, fibrates, antiretrovirals, immunosuppressants, colchicine, amiodarone, and anticancer drugs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16575599",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 283,
"text": "Muscular side effects of various anesthetics, analgetics, antibiotics, antihistaminic drugs, antiretrovirals, cardiotropics, immunosuppressants, lipid-lowering drugs, psychotropic drugs, anticancer drugs, and other substances are more frequent than assumed and are easily overlooked."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33194498",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 211,
"text": "Muscle pain is a frequent adverse effect of statins."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11869826",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 54,
"text": "Myopathy and rhabdomyolysis with lipid-lowering drugs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17143099",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "PURPOSE OF REVIEW: Lipid-lowering drugs are associated with myotoxicity, which ranges in severity from myalgias to rhabdomyolysis resulting in renal"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12426921",
"endSection": "abstract",
"offsetInBeginSection": 148,
"offsetInEndSection": 350,
"text": "Myopathy caused by HMG-CoA reductase inhibitors (statins) alone is rare, but occurs more frequently when a statin is used with gemfibrozil, a medication that likely has a direct toxic effect on muscles."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17143099",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 49,
"text": "Myotoxicity associated with lipid-lowering drugs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12426921",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Rhabdomyolysis from the combination of a statin and gemfibrozil: an uncommon but serious adverse reaction."
}
] | 11
|
BioASQ-training11b
| null | null |
601ff4a61cb411341a000076
|
bioasq_factoid
|
yesno
|
Is apremilast effective for psoriatic arthritis?
|
['yes']
|
[
"yes"
] |
['Yes, apremilast, an oral phosphodiesterase 4 inhibitor, is effective for psoriatic arthritis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26220911",
"http://www.ncbi.nlm.nih.gov/pubmed/25633241",
"http://www.ncbi.nlm.nih.gov/pubmed/27272887",
"http://www.ncbi.nlm.nih.gov/pubmed/26644232",
"http://www.ncbi.nlm.nih.gov/pubmed/27022911",
"http://www.ncbi.nlm.nih.gov/pubmed/26806620",
"http://www.ncbi.nlm.nih.gov/pubmed/26923915",
"http://www.ncbi.nlm.nih.gov/pubmed/27486641",
"http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"http://www.ncbi.nlm.nih.gov/pubmed/27747762",
"http://www.ncbi.nlm.nih.gov/pubmed/27836567",
"http://www.ncbi.nlm.nih.gov/pubmed/25973439",
"http://www.ncbi.nlm.nih.gov/pubmed/23134988",
"http://www.ncbi.nlm.nih.gov/pubmed/22257911",
"http://www.ncbi.nlm.nih.gov/pubmed/27307707",
"http://www.ncbi.nlm.nih.gov/pubmed/27168275",
"http://www.ncbi.nlm.nih.gov/pubmed/25827658",
"http://www.ncbi.nlm.nih.gov/pubmed/23569359",
"http://www.ncbi.nlm.nih.gov/pubmed/23580094",
"http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"http://www.ncbi.nlm.nih.gov/pubmed/27538241",
"http://www.ncbi.nlm.nih.gov/pubmed/26660203",
"http://www.ncbi.nlm.nih.gov/pubmed/24797159",
"http://www.ncbi.nlm.nih.gov/pubmed/26807876",
"http://www.ncbi.nlm.nih.gov/pubmed/26503917",
"http://www.ncbi.nlm.nih.gov/pubmed/26792812"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26792812",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Apremilast, an oral phosphodiesterase 4 inhibitor, in patients with psoriatic arthritis and current skin involvement: a phase III, randomised, controlled trial (PALACE 3)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26792812",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "OBJECTIVE: To evaluate apremilast treatment in patients with active psoriatic arthritis, including current skin involvement, despite prior therapy with conventional disease-modifying antirheumatic drugs and/or biologic agents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26792812",
"endSection": "abstract",
"offsetInBeginSection": 1638,
"offsetInEndSection": 1835,
"text": "CONCLUSIONS: Apremilast demonstrated clinically meaningful improvements in psoriatic arthritis and psoriasis at week 16; sustained improvements were seen with continued treatment through 52 weeks. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Apremilast: A Novel Drug for Treatment of Psoriasis and Psoriatic Arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "OBJECTIVE: To review the pharmacology, efficacy, and safety of apremilast and determine its role relative to other agents in the treatment of psoriasis and psoriatic arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1495,
"text": "CONCLUSIONS: Apremilast has a novel mechanism of action and is safe and effective for the management of psoriasis and psoriatic arthritis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26806620",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 269,
"text": " In particular, apremilast has been recently approved for the treatment of psoriasis and psoriatic arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27538241",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Apremilast, an oral phosphodiesterase 4 inhibitor, has an acceptable safety profile and is effective for treatment of plaque psoriasis and psoriatic arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27272887",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 399,
"text": "As part of the National Institute for Health and Clinical Excellence (NICE) single technology appraisal (STA) process, the manufacturer of apremilast was invited to submit evidence for its clinical and cost effectiveness for the treatment of active psoriatic arthritis (PsA) for whom disease-modifying anti-rheumatic drugs (DMARDs) have been inadequately effective, not tolerated or contraindicated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"endSection": "abstract",
"offsetInBeginSection": 84,
"offsetInEndSection": 331,
"text": "Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active psoriatic arthritis despite prior traditional disease-modifying antirheumatic drug (DMARD) and/or biologic therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27486641",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1095,
"text": "In patients with psoriatic arthritis, there are no clinical trials comparing apremilast with TNF alpha antagonists, and no interpretable trials of apremilast after failure of a TNF alpha antagonist."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"endSection": "abstract",
"offsetInBeginSection": 85,
"offsetInEndSection": 497,
"text": "Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active psoriatic arthritis despite prior traditional disease-modifying antirheumatic drug (DMARD) and/or biologic therapy.In the 24-week, placebo-controlled phase of PALACE 1, patients (N=504) were randomised (1:1:1) to placebo, apremilast 20 mg twice a day (BID) or apremilast 30 mg BID"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"endSection": "abstract",
"offsetInBeginSection": 1563,
"offsetInEndSection": 1816,
"text": "No imbalance in major adverse cardiac events, serious or opportunistic infections, malignancies or laboratory abnormalities was observed.Apremilast was effective in the treatment of psoriatic arthritis, improving signs and symptoms and physical function"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23134988",
"endSection": "abstract",
"offsetInBeginSection": 92,
"offsetInEndSection": 583,
"text": "Apremilast is a novel oral PDE4 enzyme inhibitor capable of blocking leukocyte production of IL-12, IL-23, TNF-a, INF- with subsequent suppression of Th1 and Th17-mediated immune responses, and proven clinical efficacy for psoriasis as well as rheumatoid and psoriatic arthritis.Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) showed a significant (P<0.05) decrease after 85 days of treatment with apremilast 20 mg twice daily in 8 patients with active discoid lupus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25633241",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 397,
"text": "The purpose of this study is to give an overview of the new treatments approved by the U.S. Food and Drug Administration (FDA) for use in psoriatic arthritis (PsA).FDA has approved three new drugs for PsA: Certolizumab-pegol: a PEGylated Fc-free tumour necrosis factor inhibitor (TNFi); ustekinumab: an anti interleukin (IL)-12 and IL-23 mAb; and apremilast and oral phosphodiesterase 4 inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1403,
"text": "In all trials, the drug had an acceptable safety profile, with the most common adverse effects of diarrhea, nausea, and headache.Apremilast has a novel mechanism of action and is safe and effective for the management of psoriasis and psoriatic arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27307707",
"endSection": "abstract",
"offsetInBeginSection": 418,
"offsetInEndSection": 597,
"text": "Apremilast is a well-tolerated and effective phosphodiesterase type 4 inhibitor that is indicated for the treatment of moderate-to-severe plaque psoriasis and psoriatic arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"endSection": "abstract",
"offsetInBeginSection": 85,
"offsetInEndSection": 498,
"text": "Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active psoriatic arthritis despite prior traditional disease-modifying antirheumatic drug (DMARD) and/or biologic therapy.In the 24-week, placebo-controlled phase of PALACE 1, patients (N=504) were randomised (1:1:1) to placebo, apremilast 20 mg twice a day (BID) or apremilast 30 mg BID."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23580094",
"endSection": "abstract",
"offsetInBeginSection": 756,
"offsetInEndSection": 961,
"text": "Newer drugs in the treatment armamentarium that have shown efficacy for both psoriasis and psoriatic arthritis consist of the anti-IL-17 agent, secukinumab, and a phosphodiesterase-4 inhibitor, apremilast."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 397,
"text": "To review the pharmacology, efficacy, and safety of apremilast and determine its role relative to other agents in the treatment of psoriasis and psoriatic arthritis.A PubMed search (1946 to December 2015) using the terms apremilast and CC-10004 was conducted to identify relevant articles.In vitro or in vivo evaluations of apremilast published in the English language were eligible for inclusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27486641",
"endSection": "abstract",
"offsetInBeginSection": 903,
"offsetInEndSection": 1101,
"text": "In patients with psoriatic arthritis, there are no clinical trials comparing apremilast with TNF alpha antagonists, and no interpretable trials of apremilast after failure of a TNF alpha antagonist."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"endSection": "abstract",
"offsetInBeginSection": 1563,
"offsetInEndSection": 1817,
"text": "No imbalance in major adverse cardiac events, serious or opportunistic infections, malignancies or laboratory abnormalities was observed.Apremilast was effective in the treatment of psoriatic arthritis, improving signs and symptoms and physical function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23134988",
"endSection": "abstract",
"offsetInBeginSection": 92,
"offsetInEndSection": 581,
"text": "Apremilast is a novel oral PDE4 enzyme inhibitor capable of blocking leukocyte production of IL-12, IL-23, TNF-a, INF- with subsequent suppression of Th1 and Th17-mediated immune responses, and proven clinical efficacy for psoriasis as well as rheumatoid and psoriatic arthritis.Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) showed a significant (P<0.05) decrease after 85 days of treatment with apremilast 20 mg twice daily in 8 patients with active discoid lupus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"endSection": "abstract",
"offsetInBeginSection": 1700,
"offsetInEndSection": 1817,
"text": "Apremilast was effective in the treatment of psoriatic arthritis, improving signs and symptoms and physical function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 1282,
"offsetInEndSection": 1407,
"text": "Apremilast has a novel mechanism of action and is safe and effective for the management of psoriasis and psoriatic arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25973439",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 250,
"text": "Apremilast, an oral phosphodiesterase 4 inhibitor, demonstrated effectiveness (versus placebo) for treatment of active psoriatic arthritis in the psoriatic arthritis long-term assessment of clinical efficacy (PALACE) phase III clinical trial program."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"endSection": "abstract",
"offsetInBeginSection": 85,
"offsetInEndSection": 332,
"text": "Psoriatic Arthritis Long-term Assessment of Clinical Efficacy 1 (PALACE 1) compared apremilast with placebo in patients with active psoriatic arthritis despite prior traditional disease-modifying antirheumatic drug (DMARD) and/or biologic therapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26220911",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 59,
"text": "Apremilast: A Review in Psoriasis and Psoriatic Arthritis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25827658",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Drug safety evaluation of apremilast for treating psoriatic arthritis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26503917",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 53,
"text": "Apremilast for the treatment of psoriatic arthritis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22257911",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Apremilast mechanism of action and application to psoriasis and psoriatic arthritis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27747762",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Apremilast: A Phosphodiesterase 4 Inhibitor for the Treatment of Psoriatic Arthritis."
}
] | 6
|
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015535",
"http://www.disease-ontology.org/api/metadata/DOID:9008"
] |
[
{
"o": "APREMILAST",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1678805"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A15589751",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1678805"
},
{
"o": "apremilast",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A15589751"
}
] |
5896e22078275d0c4a000014
|
bioasq_yesno
|
factoid
|
What is the role of TAD protein domain?
|
['transcription activation domain', 'transactivation domain', 'trans-activating domain']
|
[
"transcription activation domain",
"transactivation domain",
"trans-activating domain",
"transcriptional activation domain",
"transcriptional activation region",
"transcription activation region"
] |
['TAD domain is a transcription activation domain found in transcription factors.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26537679",
"http://www.ncbi.nlm.nih.gov/pubmed/17404593",
"http://www.ncbi.nlm.nih.gov/pubmed/17332356",
"http://www.ncbi.nlm.nih.gov/pubmed/27196604",
"http://www.ncbi.nlm.nih.gov/pubmed/9826771",
"http://www.ncbi.nlm.nih.gov/pubmed/27713878",
"http://www.ncbi.nlm.nih.gov/pubmed/15003254",
"http://www.ncbi.nlm.nih.gov/pubmed/16101299",
"http://www.ncbi.nlm.nih.gov/pubmed/10490619",
"http://www.ncbi.nlm.nih.gov/pubmed/18243147",
"http://www.ncbi.nlm.nih.gov/pubmed/14645574",
"http://www.ncbi.nlm.nih.gov/pubmed/11223263",
"http://www.ncbi.nlm.nih.gov/pubmed/17804822",
"http://www.ncbi.nlm.nih.gov/pubmed/22949507",
"http://www.ncbi.nlm.nih.gov/pubmed/26147604",
"http://www.ncbi.nlm.nih.gov/pubmed/24019758",
"http://www.ncbi.nlm.nih.gov/pubmed/17233836",
"http://www.ncbi.nlm.nih.gov/pubmed/27502417",
"http://www.ncbi.nlm.nih.gov/pubmed/26029824",
"http://www.ncbi.nlm.nih.gov/pubmed/8086335",
"http://www.ncbi.nlm.nih.gov/pubmed/24675874",
"http://www.ncbi.nlm.nih.gov/pubmed/15663936",
"http://www.ncbi.nlm.nih.gov/pubmed/16226227",
"http://www.ncbi.nlm.nih.gov/pubmed/25961797",
"http://www.ncbi.nlm.nih.gov/pubmed/26476216",
"http://www.ncbi.nlm.nih.gov/pubmed/19220000",
"http://www.ncbi.nlm.nih.gov/pubmed/19319663",
"http://www.ncbi.nlm.nih.gov/pubmed/15641800",
"http://www.ncbi.nlm.nih.gov/pubmed/8561893",
"http://www.ncbi.nlm.nih.gov/pubmed/16596634",
"http://www.ncbi.nlm.nih.gov/pubmed/20969867",
"http://www.ncbi.nlm.nih.gov/pubmed/8806843",
"http://www.ncbi.nlm.nih.gov/pubmed/23110116"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27713878",
"endSection": "abstract",
"offsetInBeginSection": 367,
"offsetInEndSection": 567,
"text": " Thus, nuclear ERK5 activates transcription factors by either direct phosphorylation or acting as co-activator thanks to a unique transcriptional activation TAD domain located at its C-terminal tail. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27713878",
"endSection": "abstract",
"offsetInBeginSection": 1425,
"offsetInEndSection": 1560,
"text": "Although lacking kinase activity, these forms activate transcription by interacting with transcription factors through the TAD domain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15003254",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 579,
"text": "Myc has an N-terminal transcription activation domain (TAD) that interacts with various coactivators and a C-terminal basic-helix-loop-helix-leucine zipper (bHLHZip) domain required for E box-specific DNA-binding and heterodimerization with its obligatory bHLHZip protein partner Max. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26476216",
"endSection": "abstract",
"offsetInBeginSection": 542,
"offsetInEndSection": 718,
"text": "p300 worked synergistically with MRTF-A to activate the transcription of MYH9, MYL9 and CYR61. As identified by co-IP, p300 interacted with the C-terminal TAD domain of MRTF-A."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14645574",
"endSection": "abstract",
"offsetInBeginSection": 343,
"offsetInEndSection": 709,
"text": "To investigate further the role of cytoplasmic sequestration of p53 in its inhibition by the E1B 55-kDa protein we systematically examined domains in both the Ad12 55-kDa protein and p53 that underpin their colocalization in the cytoplasmic body and show that the N-terminal transactivation domain (TAD) of p53 is essential for retaining p53 in the cytoplasmic body."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20969867",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "Physical interaction between the transactivation domain (TAD) of the mixed-lineage leukemia protein (MLL) and the KIX domain of the cyclic-AMP response element binding protein (CREB) binding protein (CBP) is necessary for MLL-mediated transcriptional activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26537679",
"endSection": "abstract",
"offsetInBeginSection": 173,
"offsetInEndSection": 388,
"text": "The IE62 possesses several domains essential for trans-activation, including an acidic trans-activation domain (TAD), a serine-rich tract (SRT), and binding domains for USF, TFIIB, and TATA box binding protein (TBP)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14645574",
"endSection": "abstract",
"offsetInBeginSection": 346,
"offsetInEndSection": 712,
"text": "To investigate further the role of cytoplasmic sequestration of p53 in its inhibition by the E1B 55-kDa protein we systematically examined domains in both the Ad12 55-kDa protein and p53 that underpin their colocalization in the cytoplasmic body and show that the N-terminal transactivation domain (TAD) of p53 is essential for retaining p53 in the cytoplasmic body."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22949507",
"endSection": "abstract",
"offsetInBeginSection": 278,
"offsetInEndSection": 473,
"text": "We have characterized two transcription activation domains (TADs) in Da, called activation domain 1 (AD1) and loop-helix (LH), and have evaluated their roles in promoting peripheral neurogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17332356",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 452,
"text": "Particularly, the intrinsic histone acetyltransferase (HAT) activity and transactivation domains (TAD) play essential roles for their coactivating function."
}
] | 6
|
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012380"
] |
[
{
"o": "TAD",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0280090"
}
] |
58dcb47c8acda34529000020
|
bioasq_factoid
|
yesno
|
Is PRDM9 essential for meiosis?
|
['yes']
|
[
"yes"
] |
['PRDM9 is essential for the progression through early meiotic prophase, including double strand break repair, homologous chromosome pairing, and sex body formation during spermatogenesis.', 'In aggregate, our data indicate that domains typically involved in regulation of gene expression do not serve that role in PRDM9, but are likely involved in setting the proper chromatin environment for initiation and completion of homologous recombination. PRDM9 Methyltransferase Activity Is Essential for Meiotic DNA Double-Strand Break Formation at Its Binding Sites.', 'yes, Our findings do not identify the nature of the underlying DNA sequences, but argue against the proposed role of Prdm9 as an essential transcription factor in mouse meiosis', 'Prdm9, is a meiosis-specific protein that trimethylates h3k4 and controls the activation of recombination hot spots. It is an essential enzyme in the progression of early meiotic prophase.', 'Yes. PRDM9 is an evolutionarily conserved protein that is essential for meiosis.', 'In many eukaryotes, sites of meiotic recombination, also called hotspots, are regions of accessible chromatin, but in many vertebrates, their location follows a distinct pattern and is specified by PR domain-containing protein 9 (PRDM9). PRDM9 Methyltransferase Activity Is Essential for Meiotic DNA Double-Strand Break Formation at Its Binding Sites.', 'Yes, PRDM9 is essential for meiosis.', 'Yes. PRDM9 is an RNA-binding protein that is essential for meiosis.', 'Yes. PRDM9 is an essential factor for meiosis.', 'PRDM9 Methyltransferase Activity Is Essential for Meiotic DNA Double-Strand Break Formation at Its Binding Sites.', 'PRDM9 is essential for the progression through early meiotic prophase, including double strand break repair, homologous chromosome pairing, and sex body formation during spermatogenesis. PRDM9 (PR domain-containing protein 9) is a meiosis-specific protein that trimethylates H3K4 and controls the activation of recombination hot spots.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29674518",
"http://www.ncbi.nlm.nih.gov/pubmed/19997497",
"http://www.ncbi.nlm.nih.gov/pubmed/24634223",
"http://www.ncbi.nlm.nih.gov/pubmed/23190393",
"http://www.ncbi.nlm.nih.gov/pubmed/30161134",
"http://www.ncbi.nlm.nih.gov/pubmed/29478809"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19997497",
"endSection": "abstract",
"offsetInBeginSection": 1468,
"offsetInEndSection": 1639,
"text": "Our findings do not identify the nature of the underlying DNA sequences, but argue against the proposed role of Prdm9 as an essential transcription factor in mouse meiosis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23190393",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "PRDM9 gene polymorphism may not be associated with defective spermatogenesis in the Chinese Han population"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23190393",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "PRDM9 is essential for the progression through early meiotic prophase, including double strand break repair, homologous chromosome pairing, and sex body formation during spermatogenesis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24634223",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "PRDM9 (PR domain-containing protein 9) is a meiosis-specific protein that trimethylates H3K4 and controls the activation of recombination hot spots. It is an essential enzyme in the progression of early meiotic prophase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30161134",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 404,
"text": "In many eukaryotes, sites of meiotic recombination, also called hotspots, are regions of accessible chromatin, but in many vertebrates, their location follows a distinct pattern and is specified by PR domain-containing protein 9 (PRDM9). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29674518",
"endSection": "abstract",
"offsetInBeginSection": 739,
"offsetInEndSection": 1252,
"text": " We found that although the post-SET zinc finger and the KRAB domains are not essential for the methyltransferase activity of PRDM9 in cell culture, the KRAB domain mutant mice show only residual PRDM9 methyltransferase activity and undergo meiotic arrest. In aggregate, our data indicate that domains typically involved in regulation of gene expression do not serve that role in PRDM9, but are likely involved in setting the proper chromatin environment for initiation and completion of homologous recombination."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29478809",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "PRDM9 Methyltransferase Activity Is Essential for Meiotic DNA Double-Strand Break Formation at Its Binding Sites."
}
] | 11
|
BioASQ-training11b
| null | null |
5d3856ca7bc3fee31f000016
|
bioasq_yesno
|
yesno
|
Can fingolimod be used during pregnancy?
|
['no']
|
[
"no"
] |
['No. Fingolimod has teratogenic potential and therefore should not be used during pregnancy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34310364",
"http://www.ncbi.nlm.nih.gov/pubmed/36174258",
"http://www.ncbi.nlm.nih.gov/pubmed/31185372",
"http://www.ncbi.nlm.nih.gov/pubmed/33443836",
"http://www.ncbi.nlm.nih.gov/pubmed/35088492",
"http://www.ncbi.nlm.nih.gov/pubmed/32564333",
"http://www.ncbi.nlm.nih.gov/pubmed/30542374",
"http://www.ncbi.nlm.nih.gov/pubmed/35390594",
"http://www.ncbi.nlm.nih.gov/pubmed/35428205",
"http://www.ncbi.nlm.nih.gov/pubmed/23961604",
"http://www.ncbi.nlm.nih.gov/pubmed/28078140",
"http://www.ncbi.nlm.nih.gov/pubmed/37307691",
"http://www.ncbi.nlm.nih.gov/pubmed/22926165",
"http://www.ncbi.nlm.nih.gov/pubmed/37341330",
"http://www.ncbi.nlm.nih.gov/pubmed/37217309"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37307691",
"endSection": "abstract",
"offsetInBeginSection": 1570,
"offsetInEndSection": 1775,
"text": "Interferon beta 1a SC was preferred over other treatments for patients with mild to moderate MS and planning for pregnancy (56.6%) or breastfeeding (60.2%). Fingolimod was not a choice for these patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35428205",
"endSection": "abstract",
"offsetInBeginSection": 1985,
"offsetInEndSection": 2389,
"text": "In total, 45 patients (18.8%) permanently discontinued treatment because of AEs related to study drug; two patients reported pregnancy after treatment initiation and subsequently discontinued the treatment; no deaths were reported.CONCLUSION: GOLEMS study demonstrated the sustained effectiveness and manageable safety profile of fingolimod under real-world conditions over 48 months in patients with MS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35390594",
"endSection": "abstract",
"offsetInBeginSection": 1568,
"offsetInEndSection": 1893,
"text": "Concerns about COVID-19 had a noticeable impact on administering high efficacy drugs like rituximab and fingolimod. However, in male patients this approach has not been the case. It may be related to more aggressive disease course in this group. The other possible explanation could be planning for pregnancy in female cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36174258",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "BACKGROUND: Authorizations of fingolimod, teriflunomide and cladribine were accompanied by risk minimization measures concerning their teratogenic potential."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33443836",
"endSection": "abstract",
"offsetInBeginSection": 503,
"offsetInEndSection": 600,
"text": "Fingolimod : contraindicated during pregnancy due to suspected risk of congenital malformations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34310364",
"endSection": "abstract",
"offsetInBeginSection": 489,
"offsetInEndSection": 706,
"text": "Drugs with a known potential of teratogenicity such as fingolimod or teriflunomide should be avoided and recommended wash-out times for medications such as cladribine, alemtuzumab or ocrelizumab should be considered. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37341330",
"endSection": "abstract",
"offsetInBeginSection": 226,
"offsetInEndSection": 433,
"text": "Caution should be exercised when prescribing fingolimod and natalizumab to patients with multiple sclerosis who are of childbearing potential because of the risk of disease rebound when they are discontinued"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28078140",
"endSection": "abstract",
"offsetInBeginSection": 980,
"offsetInEndSection": 1095,
"text": "Current evidence supports the contraindication for fingolimod during pregnancy; data on other DMTs remains limited."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23961604",
"endSection": "abstract",
"offsetInBeginSection": 436,
"offsetInEndSection": 604,
"text": "Fingolimod is suspected to be harmful for fetal development, and the use of this drug should be stopped no later than two months before discontinuing the contraception."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22926165",
"endSection": "abstract",
"offsetInBeginSection": 636,
"offsetInEndSection": 770,
"text": "Conception should be discouraged for patients on fingolimod, because of the limited information available on human pregnancy outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32564333",
"endSection": "abstract",
"offsetInBeginSection": 1081,
"offsetInEndSection": 1308,
"text": "If a patient becomes pregnant while taking fingolimod, and requires continued DMD treatment, a switch to interferon β or natalizumab after a variable washout period may be prescribed, depending on the level of disease activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31185372",
"endSection": "abstract",
"offsetInBeginSection": 254,
"offsetInEndSection": 432,
"text": "it is recommended that multiple sclerosis patients undergoing treatment with fingolimod use contraceptive methods for at least two months after discontinuation of the medication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30542374",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 522,
"text": "BACKGROUND AND METHODS: Limited data are available on the safety of fingolimod in pregnant women. We estimated the risk of adverse pregnancy outcomes in women with multiple sclerosis (MS) exposed to fingolimod either shortly before or during pregnancy in prospectively collected cases from clinical trials, observational studies, surveillance programs, and spontaneous reports.RESULTS: The prevalence of major malformations among live births does not appear to be significantly higher than those in the general population "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37217309",
"endSection": "abstract",
"offsetInBeginSection": 26,
"offsetInEndSection": 134,
"text": "Discontinuation of fingolimod ≥2 months before pregnancy is recommended to minimize potential teratogenicity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37217309",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 293,
"text": "BACKGROUND AND OBJECTIVE: Discontinuation of fingolimod ≥2 months before pregnancy is recommended to minimize potential teratogenicity. The magnitude of MS pregnancy relapse risk, particularly severe relapses, after fingolimod cessation is unclear, as is whether this risk is reduced by pregna"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33443836",
"endSection": "abstract",
"offsetInBeginSection": 503,
"offsetInEndSection": 599,
"text": "Fingolimod : contraindicated during pregnancy due to suspected risk of congenital malformations."
}
] | 13
|
BioASQ-training13b
| null | null |
65d12ae11930410b13000030
|
bioasq_yesno
|
yesno
|
Is there a dependence between chromatin organization and dorsoventral gene expression in Drosophila?
|
['no']
|
[
"no"
] |
['No. There is independence of chromatin conformation and gene regulation during Drosophila dorsoventral patterning', 'No. There is evidence for the independence of chromatin organization and dorsoventral gene expression in Drosophila. Tissue-specific chromatin conformation is not necessary for tissue-specific gene expression but rather acts as a scaffold facilitating gene expression when enhancers become active.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33795866"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33795866",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Independence of chromatin conformation and gene regulation during Drosophila dorsoventral patterning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33795866",
"endSection": "abstract",
"offsetInBeginSection": 503,
"offsetInEndSection": 1144,
"text": "Here, using the dorsoventral patterning of the Drosophila melanogaster embryo as a model system, we provide evidence for the independence of chromatin organization and dorsoventral gene expression. We define tissue-specific enhancers and link them to expression patterns using single-cell RNA-seq. Surprisingly, despite tissue-specific chromatin states and gene expression, chromatin organization is largely maintained across tissues. Our results indicate that tissue-specific chromatin conformation is not necessary for tissue-specific gene expression but rather acts as a scaffold facilitating gene expression when enhancers become active."
}
] | 11
|
BioASQ-training11b
| null | null |
6201a85cc9dfcb9c0900002a
|
bioasq_yesno
|
factoid
|
Central Vein Sign is characteristic to which disease?
|
['multiple sclerosis']
|
[
"multiple sclerosis",
"MS",
"sclerosis multiplex",
"disseminated sclerosis"
] |
['Central vein sign on FLAIR* magnetic resonance imaging is highly specific and sensitive for multiple sclerosis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28820013",
"http://www.ncbi.nlm.nih.gov/pubmed/31796822",
"http://www.ncbi.nlm.nih.gov/pubmed/30213803",
"http://www.ncbi.nlm.nih.gov/pubmed/29369733",
"http://www.ncbi.nlm.nih.gov/pubmed/29328521",
"http://www.ncbi.nlm.nih.gov/pubmed/29565219",
"http://www.ncbi.nlm.nih.gov/pubmed/27300318",
"http://www.ncbi.nlm.nih.gov/pubmed/27834394",
"http://www.ncbi.nlm.nih.gov/pubmed/31424490",
"http://www.ncbi.nlm.nih.gov/pubmed/29514948",
"http://www.ncbi.nlm.nih.gov/pubmed/31668125"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28820013",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Diagnostic performance of central vein sign for multiple sclerosis with a simplified three-lesion algorithm."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28820013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "BACKGROUND: Detection of a \"central vein sign\" (CVS) on FLAIR* magnetic resonance imaging (MRI) is highly specific and sensitive for multiple sclerosis (MS). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28820013",
"endSection": "abstract",
"offsetInBeginSection": 1164,
"offsetInEndSection": 1426,
"text": "CONCLUSION: A simplified determination of CVS in three white matter lesions on 3T FLAIR* MRI demonstrated good specificity and sensitivity and fair inter-rater reliability for a diagnosis of MS and with further study, may be a candidate for clinical application."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29328521",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Central vein sign differentiates Multiple Sclerosis from central nervous system inflammatory vasculopathies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29328521",
"endSection": "abstract",
"offsetInBeginSection": 232,
"offsetInEndSection": 544,
"text": "Detection of perivenular lesions in the brain (the \"central vein sign\") improves the pathological specificity of MS diagnosis, but comprehensive evaluation of this MRI biomarker in MS-mimicking inflammatory and/or autoimmune diseases, such as central nervous system (CNS) inflammatory vasculopathies, is lacking."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29328521",
"endSection": "abstract",
"offsetInBeginSection": 1785,
"offsetInEndSection": 1924,
"text": "INTERPRETATION: The central vein sign differentiates inflammatory CNS vasculopathies from MS at standard clinical magnetic field strengths."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29369733",
"endSection": "abstract",
"offsetInBeginSection": 337,
"offsetInEndSection": 534,
"text": "Areas covered: An overview of 7T MRI applications in MS focusing on increased sensitivity for lesion detection, specificity of the central vein sign and better understanding of MS pathophysiology. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29514948",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Value of the central vein sign at 3T to differentiate MS from seropositive NMOSD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29514948",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "OBJECTIVE: To assess the value of the central vein sign (CVS) on a clinical 3T scanner to distinguish between multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29514948",
"endSection": "abstract",
"offsetInBeginSection": 1408,
"offsetInEndSection": 1575,
"text": "CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that the CVS on 3T MRI accurately distinguishes patients with MS from those with seropositive NMOSD."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31424490",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Evaluation of the Central Vein Sign as a Diagnostic Imaging Biomarker in Multiple Sclerosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31424490",
"endSection": "abstract",
"offsetInBeginSection": 387,
"offsetInEndSection": 595,
"text": "Objective\n\nTo evaluate the sensitivity and specificity of various central vein sign lesion criteria for differentiating MS from non-MS conditions using 3T brain MRI with various commonly used pulse sequences."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31424490",
"endSection": "abstract",
"offsetInBeginSection": 2518,
"offsetInEndSection": 2655,
"text": "The sensitivity was 68.1% and specificity was 82.9% for distinguishing MS from not MS using a 35% central vein sign proportion threshold."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31424490",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "Importance\n\nThe central vein sign has been proposed as a specific imaging biomarker for distinguishing between multiple sclerosis (MS) and not MS, mainly based on findings from ultrahigh-field magnetic resonance imaging (MRI) studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31424490",
"endSection": "abstract",
"offsetInBeginSection": 2823,
"offsetInEndSection": 3125,
"text": "Conclusions and Relevance\n\nIn this study, use of the central vein sign at 3T MRI yielded a high specificity and a moderate sensitivity in differentiating MS from not MS; international, multicenter studies may be needed to ascertain whether the central vein sign-based criteria can accurately detect MS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29565219",
"endSection": "abstract",
"offsetInBeginSection": 1556,
"offsetInEndSection": 1801,
"text": "Conclusion The presence of the central vein sign on susceptibility-weighted images for MS lesions improves the understanding of the periventricular distribution of MS lesions and could contribute as adjunctive diagnostic criteria for MS disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31668125",
"endSection": "abstract",
"offsetInBeginSection": 1274,
"offsetInEndSection": 1349,
"text": "The central vein sign should be considered as a diagnostic biomarker in MS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31668125",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 247,
"text": "The central vein sign has the potential to be a non-invasive, MS-specific biomarker."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31796822",
"endSection": "abstract",
"offsetInBeginSection": 404,
"offsetInEndSection": 511,
"text": "Original articles investigating central vein sign on T2*-weighted images of patients with MS were selected."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30213803",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "BACKGROUND AND PURPOSE\n\nThe central vein sign is a promising MR imaging diagnostic biomarker for multiple sclerosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31668125",
"endSection": "abstract",
"offsetInBeginSection": 1283,
"offsetInEndSection": 1358,
"text": "The central vein sign should be considered as a diagnostic biomarker in MS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30213803",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "BACKGROUND AND PURPOSE The central vein sign is a promising MR imaging diagnostic biomarker for multiple sclerosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27834394",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 336,
"text": "The central vein sign ( CVS ) has recently been proposed as a novel MRI biomarker to improve the accuracy and speed of MS diagnosis . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30213803",
"endSection": "abstract",
"offsetInBeginSection": 94,
"offsetInEndSection": 288,
"text": "Recent studies have demonstrated that patients with MS have higher proportions of white matter lesions with the central vein sign compared with those with diseases that mimic MS on MR imaging . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29565219",
"endSection": "abstract",
"offsetInBeginSection": 1556,
"offsetInEndSection": 1802,
"text": "Conclusion The presence of the central vein sign on susceptibility-weighted images for MS lesions improves the understanding of the periventricular distribution of MS lesions and could contribute as adjunctive diagnostic criteria for MS disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29328521",
"endSection": "abstract",
"offsetInBeginSection": 1791,
"offsetInEndSection": 1930,
"text": "INTERPRETATION\nThe central vein sign differentiates inflammatory CNS vasculopathies from MS at standard clinical magnetic field strengths."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31668125",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 248,
"text": "The central vein sign has the potential to be a non-invasive, MS-specific biomarker."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31668125",
"endSection": "abstract",
"offsetInBeginSection": 1282,
"offsetInEndSection": 1358,
"text": "The central vein sign should be considered as a diagnostic biomarker in MS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27300318",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "The Central Vein Sign in Multiple Sclerosis Lesions Is Present Irrespective of the T2* Sequence at 3 T. BACKGROUND AND PURPOSE\nPrevious T2*-weighted magnetic resonance imaging (MRI) studies have used white matter lesion (WML) central veins to distinguish multiple sclerosis (MS) from its mimics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30213803",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 309,
"text": "Recent studies have demonstrated that patients with MS have higher proportions of white matter lesions with the central vein sign compared with those with diseases that mimic MS on MR imaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29328521",
"endSection": "abstract",
"offsetInBeginSection": 1597,
"offsetInEndSection": 1757,
"text": "When a threshold of 50% perivenular lesions was applied, central vein sign discriminated MS from inflammatory vasculopathies with a diagnostic accuracy of 100%."
}
] | 11
|
BioASQ-training11b
| null | null |
5e4601293f54159529000002
|
bioasq_factoid
|
yesno
|
Is muscle regeneration possible in mdx mice with the use of induced mesenchymal stem cells?
|
['yes']
|
[
"yes"
] |
['Purified induced mesenchymal stem cells (iMSCs) display fibroblast-like morphology, form three-dimensional spheroid structures, express characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105, and are capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplantation of iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowers oxidative damage, and restores the expression levels of normal dystrophin, leading to skeletal muscle regeneration.', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25102299"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 622,
"offsetInEndSection": 1147,
"text": "Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1260,
"text": "This study demonstrates the therapeutic potential of purified iMSCs in skeletal muscle regeneration in mdx mice"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17999592",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Flk-1+ adipose-derived mesenchymal stem cells differentiate into skeletal muscle satellite cells and ameliorate muscular dystrophy in mdx mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17999592",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 784,
"text": "Within mdx mice, an animal model of DMD, adipose tissue-derived Flk-1(+) MSCs (AD-MSCs) homed to and differentiated into cells that repaired injured muscle tissue. This repair correlated with reconstitution of dystrophin expression on the damaged fibers"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17999592",
"endSection": "abstract",
"offsetInBeginSection": 1076,
"offsetInEndSection": 1133,
"text": "Flk-1(+) AD-MSC transplants may repair muscular dystrophy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 1336,
"offsetInEndSection": 1531,
"text": "This study demonstrates the therapeutic potential of purified iMSCs in skeletal muscle regeneration in mdx mice, and suggests that iPSCs are a viable alternate source for deriving MSCs as needed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 1336,
"offsetInEndSection": 1531,
"text": "This study demonstrates the therapeutic potential of purified iMSCs in skeletal muscle regeneration in mdx mice, and suggests that iPSCs are a viable alternate source for deriving MSCs as needed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 935,
"offsetInEndSection": 1147,
"text": "Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1343,
"text": "This study demonstrates the therapeutic potential of purified iMSCs in skeletal muscle regeneration in mdx mice, and suggests that iPSCs are a viable alternate source for deriving MSCs as needed"
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
57134d511174fb1755000002
|
bioasq_yesno
|
yesno
|
Does GATA-1 regulate ribosomal protein genes?
|
['yes']
|
[
"yes"
] |
['Mutations in exon 2 interfere with the synthesis of the full-length isoform of GATA-1 and lead to the production of a shortened isoform, GATA-1s. These mutations have been found in patients with Diamond-Blackfan anemia (DBA), a congenital erythroid aplasia typically caused by mutations in genes encoding ribosomal proteins. Sixteen of the corresponding transcription factors are of particular interest, as they are housekeeping genes or show a direct link to hematopoiesis, tumorigenesis or leukemia (e.g. GATA-1/2, PU.1, MZF-1). ', 'in exon 2 interfere with the synthesis of the full-length isoform of gata-1 and lead to the production of a shortened isoform , gata-1s these mutations have been found in patients with diamond-blackfan anemia (dba) , a congenital erythroid aplasia typically caused by mutations in genes encoding ribosomal proteins. . of the corresponding transcription factors are of particular interest , as they are housekeeping genes or show a direct link to hematopoiesis , tumorigenesis or leukemia (e.g gata-1/2 , pu.1 , mzf-1). . ', 'These mutations have been found in patients with Diamond-Blackfan anemia (DBA), a congenital erythroid aplasia typically caused by mutations in genes encoding ribosomal proteins. Mutations in exon 2 interfere with the synthesis of the full-length isoform of GATA-1 and lead to the production of a shortened isoform, GATA-1s. Sixteen of the corresponding transcription factors are of particular interest, as they are housekeeping genes or show a direct link to hematopoiesis, tumorigenesis or leukemia (e.g. GATA-1/2, PU.1, MZF-1). ', 'These mutations have been found in patients with Diamond-Blackfan anemia (DBA), a congenital erythroid aplasia typically caused by mutations in genes encoding ribosomal proteins. Sixteen of the corresponding transcription factors are of particular interest, as they are housekeeping genes or show a direct link to hematopoiesis, tumorigenesis or leukemia (e.g.', 'These mutations have been found in patients with Diamond-Blackfan anemia (DBA), a congenital erythroid aplasia typically caused by mutations in genes encoding ribosomal proteins. The Ribosomal protein S19 gene locus (RPS19) has been linked to two kinds of red cell aplasia, Diamond-Blackfan Anemia (DBA) and Transient Erythroblastopenia in Childhood (TEC).', 'Mutations in exon 2 interfere with the synthesis of the full-length isoform of GATA-1 and lead to the production of a shortened isoform, GATA-1s. These mutations have been found in patients with Diamond-Blackfan anemia (DBA), a congenital erythroid aplasia typically caused by mutations in genes encoding ribosomal proteins.', 'mutations in exon 2 interfere with the synthesis of the full-length isoform of gata-1 and lead to the production of a shortened isoform, gata-1s.', 'yes', 'Sixteen of the corresponding transcription factors are of particular interest, as they are housekeeping genes or show a direct link to hematopoiesis, tumorigenesis or leukemia (e.g. GATA-1/2, PU.1, MZF-1). Mutations in exon 2 interfere with the synthesis of the full-length isoform of GATA-1 and lead to the production of a shortened isoform, GATA-1s. These mutations have been found in patients with Diamond-Blackfan anemia (DBA), a congenital erythroid aplasia typically caused by mutations in genes encoding ribosomal proteins.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19587786",
"http://www.ncbi.nlm.nih.gov/pubmed/10224082",
"http://www.ncbi.nlm.nih.gov/pubmed/24453067"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24453067",
"endSection": "abstract",
"offsetInBeginSection": 127,
"offsetInEndSection": 451,
"text": "Mutations in exon 2 interfere with the synthesis of the full-length isoform of GATA-1 and lead to the production of a shortened isoform, GATA-1s. These mutations have been found in patients with Diamond-Blackfan anemia (DBA), a congenital erythroid aplasia typically caused by mutations in genes encoding ribosomal proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19587786",
"endSection": "abstract",
"offsetInBeginSection": 1248,
"offsetInEndSection": 1453,
"text": "Sixteen of the corresponding transcription factors are of particular interest, as they are housekeeping genes or show a direct link to hematopoiesis, tumorigenesis or leukemia (e.g. GATA-1/2, PU.1, MZF-1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10224082",
"endSection": "abstract",
"offsetInBeginSection": 885,
"offsetInEndSection": 1028,
"text": "Deletion of PKC1 relieves the repression of both ribosomal protein and rRNA genes that occurs in response to a defect in the secretory pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10224082",
"endSection": "abstract",
"offsetInBeginSection": 1197,
"offsetInEndSection": 1360,
"text": "This stress is monitored by Pkc1p, which initiates a signal transduction pathway that leads to repression of transcription of the rRNA and ribosomal protein genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10224082",
"endSection": "abstract",
"offsetInBeginSection": 1361,
"offsetInEndSection": 1578,
"text": "The importance of the transcription of the 137 ribosomal protein genes to the economy of the cell is apparent from the existence of at least three distinct pathways that can effect the repression of this set of genes."
}
] | 6
|
BioASQ-training6b
| null | null |
58e782fd3e8b6dc87c000006
|
bioasq_yesno
|
yesno
|
Is selumetinib effective in thyroid cancer?
|
['yes']
|
[
"yes"
] |
['Yes, selumetinib was shown to be effective treatment for thyroid cancer. Selumetinib may reverse radioiodine uptake in patients with radioiodine-refractory differentiated thyroid cancer. Clinical efficacy of selumetinib was also investigated in other solid tumors.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25268371",
"http://www.ncbi.nlm.nih.gov/pubmed/25294906",
"http://www.ncbi.nlm.nih.gov/pubmed/25240824",
"http://www.ncbi.nlm.nih.gov/pubmed/24716986",
"http://www.ncbi.nlm.nih.gov/pubmed/25309778",
"http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"http://www.ncbi.nlm.nih.gov/pubmed/23435040",
"http://www.ncbi.nlm.nih.gov/pubmed/22451620"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25268371",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "A phase I trial of vertical inhibition of IGF signalling using cixutumumab, an anti-IGF-1R antibody, and selumetinib, an MEK 1/2 inhibitor, in advanced solid tumours."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25268371",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "BACKGROUND: We completed a phase I clinical trial to test the safety and toxicity of combined treatment with cixutumumab (anti-IGF-1R antibody) and selumetinib (MEK 1/2 inhibitor)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25268371",
"endSection": "abstract",
"offsetInBeginSection": 946,
"offsetInEndSection": 1272,
"text": "Two patients achieved a partial response (one unconfirmed), including a patient with BRAF wild-type thyroid carcinoma, and a patient with squamous cell carcinoma of the tongue, and six patients achieved time to progression of>6 months, including patients with thyroid carcinoma, colorectal carcinoma, and basal cell carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25268371",
"endSection": "abstract",
"offsetInBeginSection": 1389,
"offsetInEndSection": 1649,
"text": "CONCLUSIONS: Our study of anti-IGF-1R antibody cixutumumab and MEK 1/2 inhibitor selumetinib showed that the combination is safe and well-tolerated at these doses, with preliminary evidence of clinical benefit and pharmacodynamic evidence of target inhibition."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25294906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25294906",
"endSection": "abstract",
"offsetInBeginSection": 1469,
"offsetInEndSection": 1592,
"text": "Increased antigenicity following selumetinib and IFN treatment warrants further study for immunotherapy of progressive PTC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25240824",
"endSection": "abstract",
"offsetInBeginSection": 880,
"offsetInEndSection": 1032,
"text": "The role of KIs in differentiated TC may be revolutionised by the finding that selumetinib may restore a clinical response to radioactive iodine (RAI). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24716986",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "BACKGROUND AND AIM: Selumetinib is a promising and interesting targeted therapy agent as it may reverse radioiodine uptake in patients with radioiodine-refractory differentiated thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24716986",
"endSection": "abstract",
"offsetInBeginSection": 1561,
"offsetInEndSection": 1834,
"text": "CONCLUSIONS: Compared with current chemotherapy, selumetinib has modest clinical activity as monotherapy in patients with advanced cancer, but combinations of selumetinib with cytotoxic agents in patients with BRAF or KRAS mutations hold great promise for cancer treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25309778",
"endSection": "abstract",
"offsetInBeginSection": 1533,
"offsetInEndSection": 1628,
"text": "Selumetinib may be an effective redifferentiating agent and could be used within several years."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "abstract",
"offsetInBeginSection": 345,
"offsetInEndSection": 562,
"text": "METHODS: We conducted a study to determine whether the MAPK kinase (MEK) 1 and MEK2 inhibitor selumetinib (AZD6244, ARRY-142886) could reverse refractoriness to radioiodine in patients with metastatic thyroid cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "abstract",
"offsetInBeginSection": 1223,
"offsetInEndSection": 1373,
"text": "Selumetinib increased the uptake of iodine-124 in 12 of the 20 patients (4 of 9 patients with BRAF mutations and 5 of 5 patients with NRAS mutations)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "abstract",
"offsetInBeginSection": 1934,
"offsetInEndSection": 2182,
"text": "CONCLUSIONS: Selumetinib produces clinically meaningful increases in iodine uptake and retention in a subgroup of patients with thyroid cancer that is refractory to radioiodine; the effectiveness may be greater in patients with RAS-mutant disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23435040",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 518,
"text": "ECENT FINDINGS: For patients with advanced differentiated thyroid cancers, sorafenib, selumetinib, pazopanib and sunitinib have been investigated with promising results. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24716986",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Selumetinib is a promising and interesting targeted therapy agent as it may reverse radioiodine uptake in patients with radioiodine-refractory differentiated thyroid cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25294906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25309778",
"endSection": "abstract",
"offsetInBeginSection": 1616,
"offsetInEndSection": 1711,
"text": "Selumetinib may be an effective redifferentiating agent and could be used within several years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22451620",
"endSection": "abstract",
"offsetInBeginSection": 404,
"offsetInEndSection": 611,
"text": "Here, selumetinib targets the mitogen-activated protein kinase pathway in papillary thyroid carcinoma and shows limited single-agent activity in the patients with tumors that harbor the (V600E)BRAF mutation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24716986",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Selumetinib is a promising and interesting targeted therapy agent as it may reverse radioiodine uptake in patients with radioiodine-refractory differentiated thyroid cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25294906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25309778",
"endSection": "abstract",
"offsetInBeginSection": 1616,
"offsetInEndSection": 1711,
"text": "Selumetinib may be an effective redifferentiating agent and could be used within several years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22451620",
"endSection": "abstract",
"offsetInBeginSection": 404,
"offsetInEndSection": 611,
"text": "Here, selumetinib targets the mitogen-activated protein kinase pathway in papillary thyroid carcinoma and shows limited single-agent activity in the patients with tumors that harbor the (V600E)BRAF mutation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24716986",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Selumetinib is a promising and interesting targeted therapy agent as it may reverse radioiodine uptake in patients with radioiodine-refractory differentiated thyroid cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25294906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25309778",
"endSection": "abstract",
"offsetInBeginSection": 1616,
"offsetInEndSection": 1711,
"text": "Selumetinib may be an effective redifferentiating agent and could be used within several years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22451620",
"endSection": "abstract",
"offsetInBeginSection": 404,
"offsetInEndSection": 611,
"text": "Here, selumetinib targets the mitogen-activated protein kinase pathway in papillary thyroid carcinoma and shows limited single-agent activity in the patients with tumors that harbor the (V600E)BRAF mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "abstract",
"offsetInBeginSection": 1937,
"offsetInEndSection": 2185,
"text": "CONCLUSIONS: Selumetinib produces clinically meaningful increases in iodine uptake and retention in a subgroup of patients with thyroid cancer that is refractory to radioiodine; the effectiveness may be greater in patients with RAS-mutant disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25294906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "abstract",
"offsetInBeginSection": 1937,
"offsetInEndSection": 2185,
"text": "CONCLUSIONS: Selumetinib produces clinically meaningful increases in iodine uptake and retention in a subgroup of patients with thyroid cancer that is refractory to radioiodine; the effectiveness may be greater in patients with RAS-mutant disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "abstract",
"offsetInBeginSection": 1937,
"offsetInEndSection": 2185,
"text": "CONCLUSIONS: Selumetinib produces clinically meaningful increases in iodine uptake and retention in a subgroup of patients with thyroid cancer that is refractory to radioiodine; the effectiveness may be greater in patients with RAS-mutant disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "abstract",
"offsetInBeginSection": 1937,
"offsetInEndSection": 2185,
"text": "CONCLUSIONS: Selumetinib produces clinically meaningful increases in iodine uptake and retention in a subgroup of patients with thyroid cancer that is refractory to radioiodine; the effectiveness may be greater in patients with RAS-mutant disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25294906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "abstract",
"offsetInBeginSection": 1937,
"offsetInEndSection": 2185,
"text": "CONCLUSIONS: Selumetinib produces clinically meaningful increases in iodine uptake and retention in a subgroup of patients with thyroid cancer that is refractory to radioiodine; the effectiveness may be greater in patients with RAS-mutant disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25294906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23406027",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:1781",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013964",
"http://www.disease-ontology.org/api/metadata/DOID:3963"
] |
[] |
56c1f00aef6e39474100003d
|
bioasq_yesno
|
yesno
|
Do tumour-associated macrophages have a prognostic role in gliomas?
|
['yes']
|
[
"yes"
] |
['M2-like TAMs hold an unfavourable prognostic value in high-grade gliomas and may contribute to a pro-tumourigenic microenvironment.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28767130"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28767130",
"endSection": "abstract",
"offsetInBeginSection": 67,
"offsetInEndSection": 340,
"text": "Increasing evidence suggests that tumour-associated macrophages/microglia (TAMs) facilitate tumour progression by acquiring a M2-like phenotype. Our objective was to investigate the prognostic value of TAMs in gliomas using automated quantitative double immunofluorescence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28767130",
"endSection": "abstract",
"offsetInBeginSection": 1659,
"offsetInEndSection": 1932,
"text": "This is the first study to use automated quantitative immunofluorescence to determine the prognostic impact of TAMs. Our results suggest that M2-like TAMs hold an unfavourable prognostic value in high-grade gliomas and may contribute to a pro-tumourigenic microenvironment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28767130",
"endSection": "abstract",
"offsetInBeginSection": 941,
"offsetInEndSection": 1330,
"text": "Our data revealed that the amount of especially CD204+ TAMs increases with malignancy grade. In grade III-IV, high CD204 expression was associated with shorter survival, while high IBA-1 intensity correlated with a longer survival. In grade IV, CD204 showed independent prognostic value when adjusting for clinical data and the methylation status of O6-methylguanine-DNA methyltransferase."
}
] | 11
|
BioASQ-training11b
| null | null |
5c92159becadf2e73f000012
|
bioasq_yesno
|
factoid
|
Which is the process that Conserved noncoding elements mostly regulate?
|
['Development']
|
[
"Development",
"Growth",
"Progression",
"Advancement",
"Evolution",
"Maturation",
"Formation",
"Transformation"
] |
['Conserved noncoding elements play a fundamental role in regulating animal development']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23042552",
"http://www.ncbi.nlm.nih.gov/pubmed/21731768",
"http://www.ncbi.nlm.nih.gov/pubmed/21629789",
"http://www.ncbi.nlm.nih.gov/pubmed/21478460",
"http://www.ncbi.nlm.nih.gov/pubmed/21175683",
"http://www.ncbi.nlm.nih.gov/pubmed/19704032",
"http://www.ncbi.nlm.nih.gov/pubmed/19492354",
"http://www.ncbi.nlm.nih.gov/pubmed/19073165",
"http://www.ncbi.nlm.nih.gov/pubmed/18334644",
"http://www.ncbi.nlm.nih.gov/pubmed/18282512",
"http://www.ncbi.nlm.nih.gov/pubmed/18279518",
"http://www.ncbi.nlm.nih.gov/pubmed/18056681",
"http://www.ncbi.nlm.nih.gov/pubmed/17442748",
"http://www.ncbi.nlm.nih.gov/pubmed/16533910",
"http://www.ncbi.nlm.nih.gov/pubmed/19698106",
"http://www.ncbi.nlm.nih.gov/pubmed/16630819",
"http://www.ncbi.nlm.nih.gov/pubmed/17096848"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21478460",
"endSection": "sections.0",
"offsetInBeginSection": 507,
"offsetInEndSection": 681,
"text": "Much evidence suggests that CNEs are selectively constrained and not mutational cold-spots, and there is evidence that some CNEs play a role in the regulation of development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21478460",
"endSection": "sections.0",
"offsetInBeginSection": 1463,
"offsetInEndSection": 1676,
"text": "This result suggests that there is widespread adaptation in mammalian conserved noncoding DNA elements, some of which have been implicated in the regulation of crucially important processes, including development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21175683",
"endSection": "sections.0",
"offsetInBeginSection": 143,
"offsetInEndSection": 345,
"text": "Some characteristics of CNEs include their high frequency in mammalian genomes, their potential regulatory role in gene expression, and their enrichment in gene deserts nearby master developmental genes"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19704032",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Animal genomes possess highly conserved cis-regulatory sequences that are often found near genes that regulate transcription and development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19073165",
"endSection": "sections.0",
"offsetInBeginSection": 585,
"offsetInEndSection": 677,
"text": "HCNEs of both human and zebrafish function as specific developmental enhancers in zebrafish."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19073165",
"endSection": "sections.0",
"offsetInBeginSection": 1185,
"offsetInEndSection": 1391,
"text": "HCNEs from the same area often drive overlapping patterns, suggesting that multiple regulatory inputs are required to achieve robust and precise complex expression patterns exhibited by developmental genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18334644",
"endSection": "sections.0",
"offsetInBeginSection": 1401,
"offsetInEndSection": 1596,
"text": "These results suggest important roles for SINEs in the development of the mammalian neuronal network, a part of which was initiated with the exaptation of AmnSINE1 in a common mammalian ancestor."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18282512",
"endSection": "sections.0",
"offsetInBeginSection": 480,
"offsetInEndSection": 648,
"text": "Further positional analysis of these conserved noncoding elements (CNEs) in the genome demonstrates that they cluster around genes involved in developmental regulation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056681",
"endSection": "sections.0",
"offsetInBeginSection": 1277,
"offsetInEndSection": 1412,
"text": "The majority of tetrapod-specific UCEs are noncoding and associated with genes involved in regulation of transcription and development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16533910",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 304,
"text": "Fish-mammal genomic comparisons have proved powerful in identifying conserved noncoding elements likely to be cis-regulatory in nature, and the majority of those tested in vivo have been shown to act as tissue-specific enhancers associated with genes involved in transcriptional regulation of development"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16533910",
"endSection": "sections.0",
"offsetInBeginSection": 792,
"offsetInEndSection": 955,
"text": "In 74% of cases, we were able to assign a specific set of paralogous genes with annotation relating to transcriptional regulation and/or development to each family"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16630819",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "The most highly conserved noncoding elements (HCNEs) in mammalian genomes cluster within regions enriched for genes encoding developmentally important transcription factors (TFs). This suggests that HCNE-rich regions may contain key regulatory controls involved in development"
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017124"
] | null |
51387022bee46bd34c000002
|
bioasq_factoid
|
yesno
|
Can oleuropein aglycone interfere with amyloid aggregation?
|
['yes']
|
[
"yes"
] |
['Yes, oleuropein aglycone interferes in vitro and in vivo with amyloid aggregates.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29571746"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29571746",
"endSection": "abstract",
"offsetInBeginSection": 285,
"offsetInEndSection": 684,
"text": "Oleuropein, a phenolic secoiroid glycoside, is the main polyphenol in the olive oil. It has been reported that the aglycone form of Oleuropein (OleA) interferes in vitro and in vivo with amyloid aggregation of a number of proteins/peptides involved in amyloid, particularly neurodegenerative, diseases avoiding the growth of toxic oligomers and displaying protection against cognitive deterioration."
}
] | 11
|
BioASQ-training11b
| null | null |
5c890c3375a4a5d21900000e
|
bioasq_yesno
|
factoid
|
How are Arboviruses transmitted?
|
['By arthropods']
|
[
"arthropods",
"Arthropoda",
"jointed-legged animals",
"insects, arachnids, crustaceans",
"arthropod animals"
] |
['Arboviruses are transmitted by arthropods.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26141429",
"http://www.ncbi.nlm.nih.gov/pubmed/10488638",
"http://www.ncbi.nlm.nih.gov/pubmed/21658241",
"http://www.ncbi.nlm.nih.gov/pubmed/26925368",
"http://www.ncbi.nlm.nih.gov/pubmed/16893487",
"http://www.ncbi.nlm.nih.gov/pubmed/25597441",
"http://www.ncbi.nlm.nih.gov/pubmed/27220616",
"http://www.ncbi.nlm.nih.gov/pubmed/1973949",
"http://www.ncbi.nlm.nih.gov/pubmed/26363996",
"http://www.ncbi.nlm.nih.gov/pubmed/1297177",
"http://www.ncbi.nlm.nih.gov/pubmed/27869394",
"http://www.ncbi.nlm.nih.gov/pubmed/24941331",
"http://www.ncbi.nlm.nih.gov/pubmed/26283013",
"http://www.ncbi.nlm.nih.gov/pubmed/8158611",
"http://www.ncbi.nlm.nih.gov/pubmed/25053841"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25597441",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Epizootic congenital abnormalities, encephalomyelitis and febrile illnesses in cattle caused by arthropod-borne viruses (arboviruses) are prevalent in Japan"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26283013",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 97,
"text": " Zika virus (ZIKV) is an arthropod-borne virus (arbovirus) transmitted by mosquitoes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16893487",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "Nine different arboviruses are known to be transmitted by, or associated with, mosquitoes in Europe, and several (West Nile, Sindbis and Tahyna viruses) are reported to cause outbreaks of human disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24941331",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Arthropod-borne viruses (arboviruses) are transmitted to humans primarily through the bites of infected mosquitoes and ticks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21658241",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 207,
"text": "Arboviruses are transmitted among vertebrates by biting insects, chiefly mosquitoes and ticks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25053841",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Arboviruses are transmitted by distantly related arthropod vectors such as mosquitoes (class Insecta) and ticks (class Arachnida)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26363996",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "Mosquito-transmitted arthropod-borne viruses (arboviruses) such as dengue virus, chikungunya virus, and West Nile virus constitute a major public health burden and are increasing in severity and frequency worldwide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1973949",
"endSection": "abstract",
"offsetInBeginSection": 263,
"offsetInEndSection": 564,
"text": "Malaria and Japanese encephalitis are the two most serious human diseases transmitted by riceland mosquitoes, but they have been incriminated as vectors of dozens of arboviruses and other parasites and pathogens including the causal agents of West Nile and Rift Valley Fevers and lymphatic filariasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25053841",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Arboviruses are transmitted by distantly related arthropod vectors such as mosquitoes (class Insecta) and ticks (class Arachnida)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10488638",
"endSection": "abstract",
"offsetInBeginSection": 594,
"offsetInEndSection": 786,
"text": "Many of them are transmitted by insects (arboviruses, e.g. yellow fever virus) or by rodents (e.g. Hanta viruses), others by contact with patients and nosocomial infections (e.g. Ebola virus)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26141429",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Arboviruses - viruses transmitted by haematophagous arthropods - are responsible for febrile syndromes, which sometimes include haemorrhagic or neurological symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27220616",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 289,
"text": "Arboviruses are transmitted to vertebral hosts during blood feedings by mosquitoes, ticks, biting flies, mites, and nits."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26925368",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Arboviruses transmitted by mosquitoes are a major cause of human disease worldwide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27869394",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Diseases caused by arboviruses transmitted by Aedes aegypti, such as dengue, chikungunya and Zika, continue to rise in annual incidence and geographic expansion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8158611",
"endSection": "abstract",
"offsetInBeginSection": 223,
"offsetInEndSection": 414,
"text": "Arboviruses transmitted by ticks must adapt to the peculiar physiological and behavioral characteristics of ticks, particularly with regard to blood feeding, bloodmeal digestion, and molting."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26141429",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 532,
"text": "The last decade has seen significant changes in the epidemiology of arboviruses transmitted by mosquitoes of the genus Aedes, particularly in relation to the intercontinental spread of Aedes albopictus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1297177",
"endSection": "abstract",
"offsetInBeginSection": 381,
"offsetInEndSection": 687,
"text": "This technique enables the detection of 70 of the 80 arboviruses transmitted by mosquitoes in Africa and very easily detects arbovirus associations by using either monospecific or monoclonal immune ascitic fluids (dengue-1-2-3-4 and yellow fever viruses) used in the indirect immunofluorescence technique.."
}
] | 6
|
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007303",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018562",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001103",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001102"
] |
[
{
"o": "Arboviruses",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0003725"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A18608581",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0003725"
},
{
"o": "arboviruses",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A18608581"
}
] |
58f4b85f70f9fc6f0f000015
|
bioasq_factoid
|
yesno
|
Are Toll-like receptors (TLRs) induced by microbes?
|
['yes']
|
[
"yes"
] |
['Yes,\nGram-negative bacteria and endogenous molecules coordinate to trigger inflammatory cascades via Toll-like receptor 4 to induce excessive expression of cytokines such as tumor necrosis factor-α and to activate NLRP3 inflammasome, a multiprotein complex that processes pro-interleukin-1β into its mature form.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31799626",
"http://www.ncbi.nlm.nih.gov/pubmed/31462144",
"http://www.ncbi.nlm.nih.gov/pubmed/31712269",
"http://www.ncbi.nlm.nih.gov/pubmed/31865463",
"http://www.ncbi.nlm.nih.gov/pubmed/33075123"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31462144",
"endSection": "abstract",
"offsetInBeginSection": 291,
"offsetInEndSection": 439,
"text": "The C-type lectin receptor CLEC4E and Toll-like receptor TLR4 expressed by host cells are among the first line of defense in encountering pathogens."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31865463",
"endSection": "abstract",
"offsetInBeginSection": 734,
"offsetInEndSection": 1042,
"text": "Gram-negative bacteria and endogenous molecules coordinate to trigger inflammatory cascades via Toll-like receptor 4 to induce excessive expression of cytokines such as tumor necrosis factor-α and to activate NLRP3 inflammasome, a multiprotein complex that processes pro-interleukin-1β into its mature form. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31799626",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "During viral infection, viral nucleic acids are detected by virus sensor proteins including toll-like receptor 3 or retinoic acid-inducible gene I-like receptors (RLRs) in mammalian cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31712269",
"endSection": "abstract",
"offsetInBeginSection": 698,
"offsetInEndSection": 779,
"text": "Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33075123",
"endSection": "abstract",
"offsetInBeginSection": 634,
"offsetInEndSection": 782,
"text": "We determine that HBCs have the capacity to play a defensive role, where they are responsive to Toll-like receptor stimulation and are microbicidal."
}
] | 11
|
BioASQ-training11b
| null | null |
603285861cb411341a000141
|
bioasq_yesno
|
factoid
|
What gene test is recommended for clopidogrel?
|
['CYP2C19 genotyping']
|
[
"CYP2C19 genotyping",
"Cytochrome P450 2C19 genotyping",
"CYP2C19 testing",
"CYP2C19 genetic testing",
"CYP2C19 polymorphism testing"
] |
['The genetic test recommended for clopidogrel is CYP2C19 genotyping.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22974536",
"http://www.ncbi.nlm.nih.gov/pubmed/22674970",
"http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"http://www.ncbi.nlm.nih.gov/pubmed/22464343",
"http://www.ncbi.nlm.nih.gov/pubmed/22154242",
"http://www.ncbi.nlm.nih.gov/pubmed/22088980",
"http://www.ncbi.nlm.nih.gov/pubmed/21803320",
"http://www.ncbi.nlm.nih.gov/pubmed/20435227",
"http://www.ncbi.nlm.nih.gov/pubmed/20083681",
"http://www.ncbi.nlm.nih.gov/pubmed/19706858",
"http://www.ncbi.nlm.nih.gov/pubmed/18577829",
"http://www.ncbi.nlm.nih.gov/pubmed/18004210",
"http://www.ncbi.nlm.nih.gov/pubmed/17681590"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22674970",
"endSection": "sections.0",
"offsetInBeginSection": 607,
"offsetInEndSection": 677,
"text": "polymorphisms in the CYP2C19 gene affect clopidogrel pharmacokinetics."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"endSection": "sections.0",
"offsetInBeginSection": 11,
"offsetInEndSection": 212,
"text": "This study sought to evaluate the influence of single nucleotide polymorphisms (SNPs) on the pharmacodynamic effect of high- or standard-dose clopidogrel after percutaneous coronary intervention (PCI)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"endSection": "sections.0",
"offsetInBeginSection": 1621,
"offsetInEndSection": 2056,
"text": "CYP2C19, but not PON1 or ABCB1, is a significant determinant of the pharmacodynamic effects of clopidogrel, both early and late after PCI. In patients with high OTR identified by platelet function testing, the CYP2C19 genotype provides limited incremental information regarding the risk of persistently high reactivity with clopidogrel 150-mg maintenance dosing. (Genotype Information and Functional Testing Study [GIFT]; NCT00992420)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22088980",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 324,
"text": "Variants in the CYP2C19 gene influence the pharmacologic and clinical response to the standard 75-mg daily maintenance dose of the antiplatelet drug clopidogrel. OBJECTIVE: To test whether higher doses (up to 300 mg daily) improve the response to clopidogrel in the setting of loss-of-function CYP2C19 genotypes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22674970",
"endSection": "sections.0",
"offsetInBeginSection": 607,
"offsetInEndSection": 920,
"text": "polymorphisms in the CYP2C19 gene affect clopidogrel pharmacokinetics. These polymorphisms may be useful to identify clopidogrel nonresponders who may benefit from taking an alternative antiplatelet agent such as prasugrel and ticagrelor. Although both drugs have pharmacogenomic tests available for clinical use,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"endSection": "sections.0",
"offsetInBeginSection": 11,
"offsetInEndSection": 212,
"text": "This study sought to evaluate the influence of single nucleotide polymorphisms (SNPs) on the pharmacodynamic effect of high- or standard-dose clopidogrel after percutaneous coronary intervention (PCI)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"endSection": "sections.0",
"offsetInBeginSection": 1621,
"offsetInEndSection": 2056,
"text": "CYP2C19, but not PON1 or ABCB1, is a significant determinant of the pharmacodynamic effects of clopidogrel, both early and late after PCI. In patients with high OTR identified by platelet function testing, the CYP2C19 genotype provides limited incremental information regarding the risk of persistently high reactivity with clopidogrel 150-mg maintenance dosing. (Genotype Information and Functional Testing Study [GIFT]; NCT00992420)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22464343",
"endSection": "sections.0",
"offsetInBeginSection": 136,
"offsetInEndSection": 497,
"text": "The CYP2C19*2 allele is a common genetic variant associated with increased rates of major adverse events in individuals given clopidogrel after percutaneous coronary intervention (PCI). We used a novel point-of-care genetic test to identify carriers of the CYP2C19*2 allele and aimed to assess a pharmacogenetic approach to dual antiplatelet treatment after PCI"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22154242",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 401,
"text": "The antiplatelet effect of clopidogrel has been linked to cytochrome P450 2C19 (CYP2C19) carrier status. The presence of loss of function and gain of function variants were found to have a gene-dose effect on clopidogrel metabolism. However, genotyping is only one aspect of predicting response to clopidogrel and several platelet function tests are available to measure platelet response."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22088980",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 324,
"text": "Variants in the CYP2C19 gene influence the pharmacologic and clinical response to the standard 75-mg daily maintenance dose of the antiplatelet drug clopidogrel. OBJECTIVE: To test whether higher doses (up to 300 mg daily) improve the response to clopidogrel in the setting of loss-of-function CYP2C19 genotypes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21803320",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "The cytochrome P450 (CYP) 2C19*2 loss-of-function allele has been associated with impaired clopidogrel response and worse prognosis in clopidogrel-treated patients."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21803320",
"endSection": "sections.0",
"offsetInBeginSection": 357,
"offsetInEndSection": 637,
"text": "The present study was designed to evaluate the benefit of tailored therapy with a higher maintenance dose according to CYP2C19 genotypes in patients identified as nonresponders who underwent percutaneous coronary intervention for non-ST-segment elevation acute coronary syndromes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20435227",
"endSection": "sections.0",
"offsetInBeginSection": 893,
"offsetInEndSection": 977,
"text": "identify genes and mutations with known associations with disease and drug response."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20435227",
"endSection": "sections.0",
"offsetInBeginSection": 1654,
"offsetInEndSection": 1753,
"text": "The patient had a heterozygous null mutation in CYP2C19 suggesting probable clopidogrel resistance,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20083681",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 344,
"text": "The cytochrome P450 (CYP) 2C19 isoenzyme plays an important role in clopidogrel metabolization. A recently explored CYP2C19*17 allelic variant has been linked to increased transcriptional activity, resulting in extensive metabolization of CYP2C19 substrates, which may lead to an enhanced platelet response to clopidogrel treatment."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19706858",
"endSection": "sections.0",
"offsetInBeginSection": 333,
"offsetInEndSection": 395,
"text": "To identify gene variants that influence clopidogrel response."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19706858",
"endSection": "sections.0",
"offsetInBeginSection": 608,
"offsetInEndSection": 973,
"text": "A genome-wide association study was performed followed by genotyping the loss-of-function cytochrome P450 (CYP) 2C19*2 variant (rs4244285). Findings in the PAPI Study were extended by examining the relation of CYP2C19*2 genotype to platelet function and cardiovascular outcomes in an independent sample of 227 patients undergoing percutaneous coronary intervention."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18577829",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 116,
"text": "Coexisting polymorphisms of the genes affecting clopiogrel resistance may influence platelet activation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18577829",
"endSection": "sections.0",
"offsetInBeginSection": 439,
"offsetInEndSection": 754,
"text": "Genotyping revealed 7 carriers of both the C allele of P2Y12 and A allele of CYP2C19 (group 1), 14 carriers of the T allele of P2Y12 and A allele of CYP2C19 (group 2), 17 carriers of the C allele of P2Y12 and G allele of CYP2C19 (group 3) and 67 carriers of the T allele of P2Y12 and G allele of CYP2C19 (controls)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18004210",
"endSection": "sections.0",
"offsetInBeginSection": 37,
"offsetInEndSection": 285,
"text": "to evaluate the effect of polymorphisms affecting the clopidogrel metabolism (CYP3A4 IVS10+12G/A and CYP2C19*2) and the P2Y12 receptor (P2Y12 T744C) on modulating platelet function in acute coronary syndrome patients on dual antiplatelet treatment."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17681590",
"endSection": "sections.0",
"offsetInBeginSection": 260,
"offsetInEndSection": 337,
"text": "to test the influence of the CYP 2C19*2 allele on clopidogrel responsiveness."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22674970",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Genetic polymorphisms significantly influence responses to warfarin and clopidogrel."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22974536",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 286,
"text": "A recent clinical trial has demonstrated that patients with acute coronary syndromes (ACS) and the reduced function allele CYP2C19*2 (*2 allele), who are treated with thienopyridines, have an increased risk of adverse cardiac events with clopidogrel, but not with prasugrel."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4260620",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005796",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005820",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003955"
] |
[
{
"o": "http://linkedlifedata.com/resource/umls/label/A0173515",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0070166"
},
{
"o": "clopidogrel",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0173515"
},
{
"o": "http://www.w3.org/2008/05/skos-xl#Label",
"p": "http://www.w3.org/1999/02/22-rdf-syntax-ns#type",
"s": "http://linkedlifedata.com/resource/umls/label/A12101557"
},
{
"o": "Clopidogrel",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A12785306"
},
{
"o": "MeSH",
"p": "http://www.w3.org/2004/02/skos/core#note",
"s": "http://linkedlifedata.com/resource/umls/label/A0173516"
},
{
"o": "http://www.w3.org/2008/05/skos-xl#Label",
"p": "http://www.w3.org/1999/02/22-rdf-syntax-ns#type",
"s": "http://linkedlifedata.com/resource/umls/label/A10928568"
}
] |
5156be04d24251bc05000085
|
bioasq_factoid
|
yesno
|
Is diphosphatidylglycerol (cardiolipin) a phospholipid of the mitochondrial membranes?
|
['yes']
|
[
"yes"
] |
['Yes, diphosphatidylglycerol (cardiolipin) is a phospholipid of the mitochondrial membranes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21599656",
"http://www.ncbi.nlm.nih.gov/pubmed/26028302",
"http://www.ncbi.nlm.nih.gov/pubmed/24905496",
"http://www.ncbi.nlm.nih.gov/pubmed/7378435",
"http://www.ncbi.nlm.nih.gov/pubmed/4322761",
"http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"http://www.ncbi.nlm.nih.gov/pubmed/24007978",
"http://www.ncbi.nlm.nih.gov/pubmed/7794966",
"http://www.ncbi.nlm.nih.gov/pubmed/3668386",
"http://www.ncbi.nlm.nih.gov/pubmed/8143741",
"http://www.ncbi.nlm.nih.gov/pubmed/23200781",
"http://www.ncbi.nlm.nih.gov/pubmed/26301254",
"http://www.ncbi.nlm.nih.gov/pubmed/6257342",
"http://www.ncbi.nlm.nih.gov/pubmed/6509920",
"http://www.ncbi.nlm.nih.gov/pubmed/26396268",
"http://www.ncbi.nlm.nih.gov/pubmed/6807345",
"http://www.ncbi.nlm.nih.gov/pubmed/16971584",
"http://www.ncbi.nlm.nih.gov/pubmed/9370332",
"http://www.ncbi.nlm.nih.gov/pubmed/20336283",
"http://www.ncbi.nlm.nih.gov/pubmed/1213878",
"http://www.ncbi.nlm.nih.gov/pubmed/9843887",
"http://www.ncbi.nlm.nih.gov/pubmed/7459841",
"http://www.ncbi.nlm.nih.gov/pubmed/3548756",
"http://www.ncbi.nlm.nih.gov/pubmed/22634369",
"http://www.ncbi.nlm.nih.gov/pubmed/6717095",
"http://www.ncbi.nlm.nih.gov/pubmed/25182746",
"http://www.ncbi.nlm.nih.gov/pubmed/3718705",
"http://www.ncbi.nlm.nih.gov/pubmed/15460113",
"http://www.ncbi.nlm.nih.gov/pubmed/25843549",
"http://www.ncbi.nlm.nih.gov/pubmed/1550861",
"http://www.ncbi.nlm.nih.gov/pubmed/24443516",
"http://www.ncbi.nlm.nih.gov/pubmed/20637181",
"http://www.ncbi.nlm.nih.gov/pubmed/8977117",
"http://www.ncbi.nlm.nih.gov/pubmed/1247555",
"http://www.ncbi.nlm.nih.gov/pubmed/24769127"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24007978",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 341,
"text": "A unique organelle for studying membrane biochemistry is the mitochondrion whose functionality depends on a coordinated supply of proteins and lipids. Mitochondria are capable of synthesizing several lipids autonomously such as phosphatidylglycerol, cardiolipin and in part phosphatidylethanolamine, phosphatidic acid and CDP-diacylglycerol."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7459841",
"endSection": "abstract",
"offsetInBeginSection": 372,
"offsetInEndSection": 474,
"text": "A small decrease of diphosphatidylglycerol also occurred in the hepatoma mitochondria inner membrane. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6807345",
"endSection": "abstract",
"offsetInBeginSection": 492,
"offsetInEndSection": 624,
"text": "Diphosphatidylglycerol was confined to the mitochondrial fraction, where it represented about 7% of the total phosphoacylglycerols. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6717095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 401,
"text": "Mitochondrial membranes were isolated from the myocardium of young (4-month-old) and aged (33-month-old) male Long-Evans rats and compared in terms of cholesterol content and phospholipid and fatty acid composition. In aged rats, as compared to young, the major observations include: markedly higher cholesterol content; increased percentage of sphingomyelin and diphosphatidylglycerol (cardiolipin); "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3548756",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 632,
"text": "The polyglycerophosphatides (typified by diphosphatidylglycerol) were apparently synthesized in situ by intramitochondrial membrane-bound enzymes using CDP-diglycerides as intermediates. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6509920",
"endSection": "abstract",
"offsetInBeginSection": 538,
"offsetInEndSection": 875,
"text": "Both the mitochondrial and microsomal fractions contained significant proportions of solvent front phospholipid (SFP) and whereas the mitochondrial SFP displayed the relatively unsaturated fatty acid composition characteristic of diphosphatidylglycerol (cardiolipin), the fatty acids of the microsomal SFP were distinctly more saturated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3718705",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 764,
"text": "Ten to 15% of microsomal radioactive CDP-diglycerides was transferred to mitochondrial membranes and incorporated into mitochondrial radioactive lipids identified as phosphatidylglycerol, phosphatidylglycerophosphate, and, when [14C]linoleoyl CDP-diglycerides were used, diphosphatidylglycerol (cardiolipin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6257342",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "The enzyme responsible for the conversion of phosphatidylglycerol to diphosphatidylglycerol (cardiolipin) in the presence of cytidine diphosphate diacylglycerol is firmly associated with mitochondrial membranes and is not extracted with hypotonic or hypertonic media or with nonionic detergents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 347,
"text": "The mechanism of cardiolipin (diphosphatidylglycerol) biosynthesis was examined in mitochondria and outer and inner mitochondrial membranes prepared from guinea pig and rat livers to determine whether this formation from phosphatidylglycerol was absolutely dependent on cytidinediphosphodiglyceride, as previously reported for intact mitochondria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21599656",
"endSection": "abstract",
"offsetInBeginSection": 454,
"offsetInEndSection": 597,
"text": "In isolated mitochondrial outer membranes, cardiolipin (diphosphatidylglycerol) increased CPT1 activity 4-fold and the Km for carnitine 6-fold."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3718705",
"endSection": "abstract",
"offsetInBeginSection": 457,
"offsetInEndSection": 765,
"text": "Ten to 15% of microsomal radioactive CDP-diglycerides was transferred to mitochondrial membranes and incorporated into mitochondrial radioactive lipids identified as phosphatidylglycerol, phosphatidylglycerophosphate, and, when [14C]linoleoyl CDP-diglycerides were used, diphosphatidylglycerol (cardiolipin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/4322761",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 615,
"text": "90% or more of the phospholipid, cardiolipin was found in the mitochondrial membranes of wild type and petite yeast."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 760,
"text": "Furthermore, the same mechanism for the biosynthesis of cardiolipin was operational in the outer and inner mitochondrial membranes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 346,
"text": "The mechanism of cardiolipin (diphosphatidylglycerol) biosynthesis was examined in mitochondria and outer and inner mitochondrial membranes prepared from guinea pig and rat livers to determine whether this formation from phosphatidylglycerol was absolutely dependent on cytidinediphosphodiglyceride, as previously reported for intact mitochondria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24443516",
"endSection": "abstract",
"offsetInBeginSection": 65,
"offsetInEndSection": 246,
"text": "Cardiolipin (CL) is a key phospholipid in mitochondrial membranes, playing important roles in maintaining the functional integrity and dynamics of mitochondria in animals and yeasts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23200781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Cardiolipin, the specific phospholipid of mitochondria, is involved in the biogenesis, the dynamics, and the supramolecular organization of mitochondrial membranes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26301254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Cardiolipin (CL), the signature phospholipid of mitochondrial membranes, is crucial for both mitochondrial function and cellular processes outside of the mitochondria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24769127",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 231,
"text": "Since it has been recognized that mitochondria are crucial not only for energy metabolism but also for other cellular functions, there has been a growing interest in cardiolipin, the specific phospholipid of mitochondrial membranes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25843549",
"endSection": "abstract",
"offsetInBeginSection": 72,
"offsetInEndSection": 259,
"text": "Cardiolipin, the main anionic phospholipid in mitochondrial membranes, is expected to be a determinant in this adaptive mechanism since it modulates the activity of most membrane proteins"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3718705",
"endSection": "abstract",
"offsetInBeginSection": 457,
"offsetInEndSection": 764,
"text": "Ten to 15% of microsomal radioactive CDP-diglycerides was transferred to mitochondrial membranes and incorporated into mitochondrial radioactive lipids identified as phosphatidylglycerol, phosphatidylglycerophosphate, and, when [14C]linoleoyl CDP-diglycerides were used, diphosphatidylglycerol (cardiolipin)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26396268",
"endSection": "abstract",
"offsetInBeginSection": 247,
"offsetInEndSection": 530,
"text": "Cardiolipin is normally localized to the inner mitochondrial membrane; however, when cardiolipin becomes externalized to the surface of dysregulated mitochondria, it promotes inflammasome activation and stimulates the elimination of damaged or nonfunctional mitochondria by mitophagy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21599656",
"endSection": "abstract",
"offsetInBeginSection": 454,
"offsetInEndSection": 598,
"text": "In isolated mitochondrial outer membranes, cardiolipin (diphosphatidylglycerol) increased CPT1 activity 4-fold and the Km for carnitine 6-fold. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24905496",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Increasing levels of cardiolipin differentially influence packing of phospholipids found in the mitochondrial inner membrane."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25843549",
"endSection": "abstract",
"offsetInBeginSection": 261,
"offsetInEndSection": 440,
"text": "Here, we used Saccharomyces cerevisiae subjected to conditions that affect mitochondrial metabolism as a model to determine the possible role of cardiolipin in stress adaptation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8977117",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 684,
"text": "This decline of respiration was attributed to a progressive diminution of the number of mitochondria in copper-treated cells, based on the demonstration of the concomitant decline of (1) cardiolipin (diphosphatidylglycerol) and cytochrome aa3 (cytochrome oxidase), two specific markers of mitochondrial inner membrane, and (2) fumarase activity, a specific marker of mitochondrial matrix space."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15460113",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 477,
"text": "Diphosphatidylglycerol (DPG) or cardiolipin, a specific component of the inner mitochondrial membrane, represents about 4% of the total lipid content."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 628,
"text": "Experimental results confirmed that the biosynthesis of cardiolipin, from the membrane-bound radioactive phosphatidylglycerol in intact mitochondria isolated from guinea pig and rat liver, was absolutely dependent on CDP-diglycerides and required the addition of divalent cations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7378435",
"endSection": "abstract",
"offsetInBeginSection": 561,
"offsetInEndSection": 776,
"text": "We have shown that decrease of cardiolipin in mitochondrial membrane occurs early during ischemia, and only during the irreversible phase of ischemia are phosphatidylethanolamine and phosphatidylcholine broken down."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6257342",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Partial purification of diphosphatidylglycerol synthetase from liver mitochondrial membranes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7459841",
"endSection": "abstract",
"offsetInBeginSection": 372,
"offsetInEndSection": 473,
"text": "A small decrease of diphosphatidylglycerol also occurred in the hepatoma mitochondria inner membrane."
}
] | 6
|
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002308",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008566",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008563",
"http://www.biosemantics.org/jochem#http://www.biosemantics.org/jochem#:4244279",
"http://www.biosemantics.org/jochem#4001026",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008928",
"http://www.biosemantics.org/jochem#4244279",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051336"
] |
[
{
"o": "Phospholipid",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0202177"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17997459",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0007188"
},
{
"o": "Cardiolipins",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17997459"
},
{
"o": "http://linkedlifedata.com/resource/rxnorm/label/3130515",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/rxnorm/id/2083"
},
{
"o": "Cardiolipins",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/rxnorm/label/3130515"
},
{
"o": "cardiolipin",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0007188"
},
{
"o": "http://linkedlifedata.com/resource/rxnorm/label/3130514",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/rxnorm/id/2083"
},
{
"o": "Cardiolipin",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/rxnorm/label/3130514"
}
] |
58d90f228acda3452900000f
|
bioasq_yesno
|
factoid
|
What is another name for the drug AMG334?
|
['Erenumab']
|
[
"Erenumab",
"Aimovig"
] |
['AMG334 is also called erenumab.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28240610"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28240610",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 396,
"text": "The results of phase 2 randomized controlled trials for the prevention of episodic and chronic migraine demonstrating the efficacy and safety of four mAbs targeting the calcitonin gene-related peptide (CGRP) pathway [ALD403 (eptinezumab), AMG334 (erenumab), LY2951742 (galcanezumab) and TEV48125 (fremanezumab)] have been published recently, and phase 3 trials are in process. "
}
] | 11
|
BioASQ-training11b
| null | null |
6026ed981cb411341a0000d2
|
bioasq_factoid
|
yesno
|
Are breaks in double stranded DNA associated with ionizing radiation?
|
['yes']
|
[
"yes"
] |
['Yes, double-strand breaks in double stranded DNA may be associated with ionizing radiation risk.', 'Yes, breaks in double stranded DNA are associated with ionizing radiation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/10639091",
"http://www.ncbi.nlm.nih.gov/pubmed/1540967",
"http://www.ncbi.nlm.nih.gov/pubmed/16650867",
"http://www.ncbi.nlm.nih.gov/pubmed/31652722",
"http://www.ncbi.nlm.nih.gov/pubmed/9665145",
"http://www.ncbi.nlm.nih.gov/pubmed/29043625",
"http://www.ncbi.nlm.nih.gov/pubmed/26089209",
"http://www.ncbi.nlm.nih.gov/pubmed/20079875",
"http://www.ncbi.nlm.nih.gov/pubmed/6445538",
"http://www.ncbi.nlm.nih.gov/pubmed/29787435",
"http://www.ncbi.nlm.nih.gov/pubmed/29956296",
"http://www.ncbi.nlm.nih.gov/pubmed/7683090",
"http://www.ncbi.nlm.nih.gov/pubmed/23948232"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29043625",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 282,
"text": "DNA double-strand breaks (DSBs) are major DNA lesions that are constantly formed during physiological processes such as DNA replication, transcription, and recombination, or as a result of exogenous agents such as ionizing radiation, radiomimetic drugs, and genome editing nucleases"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29956296",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "Whereas most endogenous and exogenous DNA damaging agents typically generate lesions that are relatively isolated and can be repaired easily, ionizing radiation (IR) also induces clustered lesions causing DNA double strand breaks (DSBs)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20079875",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "The induction of DNA interstrand cross-links by ionizing radiation has been largely ignored in favour of studies on double-strand break formation and repair."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23948232",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "While much is known about radiation-induced DNA double-strand breaks (DSBs) and their repair, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29787435",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Exposure of cells to ionizing radiation induces DNA double-strand breaks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7683090",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "DNA double-strand breaks are considered to be the most deleterious lesion induced by ionizing radiation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1540967",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Influence of chromatin structure on the induction of DNA double strand breaks by ionizing radiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10639091",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Ionizing radiation and radiomimetic drugs such as bleomycin, calichieamycin, neocarzinostatin chromophore, and other synthetic agents can produce both single and double strand breaks in DNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9665145",
"endSection": "abstract",
"offsetInBeginSection": 816,
"offsetInEndSection": 927,
"text": "RESULTS BRCA2-defective cells were unable to repair the double-strand DNA breaks induced by ionizing radiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16650867",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "BACKGROUND Induction of DNA double strand breaks and alterations in the repair of these breaks is implicated in breast carcinogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31652722",
"endSection": "abstract",
"offsetInBeginSection": 134,
"offsetInEndSection": 298,
"text": "Double-stranded breaks ( DSBs ) are the most injurious type of DNA damage , being induced by ionizing radiation ( IR ) and cytotoxic agents used in cancer treatment"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089209",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Double-stranded breaks ( DSBs ) are cytotoxic DNA lesions caused by oxygen radicals , ionizing radiation , and radiomimetic chemicals"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6445538",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Gamma-ray irradiation introduces single and/or double strand breaks into the DNA molecule of the cells."
}
] | 11
|
BioASQ-training11b
| null | null |
5e3c6e15b5b409ea53000023
|
bioasq_yesno
|
yesno
|
Without immunization, rabies is a lethal disease.
|
['yes']
|
[
"yes"
] |
['Rabies lethality is close to 100% without immunization.', 'Yes, without immunization, rabies is almost always a lethal disease. Rabies is a viral encephalitis that is statistically 100% fatal if left untreated. However, rabies is also one of the few infectious diseases that can be prevented through vaccination, providing almost 100% protection if administered early enough after exposure.', 'Rabies is a zoonotic disease caused primarily by the rabies virus (RABV) and is considered fatal without vaccination or treatment. The RABV infects the central nervous system, leading to symptoms such as fever, headache, fatigue, nausea, and ultimately progressing to more severe neurological signs like seizures, paralysis, and encephalitis. Without immunization through vaccination or post-exposure prophylaxis, rabies is almost always fatal once clinical symptoms appear.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37728394",
"http://www.ncbi.nlm.nih.gov/pubmed/35931921",
"http://www.ncbi.nlm.nih.gov/pubmed/36343866"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35931921",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Rabies is a lethal zoonotic disease mainly transmitted to humans by dog bites"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36343866",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 89,
"text": "Rabies is an acute lethal infectious disease caused by a lyssavirus infection"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37728394",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 38,
"text": "Rabies, a lethal zoonotic encephalitis"
}
] | 13
|
BioASQ-training13b
| null | null |
660d6a97fdcbea915f00003c
|
bioasq_yesno
|
yesno
|
Is Phospholemman a membrane protein?
|
['yes']
|
[
"yes"
] |
['Yes, FXYD1 (encoding phospholemman) is a transmembrane protein.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31840988",
"http://www.ncbi.nlm.nih.gov/pubmed/26429909",
"http://www.ncbi.nlm.nih.gov/pubmed/23246925"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31840988",
"endSection": "abstract",
"offsetInBeginSection": 772,
"offsetInEndSection": 824,
"text": " the transmembrane lipoprotein phospholemman (FXYD1)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26429909",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Phospholemman (FXYD1) is a single-transmembrane protein regulator of Na,K-ATPase, expressed strongly in heart, skeletal muscle, and brain and phosphorylated by protein kinases A and C at Ser-68 and Ser-63, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23246925",
"endSection": "abstract",
"offsetInBeginSection": 148,
"offsetInEndSection": 347,
"text": "We previously identified FXYD1 (encoding phospholemman; a protein containing the motif phenylalanine-X-tyrosine-aspartate), a gene encoding a transmembrane modulator of the Na, K-ATPase (NKA) enzyme,"
}
] | 11
|
BioASQ-training11b
| null | null |
6251465ae764a53204000017
|
bioasq_yesno
|
yesno
|
Is the optogenetics tool ChR2 light-sensitive?
|
['yes']
|
[
"yes"
] |
['Channelrhodospin-2 (ChR2) is a light-sensitive ion channel that has emerged as new optogenetics tool.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"http://www.ncbi.nlm.nih.gov/pubmed/23002710",
"http://www.ncbi.nlm.nih.gov/pubmed/25518365",
"http://www.ncbi.nlm.nih.gov/pubmed/23664865",
"http://www.ncbi.nlm.nih.gov/pubmed/24518144",
"http://www.ncbi.nlm.nih.gov/pubmed/25483880",
"http://www.ncbi.nlm.nih.gov/pubmed/25303540",
"http://www.ncbi.nlm.nih.gov/pubmed/24022017",
"http://www.ncbi.nlm.nih.gov/pubmed/23056472",
"http://www.ncbi.nlm.nih.gov/pubmed/25060859",
"http://www.ncbi.nlm.nih.gov/pubmed/24555016",
"http://www.ncbi.nlm.nih.gov/pubmed/24026336",
"http://www.ncbi.nlm.nih.gov/pubmed/23366158",
"http://www.ncbi.nlm.nih.gov/pubmed/25571406",
"http://www.ncbi.nlm.nih.gov/pubmed/24509078",
"http://www.ncbi.nlm.nih.gov/pubmed/25796616",
"http://www.ncbi.nlm.nih.gov/pubmed/23380919"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23002710",
"endSection": "abstract",
"offsetInBeginSection": 799,
"offsetInEndSection": 993,
"text": "Light-sensitive genes chiefly including the genetically targeted light-gated channels channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR) cause intracellular ion flow during optical illumination."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Computational optogenetics: empirically-derived voltage- and light-sensitive channelrhodopsin-2 model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25303540",
"endSection": "abstract",
"offsetInBeginSection": 561,
"offsetInEndSection": 979,
"text": "The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24026336",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Channelrhodopsins-2 (ChR2) are a class of light sensitive proteins that offer the ability to use light stimulation to regulate neural activity with millisecond precision."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25303540",
"endSection": "abstract",
"offsetInBeginSection": 561,
"offsetInEndSection": 979,
"text": "The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25060859",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "The most widely used optogenetic tool, Channelrhodopsin2 (ChR2), is both light- and voltage-sensitive."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Computational optogenetics: empirically-derived voltage- and light-sensitive channelrhodopsin-2 model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25303540",
"endSection": "abstract",
"offsetInBeginSection": 561,
"offsetInEndSection": 979,
"text": "The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24026336",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Channelrhodopsins-2 (ChR2) are a class of light sensitive proteins that offer the ability to use light stimulation to regulate neural activity with millisecond precision."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24022017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 432,
"text": "Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., halorhodopsin, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24022017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 432,
"text": "Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., halorhodopsin, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509078",
"endSection": "abstract",
"offsetInBeginSection": 1136,
"offsetInEndSection": 1334,
"text": "Virus-mediated expression of a ChR2 variant with greater light sensitivity in SGNs reduced the amount of light required for responses and allowed neuronal spiking following stimulation up to 60 Hz. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25796616",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 250,
"text": "Channelrhodopsin-2 (ChR2) from the green alga Chlamydomonas reinhardtii functions as a light-gated cation channel that has been developed as an optogenetic tool to stimulate specific nerve cells in animals and control their behavior by illumination. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509078",
"endSection": "abstract",
"offsetInBeginSection": 360,
"offsetInEndSection": 562,
"text": "Here, we used animal models to characterize optogenetic stimulation, which is the optical stimulation of neurons genetically engineered to express the light-gated ion channel channelrhodopsin-2 (ChR2). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24022017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 432,
"text": "Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., halorhodopsin, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509078",
"endSection": "abstract",
"offsetInBeginSection": 1136,
"offsetInEndSection": 1334,
"text": "Virus-mediated expression of a ChR2 variant with greater light sensitivity in SGNs reduced the amount of light required for responses and allowed neuronal spiking following stimulation up to 60 Hz. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25796616",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 250,
"text": "Channelrhodopsin-2 (ChR2) from the green alga Chlamydomonas reinhardtii functions as a light-gated cation channel that has been developed as an optogenetic tool to stimulate specific nerve cells in animals and control their behavior by illumination. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509078",
"endSection": "abstract",
"offsetInBeginSection": 360,
"offsetInEndSection": 562,
"text": "Here, we used animal models to characterize optogenetic stimulation, which is the optical stimulation of neurons genetically engineered to express the light-gated ion channel channelrhodopsin-2 (ChR2). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24022017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 432,
"text": "Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., halorhodopsin, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24022017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 432,
"text": "Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., halorhodopsin, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25303540",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 563,
"text": "The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25060859",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "The most widely used optogenetic tool, Channelrhodopsin2 (ChR2), is both light- and voltage-sensitive. A light-triggered action potential or light-driven perturbations of ongoing electrical activity provide instant voltage feedback, shaping ChR2 current."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24022017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 432,
"text": " Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., halorhodopsin, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23002710",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 994,
"text": "It allows neurons to express light-sensitive genes that enable the identification, dissection, and manipulation of specific neural populations and their connections in the tissues and organs of awake animals with unprecedented spatial and temporal precision. Light-sensitive genes chiefly including the genetically targeted light-gated channels channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR) cause intracellular ion flow during optical illumination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25303540",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 563,
"text": "The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25060859",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "The most widely used optogenetic tool, Channelrhodopsin2 (ChR2), is both light- and voltage-sensitive. A light-triggered action potential or light-driven perturbations of ongoing electrical activity provide instant voltage feedback, shaping ChR2 current."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25796616",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 512,
"text": "Channelrhodopsin-2 (ChR2) from the green alga Chlamydomonas reinhardtii functions as a light-gated cation channel that has been developed as an optogenetic tool to stimulate specific nerve cells in animals and control their behavior by illumination. The molecular mechanism of ChR2 has been extensively studied by a variety of spectroscopic methods, including light-induced difference Fourier transform infrared (FTIR) spectroscopy, which is sensitive to structural changes in the protein upon light activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25060859",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "The most widely used optogenetic tool, Channelrhodopsin2 (ChR2), is both light- and voltage-sensitive. A light-triggered action potential or light-driven perturbations of ongoing electrical activity provide instant voltage feedback, shaping ChR2 current."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25303540",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 563,
"text": "The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25796616",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 512,
"text": "Channelrhodopsin-2 (ChR2) from the green alga Chlamydomonas reinhardtii functions as a light-gated cation channel that has been developed as an optogenetic tool to stimulate specific nerve cells in animals and control their behavior by illumination. The molecular mechanism of ChR2 has been extensively studied by a variety of spectroscopic methods, including light-induced difference Fourier transform infrared (FTIR) spectroscopy, which is sensitive to structural changes in the protein upon light activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25303540",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 563,
"text": "The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25060859",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "The most widely used optogenetic tool, Channelrhodopsin2 (ChR2), is both light- and voltage-sensitive. A light-triggered action potential or light-driven perturbations of ongoing electrical activity provide instant voltage feedback, shaping ChR2 current."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24022017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 432,
"text": " Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., halorhodopsin, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23002710",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 994,
"text": "It allows neurons to express light-sensitive genes that enable the identification, dissection, and manipulation of specific neural populations and their connections in the tissues and organs of awake animals with unprecedented spatial and temporal precision. Light-sensitive genes chiefly including the genetically targeted light-gated channels channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR) cause intracellular ion flow during optical illumination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25060859",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "The most widely used optogenetic tool, Channelrhodopsin2 (ChR2), is both light- and voltage-sensitive. A light-triggered action potential or light-driven perturbations of ongoing electrical activity provide instant voltage feedback, shaping ChR2 current."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25303540",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 563,
"text": "The versatility and the electrophysiologic characteristics of the light-sensitive ion-channels channelrhodopsin-2 (ChR2), halorhodopsin (NpHR), and the light-sensitive proton pump archaerhodopsin-3 (Arch) make these optogenetic tools potent candidates in controlling neuronal firing in models of epilepsy and in providing insights into the physiology and pathology of neuronal network organization and synchronization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24022017",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 432,
"text": " Optogenetic methods have emerged as a powerful tool for elucidating neural circuit activity underlying a diverse set of behaviors across a broad range of species. Optogenetic tools of microbial origin consist of light-sensitive membrane proteins that are able to activate (e.g., channelrhodopsin-2, ChR2) or silence (e.g., halorhodopsin, NpHR) neural activity ingenetically-defined cell types over behaviorally-relevant timescales."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Channelrhodospin-2 (ChR2), a light-sensitive ion channel, and its variants have emerged as new excitatory optogenetic tools not only in neuroscience, but also in other areas, including cardiac electrophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23002710",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 994,
"text": "It allows neurons to express light-sensitive genes that enable the identification, dissection, and manipulation of specific neural populations and their connections in the tissues and organs of awake animals with unprecedented spatial and temporal precision. Light-sensitive genes chiefly including the genetically targeted light-gated channels channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR) cause intracellular ion flow during optical illumination."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D062308"
] |
[] |
56e073ad51531f7e3300000e
|
bioasq_yesno
|
factoid
|
Which enzyme is targeted by Evolocumab?
|
[['proprotein convertase subtilisin/kexin type 9']]
|
[
"proprotein convertase subtilisin/kexin type 9",
"PCSK9",
"proprotein convertase 9",
"subtilisin/kexin type 9",
"proprotein convertase 9",
"kexin-9"
] |
['Evolocumab (AMG145) is a fully human monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9) that demonstrated marked reductions in plasma low-density lipoprotein cholesterol concentrations in statin-intolerant patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"http://www.ncbi.nlm.nih.gov/pubmed/24598985",
"http://www.ncbi.nlm.nih.gov/pubmed/24509273",
"http://www.ncbi.nlm.nih.gov/pubmed/24481874",
"http://www.ncbi.nlm.nih.gov/pubmed/24477778",
"http://www.ncbi.nlm.nih.gov/pubmed/24284914",
"http://www.ncbi.nlm.nih.gov/pubmed/24255061",
"http://www.ncbi.nlm.nih.gov/pubmed/25470376",
"http://www.ncbi.nlm.nih.gov/pubmed/25410046",
"http://www.ncbi.nlm.nih.gov/pubmed/25282520",
"http://www.ncbi.nlm.nih.gov/pubmed/25282519",
"http://www.ncbi.nlm.nih.gov/pubmed/25079474",
"http://www.ncbi.nlm.nih.gov/pubmed/25052769",
"http://www.ncbi.nlm.nih.gov/pubmed/25002170",
"http://www.ncbi.nlm.nih.gov/pubmed/24961142",
"http://www.ncbi.nlm.nih.gov/pubmed/24953396",
"http://www.ncbi.nlm.nih.gov/pubmed/24953393",
"http://www.ncbi.nlm.nih.gov/pubmed/24859266",
"http://www.ncbi.nlm.nih.gov/pubmed/24825642",
"http://www.ncbi.nlm.nih.gov/pubmed/24694531",
"http://www.ncbi.nlm.nih.gov/pubmed/24691094",
"http://www.ncbi.nlm.nih.gov/pubmed/24678979",
"http://www.ncbi.nlm.nih.gov/pubmed/24662398",
"http://www.ncbi.nlm.nih.gov/pubmed/24373748"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Efficacy and safety profile of evolocumab (AMG145), an injectable inhibitor of the proprotein convertase subtilisin/kexin type 9: the available clinical evidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 582,
"text": "AREAS COVERED: Evolocumab (AMG145) is a monoclonal antibody inhibiting the proprotein convertase subtilisin/kexin type 9 that binds to the liver LDL receptor and prevents it from normal recycling by targeting it for degradation. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24598985",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Efficacy and safety of evolocumab (AMG 145), a fully human monoclonal antibody to PCSK9, in hyperlipidaemic patients on various background lipid therapies: pooled analysis of 1359 patients in four phase 2 trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24598985",
"endSection": "abstract",
"offsetInBeginSection": 449,
"offsetInEndSection": 560,
"text": "We report a pooled analysis from four phase 2 studies of evolocumab (AMG 145), a monoclonal antibody to PCSK9. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509273",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Reduction in lipoprotein(a) with PCSK9 monoclonal antibody evolocumab (AMG 145): a pooled analysis of more than 1,300 patients in 4 phase II trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509273",
"endSection": "abstract",
"offsetInBeginSection": 449,
"offsetInEndSection": 775,
"text": "METHODS: A pooled analysis of data from 1,359 patients in 4 phase II trials assessed the effects of evolocumab, a fully human monoclonal antibody to PCSK9, on Lp(a), the relationship between Lp(a) and lowering of low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B, and the influence of background statin therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509273",
"endSection": "abstract",
"offsetInBeginSection": 1490,
"offsetInEndSection": 1597,
"text": "CONCLUSIONS: Inhibition of PCSK9 with evolocumab resulted in significant dose-related reductions in Lp(a). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24481874",
"endSection": "abstract",
"offsetInBeginSection": 467,
"offsetInEndSection": 703,
"text": "Monoclonal antibodies that inhibit proprotein convertase subtilisin/kexin type 9, including evolocumab (previously AMG 145), dramatically lowered LDL-C in phase 2 clinical trials when administered alone or in combination with a statin. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24477778",
"endSection": "abstract",
"offsetInBeginSection": 545,
"offsetInEndSection": 722,
"text": "Evolocumab (AMG 145) is a fully human monoclonal antibody that binds PCSK9, inhibiting its interaction with the LDL receptor to preserve LDL-receptor recycling and reduce LDL-C."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24284914",
"endSection": "abstract",
"offsetInBeginSection": 701,
"offsetInEndSection": 1082,
"text": "Antibody therapeutics in Phase 3 studies are described, with an emphasis on those with study completion dates in 2014, including antibodies targeting interleukin-17a or the interleukin-17a receptor (secukinumab, ixekizumab, brodalumab), proprotein convertase subtilisin/kexin type 9 (alirocumab, evolocumab, bococizumab), and programmed death 1 receptor (lambrolizumab, nivolumab)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24255061",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "BACKGROUND: Evolocumab (AMG 145), a monoclonal antibody against proprotein convertase subtilisin/kexin type 9 (PCSK9), significantly reduced low-density lipoprotein cholesterol (LDL-C) in phase 2 studies of 12 weeks' duration. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25410046",
"endSection": "abstract",
"offsetInBeginSection": 479,
"offsetInEndSection": 876,
"text": "These compounds act either by reducing low-density lipoprotein (LDL) production by inhibiting apolipoprotein B synthesis with an antisense oligonucleotide (mipomersen) or by inhibiting microsomal triglyceride transfer protein (lomitapide), or by enhancing LDL catabolism via monoclonal antibody-mediated inhibition of the activity of proprotein convertase subtilisin/kexin 9 (PCSK9) (evolocumab). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25282520",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Inhibition of PCSK9 with evolocumab in homozygous familial hypercholesterolaemia (TESLA Part B): a randomised, double-blind, placebo-controlled trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25282520",
"endSection": "abstract",
"offsetInBeginSection": 292,
"offsetInEndSection": 433,
"text": "Evolocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), reduced LDL cholesterol by 16% in a pilot study. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25282519",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "PCSK9 inhibition with evolocumab (AMG 145) in heterozygous familial hypercholesterolaemia (RUTHERFORD-2): a randomised, double-blind, placebo-controlled trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25282519",
"endSection": "abstract",
"offsetInBeginSection": 346,
"offsetInEndSection": 470,
"text": "We investigated the effect of PCSK9 inhibition with evolocumab (AMG 145) on LDL cholesterol in patients with this disorder. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25079474",
"endSection": "abstract",
"offsetInBeginSection": 989,
"offsetInEndSection": 1099,
"text": "Some of the anti-dyslipidemic drugs which work by PCSK9 inhibition include evolocumab, alirocumab and ALN-PCS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25052769",
"endSection": "abstract",
"offsetInBeginSection": 615,
"offsetInEndSection": 842,
"text": "We highlight the different steps of this adventure and review the published clinical trials especially those with the anti-PCSK9 antibodies evolocumab (AMG 145) and alirocumab (SAR236553/REGN727), which are in phase III trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25002170",
"endSection": "abstract",
"offsetInBeginSection": 744,
"offsetInEndSection": 930,
"text": "Monoclonal antibodies against PCSK9 represent so far the most advanced approach in clinical development, with alirocumab, evolocumab and bococizumab under advanced clinical development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24961142",
"endSection": "abstract",
"offsetInBeginSection": 301,
"offsetInEndSection": 554,
"text": "AREAS COVERED: Evolocumab and alirocumab are fully human monoclonal antibodies inhibiting the proprotein convertase subtilisin/kexin type 9 (PCSK9) that binds to hepatic LDL receptor and prevents it from normal recycling by targeting it for degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24961142",
"endSection": "abstract",
"offsetInBeginSection": 692,
"offsetInEndSection": 939,
"text": "Phase II (for evolocumab and alirocumab) and III (for evolocumab) trials show that PCSK9 inhibitors are equally well tolerated, with adverse events mainly limited to mild-to-moderate nasopharyngitis, injection-site pain, arthralgia and back pain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24953396",
"endSection": "abstract",
"offsetInBeginSection": 837,
"offsetInEndSection": 1208,
"text": "Four classes of newer lipid-lowering drugs offer promising advances in treating FH, namely the apolipoprotein-B synthesis inhibitors (mipomersen), the microsomal transfer protein inhibitors (lomitapide), the cholesterol ester transfer protein inhibitors (anacetrapib, evacetrapib) and the proprotein convertase subtilisin/kexin type 9 inhibitors (evolocumab, alirocumab)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24953393",
"endSection": "abstract",
"offsetInBeginSection": 584,
"offsetInEndSection": 762,
"text": "Monoclonal antibodies that inhibit proprotein convertase subtilisin/ kexin type 9 (PCSK9), which degrades the LDL receptor, like alirocumab and evolocumab, are in phase 3 trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24859266",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 462,
"text": "In support of the drug development program for Evolocumab, a fully human IgGâ‚‚ antibody that targets PCSK9, a quantitative ELISA to measure free PCSK9 in human serum was developed. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24825642",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "IMPORTANCE: In phase 2 studies, evolocumab, a fully human monoclonal antibody to PCSK9, reduced LDL-C levels in patients receiving statin therapy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24694531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "Anti-PCSK9 antibody effectively lowers cholesterol in patients with statin intolerance: the GAUSS-2 randomized, placebo-controlled phase 3 clinical trial of evolocumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24694531",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 580,
"text": "Evolocumab, a fully human monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), demonstrated marked reductions in plasma low-density lipoprotein cholesterol (LDL-C) in a phase 2 study in statin-intolerant patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24691094",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Anti-PCSK9 monotherapy for hypercholesterolemia: the MENDEL-2 randomized, controlled phase III clinical trial of evolocumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24691094",
"endSection": "abstract",
"offsetInBeginSection": 173,
"offsetInEndSection": 342,
"text": "BACKGROUND: Evolocumab, a fully human monoclonal antibody against proprotein convertase subtilisin/kexin type 9 (PCSK9), significantly reduced LDL-C in phase II trials. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24678979",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "BACKGROUND: Evolocumab, a monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9), significantly reduced low-density lipoprotein (LDL) cholesterol levels in phase 2 studies. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24662398",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Effects of evolocumab (AMG 145), a monoclonal antibody to PCSK9, in hypercholesterolemic, statin-treated Japanese patients at high cardiovascular risk--primary results from the phase 2 YUKAWA study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Efficacy and safety profile of evolocumab (AMG145), an injectable inhibitor of the proprotein convertase subtilisin/kexin type 9: the available clinical evidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 582,
"text": "AREAS COVERED: Evolocumab (AMG145) is a monoclonal antibody inhibiting the proprotein convertase subtilisin/kexin type 9 that binds to the liver LDL receptor and prevents it from normal recycling by targeting it for degradation. "
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
54e0d1491388e8454a000014
|
bioasq_factoid
|
factoid
|
Which tool exists for microsatellite (SSR) loci detection and primer design?
|
['FullSSR']
|
[
"FullSSR",
"Full SSR",
"Full SSR model",
"Full SSR analysis"
] |
['Microsatellites are genomic sequences comprised of tandem repeats of short nucleotide motifs widely used as molecular markers in population genetics. FullSSR is a new bioinformatic tool for microsatellite (SSR) loci detection and primer design using genomic data from NGS assay.', 'FullSSR is a new bioinformatic tool for microsatellite (SSR) loci detection and primer design using genomic data from NGS assay. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27366148"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 51,
"text": "FullSSR: Microsatellite Finder and Primer Designer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 278,
"text": "Microsatellites are genomic sequences comprised of tandem repeats of short nucleotide motifs widely used as molecular markers in population genetics. FullSSR is a new bioinformatic tool for microsatellite (SSR) loci detection and primer design using genomic data from NGS assay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "abstract",
"offsetInBeginSection": 150,
"offsetInEndSection": 278,
"text": "FullSSR is a new bioinformatic tool for microsatellite (SSR) loci detection and primer design using genomic data from NGS assay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "abstract",
"offsetInBeginSection": 849,
"offsetInEndSection": 926,
"text": "FullSSR simplifies the detection of SSRs and primer design on a big data set."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "abstract",
"offsetInBeginSection": 850,
"offsetInEndSection": 927,
"text": "FullSSR simplifies the detection of SSRs and primer design on a big data set."
}
] | 11
|
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D018895",
"https://meshb.nlm.nih.gov/record/ui?ui=D017931"
] | null |
5a6fa61ab750ff4455000060
|
bioasq_factoid
|
factoid
|
What is the cause of the Kleefstra syndrome?
|
['Mutations in the Euchromatic Histone Methyltransferase 1 (EHMT1)']
|
[
"Euchromatic Histone Methyltransferase 1",
"EHMT1",
"EHMT1 protein",
"KMT1D",
"Histone methyltransferase EHMT1",
"Euchromatic histone methyltransferase 1"
] |
['Mutations in the Euchromatic Histone Methyltransferase 1 (EHMT1) gene cause Kleefstra syndrome, a rare form of intellectual disability (ID) with strong autistic traits and sensory processing deficits.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32531423",
"http://www.ncbi.nlm.nih.gov/pubmed/32975655",
"http://www.ncbi.nlm.nih.gov/pubmed/30585561",
"http://www.ncbi.nlm.nih.gov/pubmed/31750954",
"http://www.ncbi.nlm.nih.gov/pubmed/32539280"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31750954",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Kleefstra syndrome is a rare neurogenetic disorder caused by a subtelomeric 9q34.3 deletion or by an intragenic mutation of the euchromatin histone methyl transferase 1 gene (EHMT1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32531423",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Kleefstra syndrome is a disorder caused by a mutation in the EHMT1 gene characterized in humans by general developmental delay, mild to severe intellectual disability and autism. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32539280",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Kleefstra syndrome (KS) is an autosomal dominant disorder caused by a chromosomal deletion at 9q34.3 resulting in pathogenic variants of the gene that codes for the enzyme, euchromatin histone methyltransferase 1 (EHMT1). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32975655",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "Mutations in the Euchromatic Histone Methyltransferase 1 (EHMT1) gene cause Kleefstra syndrome, a rare form of intellectual disability (ID) with strong autistic traits and sensory processing deficits."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30585561",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Kleefstra syndrome (chromosome 9q34.3 deletion) is a rare genetic disorder with less than 110 patients reported till date. "
}
] | 11
|
BioASQ-training11b
| null | null |
60805e204e6a4cf630000002
|
bioasq_factoid
|
yesno
|
Do carmustine wafers improve survival of glioblastoma patients?
|
['yes']
|
[
"yes"
] |
['Yes, it has been documented that implantation of carmustine wafers improves survival of newly diagnosed and recurrent glioblastoma patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25054300",
"http://www.ncbi.nlm.nih.gov/pubmed/22715955",
"http://www.ncbi.nlm.nih.gov/pubmed/21330749",
"http://www.ncbi.nlm.nih.gov/pubmed/21300471",
"http://www.ncbi.nlm.nih.gov/pubmed/20706757",
"http://www.ncbi.nlm.nih.gov/pubmed/20511192",
"http://www.ncbi.nlm.nih.gov/pubmed/19123896",
"http://www.ncbi.nlm.nih.gov/pubmed/19046047",
"http://www.ncbi.nlm.nih.gov/pubmed/18636295",
"http://www.ncbi.nlm.nih.gov/pubmed/18366283",
"http://www.ncbi.nlm.nih.gov/pubmed/18035958",
"http://www.ncbi.nlm.nih.gov/pubmed/17350791",
"http://www.ncbi.nlm.nih.gov/pubmed/16482400",
"http://www.ncbi.nlm.nih.gov/pubmed/15937647",
"http://www.ncbi.nlm.nih.gov/pubmed/15015668",
"http://www.ncbi.nlm.nih.gov/pubmed/12672279",
"http://www.ncbi.nlm.nih.gov/pubmed/12074689",
"http://www.ncbi.nlm.nih.gov/pubmed/20155992",
"http://www.ncbi.nlm.nih.gov/pubmed/19514083",
"http://www.ncbi.nlm.nih.gov/pubmed/23662801",
"http://www.ncbi.nlm.nih.gov/pubmed/23535992",
"http://www.ncbi.nlm.nih.gov/pubmed/21756557",
"http://www.ncbi.nlm.nih.gov/pubmed/21479583",
"http://www.ncbi.nlm.nih.gov/pubmed/21390826",
"http://www.ncbi.nlm.nih.gov/pubmed/10414561",
"http://www.ncbi.nlm.nih.gov/pubmed/25269031",
"http://www.ncbi.nlm.nih.gov/pubmed/24246204",
"http://www.ncbi.nlm.nih.gov/pubmed/23118709",
"http://www.ncbi.nlm.nih.gov/pubmed/23350777",
"http://www.ncbi.nlm.nih.gov/pubmed/18240917",
"http://www.ncbi.nlm.nih.gov/pubmed/21344976",
"http://www.ncbi.nlm.nih.gov/pubmed/17938702",
"http://www.ncbi.nlm.nih.gov/pubmed/15069758",
"http://www.ncbi.nlm.nih.gov/pubmed/22718138",
"http://www.ncbi.nlm.nih.gov/pubmed/17334672",
"http://www.ncbi.nlm.nih.gov/pubmed/25085219",
"http://www.ncbi.nlm.nih.gov/pubmed/21983866"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25054300",
"endSection": "abstract",
"offsetInBeginSection": 338,
"offsetInEndSection": 472,
"text": "At recurrence, treatment options include repeat surgery (with or without Gliadel wafer placement), reirradiation or systemic therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22715955",
"endSection": "abstract",
"offsetInBeginSection": 1563,
"offsetInEndSection": 1909,
"text": "DISCUSSION: Carmustine wafers for primary HGG surgery in accordance with the NICE TA121 were associated with a median survival of 15.3 months; this is improved compared with previously reported randomised trials. Multimodal treatment with carmustine wafers, radical radiotherapy and concomitant temozolomide was associated with improved survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21330749",
"endSection": "abstract",
"offsetInBeginSection": 642,
"offsetInEndSection": 886,
"text": "Gliadel wafer is a new approach to the treatment of glioblastoma, which involves controlled release delivery of carmustine from biodegradable polymer wafers. It has shown promising results and provides a silver lining for glioblastoma patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21300471",
"endSection": "abstract",
"offsetInBeginSection": 613,
"offsetInEndSection": 745,
"text": "For patient with and without Gliadel, median and 1-year RFS were 12.9 months and 52% vs. 14 months and 42%, respectively (p = 0.89)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21300471",
"endSection": "abstract",
"offsetInBeginSection": 1276,
"offsetInEndSection": 1371,
"text": "According to pathology, Gliadel did not influence OS of patients with Grade III or glioblastoma"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21300471",
"endSection": "abstract",
"offsetInBeginSection": 1821,
"offsetInEndSection": 1945,
"text": "CONCLUSION: In patients with high-grade gliomas, adding Gliadel before performing a Stupp protocol did not improve survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20706757",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Randomized phase III trials have shown significant improvement of survival 1, 2, and 3 years after implantation of 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) wafers for patients with newly diagnosed malignant glioma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19123896",
"endSection": "abstract",
"offsetInBeginSection": 2138,
"offsetInEndSection": 2438,
"text": "CONCLUSIONS: The combination of aggressive resection, Gliadel wafer implantation, and GKS in addition to standard fractionated RT in selected patients resulted in increased local control and increased survival compared with a historical control group treated with surgery and involved-field RT alone."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19046047",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 230,
"text": "OBJECT: Gliadel (BCNU) wafer and concomitant temozolomide (TMZ) therapy, when used individually as adjuvant therapies, extend survival from that achieved by resection and radiation therapy (XRT) for glioblastoma multiforme (GBM). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18636295",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "BACKGROUND: Gliadel (polifeprosan 20 with carmustine [BCNU] implant) is commonly used for local delivery of BCNU to high-grade gliomas after resection and is associated with increased survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17350791",
"endSection": "abstract",
"offsetInBeginSection": 546,
"offsetInEndSection": 719,
"text": "Temozolomide administered according to this protocol produced a median survival benefit of 2 months in glioblastomas, and carmustine a similar benefit in high-grade gliomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16482400",
"endSection": "abstract",
"offsetInBeginSection": 283,
"offsetInEndSection": 455,
"text": "Analysis of a large trial by Westphal and colleagues (n = 240) showed a 29% risk reduction (P = 0.03) in the BCNU wafer-treated group over the course of the 30-month trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16482400",
"endSection": "abstract",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1360,
"text": "Median survival of patients treated with BCNU wafers was 13.8 months vs 11.6 months in placebo-treated patients (P = 0.017) with a hazard ratio of 0.73 (P = 0.018), representing a 27% significant risk reduction. This survival advantage was maintained at 1, 2, and 3 years and was statistically significant (P = 0.01) at 3 years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16482400",
"endSection": "abstract",
"offsetInBeginSection": 1474,
"offsetInEndSection": 1689,
"text": "CONCLUSION: Malignant glioma patients treated with BCNU wafers at the time of initial surgery in combination with radiation therapy demonstrated a survival advantage at 2 and 3 years follow-up compared with placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15015668",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "OBJECTIVE: Recently a randomized placebo-controlled phase III trial of biodegradable polymers containing carmustine has demonstrated a significant survival benefit for patients treated with local chemotherapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15015668",
"endSection": "abstract",
"offsetInBeginSection": 1810,
"offsetInEndSection": 2051,
"text": "CONCLUSION: In this subgroup analysis of a phase III trial population both the clinical progression and radiological progression were significantly delayed in patients treated with local chemotherapy, resulting in an increased survival time."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12672279",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 399,
"text": "A previous placebo-controlled trial has shown that biodegradable 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) wafers (Gliadel wafers) prolong survival in patients with recurrent glioblastoma multiforme. A previously completed phase 3 trial, also placebo controlled, in 32 patients with newly diagnosed malignant glioma also demonstrated a survival benefit in those patients treated with BCNU wafers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12672279",
"endSection": "abstract",
"offsetInBeginSection": 815,
"offsetInEndSection": 1198,
"text": "Median survival in the intent-to-treat group was 13.9 months for the BCNU wafer-treated group and 11.6 months for the placebo-treated group (log-rank P -value stratified by country = 0.03), with a 29% reduction in the risk of death in the treatment group. When adjusted for factors affecting survival, the treatment effect remained positive with a risk reduction of 28% ( P = 0.03). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12074689",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Controlled release delivery of carmustine from biodegradable polymer wafers was approved as an adjunct to surgical resection in the treatment of recurrent glioblastoma multiforme after it was shown in clinical trials to be well tolerated and effective. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20155992",
"endSection": "abstract",
"offsetInBeginSection": 349,
"offsetInEndSection": 513,
"text": "Clinical trials have demonstrated significant improvements in survival and quality of life for patients after complete tumour resection and BCNU wafer implantation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20155992",
"endSection": "abstract",
"offsetInBeginSection": 1553,
"offsetInEndSection": 1767,
"text": "BCNU wafers are an effective means of increasing survival and quality of life in patients diagnosed with malignant glioma, and are a valuable addition to the overall multimodal treatment strategy for these tumours."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19514083",
"endSection": "abstract",
"offsetInBeginSection": 1520,
"offsetInEndSection": 1717,
"text": "CONCLUSIONS: Carmustine wafer with concurrent TMZ and radiation followed by rotational chemotherapy is a well tolerated, effective therapy, and has a survival benefit compared with radiation alone."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23535992",
"endSection": "abstract",
"offsetInBeginSection": 1297,
"offsetInEndSection": 1518,
"text": "Median overall survival in 14 studies of newly-diagnosed patients suggested a modest improvement versus resection followed by Stupp protocol or resection with BCNU wafers, with an acceptable and manageable safety profile."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21756557",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "The efficacy of carmustine wafers for older patients with glioblastoma multiforme: prolonging survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21756557",
"endSection": "abstract",
"offsetInBeginSection": 1607,
"offsetInEndSection": 1826,
"text": "DISCUSSION: Older patients with GBM may benefit from carmustine wafers. The survival for older patients who received carmustine wafers is significantly longer than matched patients who did not receive carmustine wafers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21479583",
"endSection": "abstract",
"offsetInBeginSection": 668,
"offsetInEndSection": 958,
"text": "For glioblastoma patients who received ≥90% resection in the BCNU wafer study, median survival increased for BCNU wafer versus placebo (14.5 versus 12.4 months, respectively; P = 0.02), but no survival increase was found for <90% resection (11.7 versus 10.6 months, respectively; P = 0.98)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21390826",
"endSection": "abstract",
"offsetInBeginSection": 1923,
"offsetInEndSection": 2144,
"text": "A wafer impregnated with carmustine, for use as an implant after surgical removal of recurrent GBM showed a prolongation in the median survival time of only 2 mo, from 20 to 28 wk in a study with a total of 222 patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10414561",
"endSection": "abstract",
"offsetInBeginSection": 1620,
"offsetInEndSection": 1696,
"text": "No clear survival benefit associated with wafer implantation was identified."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25269031",
"endSection": "abstract",
"offsetInBeginSection": 710,
"offsetInEndSection": 866,
"text": "In three of the trials, patients with GBM who received carmustine wafers had significantly longer median survival than patients who did not receive wafers. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24246204",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1298,
"text": "TMZ and carmustine (BCNU) biodegradable wafer (Gliadel) are the only adjuvant chemotherapies that have improved survival in randomised GB clinical trials . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23118709",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 519,
"text": "The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent malignant glioma, with little increased risk of adverse events. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23118709",
"endSection": "abstract",
"offsetInBeginSection": 1365,
"offsetInEndSection": 1644,
"text": "For patients undergoing repeat resection for malignant glioma, a randomized, blinded, placebo-controlled trial demonstrated a median survival for 110 patients who received carmustine polymers of 31 weeks compared with 23 weeks for 122 patients who only received placebo polymers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23118709",
"endSection": "abstract",
"offsetInBeginSection": 1977,
"offsetInEndSection": 2261,
"text": "Median survival was improved from 11.6 to 13.9 months (P = 0.03), with a 29% reduction in the risk of death. When patients with glioblastoma multiforme alone were analyzed, the median survival improved from 11.4 to 13.5 months, but this improvement was not statistically significant. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23350777",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 252,
"text": "OBJECT: Locoregional chemotherapy with carmustine wafers, positioned at surgery and followed by radiation therapy, has been shown to prolong survival in patients with newly diagnosed glioblastoma, as has concomitant radiochemotherapy with temozolomide."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21756557",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "The efficacy of carmustine wafers for older patients with glioblastoma multiforme: prolonging survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17334672",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 250,
"text": "Following the resection of newly diagnosed or recurrent glioblastomas, local implantation of carmustine-impregnated biodegradable wafers (Gliadel) in the resection cavity constitutes an adjuvant therapy that can improve the possibilities of survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23118709",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 518,
"text": "The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent malignant glioma, with little increased risk of adverse events."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21756557",
"endSection": "abstract",
"offsetInBeginSection": 1154,
"offsetInEndSection": 1266,
"text": "However, patients with carmustine wafers demonstrated prolonged survival as compared to patients without wafers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21756557",
"endSection": "abstract",
"offsetInBeginSection": 1267,
"offsetInEndSection": 1414,
"text": "The median survival for patients with carmustine wafers was 8.7 months, while median survival for patients without wafers was 5.5 months (P=0.007)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21756557",
"endSection": "abstract",
"offsetInBeginSection": 1415,
"offsetInEndSection": 1606,
"text": "Likewise, in subgroup analysis, patients older than 70 years (P=0.0003) and 75 years (P=0.04) who had carmustine wafers had significantly longer survival than matched patients without wafers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22715955",
"endSection": "abstract",
"offsetInBeginSection": 1563,
"offsetInEndSection": 1909,
"text": "DISCUSSION: Carmustine wafers for primary HGG surgery in accordance with the NICE TA121 were associated with a median survival of 15.3 months; this is improved compared with previously reported randomised trials. Multimodal treatment with carmustine wafers, radical radiotherapy and concomitant temozolomide was associated with improved survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25269031",
"endSection": "abstract",
"offsetInBeginSection": 865,
"offsetInEndSection": 954,
"text": "Implantation of carmustine wafers did not significantly improve progression-free survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25269031",
"endSection": "abstract",
"offsetInBeginSection": 709,
"offsetInEndSection": 863,
"text": "In three of the trials, patients with GBM who received carmustine wafers had significantly longer median survival than patients who did not receive wafers"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12672279",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "A previous placebo-controlled trial has shown that biodegradable 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) wafers (Gliadel wafers) prolong survival in patients with recurrent glioblastoma multiforme"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12672279",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 397,
"text": "A previously completed phase 3 trial, also placebo controlled, in 32 patients with newly diagnosed malignant glioma also demonstrated a survival benefit in those patients treated with BCNU wafers"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17334672",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Following the resection of newly diagnosed or recurrent glioblastomas, local implantation of carmustine-impregnated biodegradable wafers (Gliadel) in the resection cavity constitutes an adjuvant therapy that can improve the possibilities of survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22715955",
"endSection": "abstract",
"offsetInBeginSection": 1722,
"offsetInEndSection": 1854,
"text": "Multimodal treatment with carmustine wafers, radical radiotherapy and concomitant temozolomide was associated with improved survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23118709",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 517,
"text": "The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent malignant glioma, with little increased risk of adverse events"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24246204",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1296,
"text": "TMZ and carmustine (BCNU) biodegradable wafer (Gliadel) are the only adjuvant chemotherapies that have improved survival in randomised GB clinical trials "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17334672",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Following the resection of newly diagnosed or recurrent glioblastomas, local implantation of carmustine-impregnated biodegradable wafers (Gliadel) in the resection cavity constitutes an adjuvant therapy that can improve the possibilities of survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22715955",
"endSection": "abstract",
"offsetInBeginSection": 1722,
"offsetInEndSection": 1854,
"text": "Multimodal treatment with carmustine wafers, radical radiotherapy and concomitant temozolomide was associated with improved survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23118709",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 517,
"text": "The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent malignant glioma, with little increased risk of adverse events"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24246204",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1296,
"text": "TMZ and carmustine (BCNU) biodegradable wafer (Gliadel) are the only adjuvant chemotherapies that have improved survival in randomised GB clinical trials "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17334672",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Following the resection of newly diagnosed or recurrent glioblastomas, local implantation of carmustine-impregnated biodegradable wafers (Gliadel) in the resection cavity constitutes an adjuvant therapy that can improve the possibilities of survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22715955",
"endSection": "abstract",
"offsetInBeginSection": 1722,
"offsetInEndSection": 1854,
"text": "Multimodal treatment with carmustine wafers, radical radiotherapy and concomitant temozolomide was associated with improved survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23118709",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 517,
"text": "The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent malignant glioma, with little increased risk of adverse events"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24246204",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1296,
"text": "TMZ and carmustine (BCNU) biodegradable wafer (Gliadel) are the only adjuvant chemotherapies that have improved survival in randomised GB clinical trials "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17334672",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Following the resection of newly diagnosed or recurrent glioblastomas, local implantation of carmustine-impregnated biodegradable wafers (Gliadel) in the resection cavity constitutes an adjuvant therapy that can improve the possibilities of survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22715955",
"endSection": "abstract",
"offsetInBeginSection": 1722,
"offsetInEndSection": 1854,
"text": "Multimodal treatment with carmustine wafers, radical radiotherapy and concomitant temozolomide was associated with improved survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23118709",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 517,
"text": "The carmustine implant wafer was demonstrated to improve survival in blinded placebo-controlled trials in selected patients with newly diagnosed or recurrent malignant glioma, with little increased risk of adverse events"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24246204",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1296,
"text": "TMZ and carmustine (BCNU) biodegradable wafer (Gliadel) are the only adjuvant chemotherapies that have improved survival in randomised GB clinical trials "
}
] | 5
|
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4275776"
] |
[] |
54d630283706e89528000004
|
bioasq_yesno
|
factoid
|
Which web resource for LIR motif-containing proteins in eukaryotes has been developed?
|
['The iLIR database']
|
[
"iLIR database",
"iLIR",
"iLIRdb",
"iLIR Database"
] |
['In the past few years it has been revealed that Atg8-interacting proteins include not only receptors but also components of the core autophagic machinery, proteins associated with vesicles and their transport, and specific proteins that are selectively degraded by autophagy. Atg8-interacting proteins contain a short linear LC3-interacting region/LC3 recognition sequence/Atg8-interacting motif (LIR/LRS/AIM) motif which is responsible for their interaction with Atg8-family proteins. These proteins are referred to as LIR-containing proteins (LIRCPs). So far, many experimental efforts have been carried out to identify new LIRCPs, leading to the characterization of some of them in the past 10 years. Given the need for the identification of LIRCPs in various organisms, the iLIR database ( https://ilir.warwick.ac.uk ) has been developed as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27484196"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "iLIR database: A web resource for LIR motif-containing proteins in eukaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1848,
"text": "In the past few years it has been revealed that Atg8-interacting proteins include not only receptors but also components of the core autophagic machinery, proteins associated with vesicles and their transport, and specific proteins that are selectively degraded by autophagy. Atg8-interacting proteins contain a short linear LC3-interacting region/LC3 recognition sequence/Atg8-interacting motif (LIR/LRS/AIM) motif which is responsible for their interaction with Atg8-family proteins. These proteins are referred to as LIR-containing proteins (LIRCPs). So far, many experimental efforts have been carried out to identify new LIRCPs, leading to the characterization of some of them in the past 10Â years. Given the need for the identification of LIRCPs in various organisms, we developed the iLIR database ( https://ilir.warwick.ac.uk ) as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis. Additionally, a curated text-mining analysis of the literature permitted us to identify novel putative LICRPs in mammals that have not previously been associated with autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "abstract",
"offsetInBeginSection": 1329,
"offsetInEndSection": 1670,
"text": "Given the need for the identification of LIRCPs in various organisms, we developed the iLIR database ( https://ilir.warwick.ac.uk ) as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "iLIR database: a web resource for LIR motif-containing proteins in eukaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "abstract",
"offsetInBeginSection": 1330,
"offsetInEndSection": 1671,
"text": "Given the need for the identification of LIRCPs in various organisms, we developed the iLIR database ( https://ilir.warwick.ac.uk ) as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "iLIR database: A web resource for LIR motif-containing proteins in eukaryotes."
}
] | 11
|
BioASQ-training11b
| null | null |
5a8056a2faa1ab7d2e00001f
|
bioasq_factoid
|
yesno
|
Is apremilast effective for psoriasis?
|
['yes']
|
[
"yes"
] |
['Yes, apremilast is effective for treatment of psoriasis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27376729",
"http://www.ncbi.nlm.nih.gov/pubmed/26923915",
"http://www.ncbi.nlm.nih.gov/pubmed/26220911",
"http://www.ncbi.nlm.nih.gov/pubmed/22712800",
"http://www.ncbi.nlm.nih.gov/pubmed/26243735",
"http://www.ncbi.nlm.nih.gov/pubmed/26644232",
"http://www.ncbi.nlm.nih.gov/pubmed/26806620",
"http://www.ncbi.nlm.nih.gov/pubmed/26549249",
"http://www.ncbi.nlm.nih.gov/pubmed/27486641",
"http://www.ncbi.nlm.nih.gov/pubmed/23663752",
"http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"http://www.ncbi.nlm.nih.gov/pubmed/26954311",
"http://www.ncbi.nlm.nih.gov/pubmed/26357944",
"http://www.ncbi.nlm.nih.gov/pubmed/20419594",
"http://www.ncbi.nlm.nih.gov/pubmed/26267722",
"http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"http://www.ncbi.nlm.nih.gov/pubmed/23569359",
"http://www.ncbi.nlm.nih.gov/pubmed/26892034",
"http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"http://www.ncbi.nlm.nih.gov/pubmed/27538241",
"http://www.ncbi.nlm.nih.gov/pubmed/26660203",
"http://www.ncbi.nlm.nih.gov/pubmed/26820148",
"http://www.ncbi.nlm.nih.gov/pubmed/26837052",
"http://www.ncbi.nlm.nih.gov/pubmed/27021239",
"http://www.ncbi.nlm.nih.gov/pubmed/23030767",
"http://www.ncbi.nlm.nih.gov/pubmed/26792812"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26549249",
"endSection": "abstract",
"offsetInBeginSection": 1630,
"offsetInEndSection": 1698,
"text": "CONCLUSION: Apremilast reduces the severity of nail/scalp psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26792812",
"endSection": "abstract",
"offsetInBeginSection": 1638,
"offsetInEndSection": 1834,
"text": "CONCLUSIONS: Apremilast demonstrated clinically meaningful improvements in psoriatic arthritis and psoriasis at week 16; sustained improvements were seen with continued treatment through 52 weeks."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Apremilast: A Novel Drug for Treatment of Psoriasis and Psoriatic Arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 634,
"offsetInEndSection": 910,
"text": "In those that involved doses of 30 mg twice daily, a significantly greater percentage of patients receiving apremilast (28.8% to 40.9%) compared with placebo (5.3% to 5.8%) achieved at least 75% improvement from baseline in Psoriasis Area and Severity Index score at 16 weeks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1605,
"text": "CONCLUSIONS: Apremilast has a novel mechanism of action and is safe and effective for the management of psoriasis and psoriatic arthritis. At this time, apremilast should be reserved for patients unable to take disease-modifying antirheumatic drugs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor, in patients with moderate to severe plaque psoriasis: Results of a phase III, randomized, controlled trial (Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis [ESTEEM] 1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23569359",
"endSection": "abstract",
"offsetInBeginSection": 938,
"offsetInEndSection": 1338,
"text": "More recently, three larger double-blinded, and randomized multicenter studies demonstrate that apremilast is efficacious in the treatment of psoriasis and PsA, with significantly higher numbers of apremilast-treated patients achieving endpoints of a 75% reduction compared to baseline in Psoriasis Area and Severity Index (PASI-75) or American College of Rheumatology-20 scores, relative to placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"endSection": "abstract",
"offsetInBeginSection": 1284,
"offsetInEndSection": 1664,
"text": "No new significant adverse events emerged with continued apremilast exposure versus the placebo-controlled period.Data were limited to 52 weeks and may not generalize to nonplaque psoriasis.Apremilast was effective in moderate to severe plaque psoriasis.<CopyrightInformation>Copyright © 2015 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.</"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23030767",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 596,
"text": "Apremilast, a small molecule specific inhibitor of phosphodiesterase 4, works intracellularly to modulate pro-inflammatory and anti-inflammatory mediator production.Assess apremilast efficacy and safety in moderate to severe plaque psoriasis.Phase II, 12-week, multicenter, double-blind, placebo-controlled, parallel-group, dose-comparison study of 259 subjects randomized 1 : 1 : 1 to placebo, apremilast 20 mg QD or apremilast 20 mg BID.More subjects receiving apremilast 20 mg BID achieved ≥ 75% reduction in Psoriasis Area and Severity Index (PASI-75) vs. placebo (24.4% vs. 10.3%; P = 0.023)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23663752",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 449,
"text": "Apremilast, a specific inhibitor of phosphodiesterase 4, modulates pro-inflammatory and anti-inflammatory cytokine production.Apremilasts effect on patient-reported outcomes (PROs) in patients with moderate to severe psoriasis was evaluated in a phase IIb randomized, controlled trial (NCT00773734).In this 16-week, placebo-controlled study, 352 patients with moderate to severe plaque psoriasis received placebo or apremilast (10, 20, or 30 mg BID)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26220911",
"endSection": "abstract",
"offsetInBeginSection": 1278,
"offsetInEndSection": 1517,
"text": "Although further longer-term and comparative efficacy and tolerability data would be beneficial, the current clinical data indicate that apremilast is an effective and well tolerated option for the management of psoriasis and PsA in adults"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23569359",
"endSection": "abstract",
"offsetInBeginSection": 944,
"offsetInEndSection": 1343,
"text": "More recently, three larger double-blinded, and randomized multicenter studies demonstrate that apremilast is efficacious in the treatment of psoriasis and PsA, with significantly higher numbers of apremilast-treated patients achieving endpoints of a 75% reduction compared to baseline in Psoriasis Area and Severity Index (PASI-75) or American College of Rheumatology-20 scores, relative to placebo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23030767",
"endSection": "abstract",
"offsetInBeginSection": 1601,
"offsetInEndSection": 1813,
"text": "No deaths or opportunistic infections were reported.Apremilast 20 mg BID for 12 weeks was effective and well tolerated in subjects with moderate to severe plaque psoriasis.<CopyrightInformation>© 2012 The Authors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20419594",
"endSection": "abstract",
"offsetInBeginSection": 686,
"offsetInEndSection": 934,
"text": "In addition, GlaxoSmithKline plc is developing 256066, an inhaled formulation of a PDE4 inhibitor that has demonstrated efficacy in trials in asthma, and apremilast from Celgene Corp has been reported to be effective for the treatment of psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26220911",
"endSection": "abstract",
"offsetInBeginSection": 1278,
"offsetInEndSection": 1518,
"text": "Although further longer-term and comparative efficacy and tolerability data would be beneficial, the current clinical data indicate that apremilast is an effective and well tolerated option for the management of psoriasis and PsA in adults."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"endSection": "abstract",
"offsetInBeginSection": 1284,
"offsetInEndSection": 1665,
"text": "No new significant adverse events emerged with continued apremilast exposure versus the placebo-controlled period.Data were limited to 52 weeks and may not generalize to nonplaque psoriasis.Apremilast was effective in moderate to severe plaque psoriasis.<CopyrightInformation>Copyright © 2015 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.</C"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26243735",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1344,
"text": "Several drug peculiarities, such as the low frequency of adverse events and the oral route of administration, make apremilast an innovative treatment for moderate-to-severe psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26267722",
"endSection": "abstract",
"offsetInBeginSection": 244,
"offsetInEndSection": 673,
"text": "Two new oral medications, apremilast and tofacitinib, have been developed for their immunomodulatory properties, and their potential efficacy in treating psoriasis is being evaluated.We reviewed phase III randomized, placebo-controlled clinical trial results for apremilast and tofacitinib for efficacy and safety in psoriasis.Psoriasis Area and Severity Index (PASI) 75 after 16 weeks for apremilast was between 28.8% and 33.1%."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"endSection": "abstract",
"offsetInBeginSection": 1476,
"offsetInEndSection": 1541,
"text": "Apremilast was effective in moderate to severe plaque psoriasis.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26267722",
"endSection": "abstract",
"offsetInBeginSection": 1009,
"offsetInEndSection": 1109,
"text": "Both new oral medications, apremilast and tofacitinib, appear to be effective in treating psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26357944",
"endSection": "abstract",
"offsetInBeginSection": 1516,
"offsetInEndSection": 1612,
"text": "Apremilast was effective in the treatment of moderate-to-severe plaque psoriasis over 52Â weeks.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27376729",
"endSection": "abstract",
"offsetInBeginSection": 963,
"offsetInEndSection": 1064,
"text": "Apremilast is an effective and well-tolerated option in treating moderate-to-severe plaque psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 1282,
"offsetInEndSection": 1407,
"text": "Apremilast has a novel mechanism of action and is safe and effective for the management of psoriasis and psoriatic arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23030767",
"endSection": "abstract",
"offsetInBeginSection": 1651,
"offsetInEndSection": 1772,
"text": "Apremilast 20 mg BID for 12 weeks was effective and well tolerated in subjects with moderate to severe plaque psoriasis.."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26243735",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 43,
"text": "Apremilast for the treatment of psoriasis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27021239",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 309,
"text": "Apremilast, an oral phosphodiesterase-4 inhibitor, in the treatment of palmoplantar psoriasis: Results of a pooled analysis from phase II PSOR-005 and phase III Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis (ESTEEM) clinical trials in patients with moderate to severe psoriasis."
}
] | 6
|
BioASQ-training6b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:8893",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011565"
] |
[
{
"o": "psoriasis",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0033860"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0487662",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0033860"
},
{
"o": "psoriasis",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0487662"
},
{
"o": "APREMILAST",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1678805"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A15589751",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1678805"
},
{
"o": "apremilast",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A15589751"
}
] |
589a246d78275d0c4a000033
|
bioasq_yesno
|
factoid
|
Which form of breast cancer has Keytruda been FDA approved for?
|
['triple-negative breast cancer']
|
[
"triple-negative breast cancer",
"TNBC",
"triple-negative tumor",
"triple-negative carcinoma",
"triple-negative breast carcinoma"
] |
['Keytruda has been FDA approved for use in combination with chemotherapy for treating PD-L1-positive mTNBC.', 'FDA has approved pembrolizumab (Keytruda) for the treatment of triple-negative breast cancer in combination with chemotherapy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33983696"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33983696",
"endSection": "abstract",
"offsetInBeginSection": 497,
"offsetInEndSection": 724,
"text": "The combination of chemotherapy and immunotherapy is a potential therapeutic option for PD-L1-positive mTNBC, as the FDA recently approved atezolizumab (Tecentriq) and pembrolizumab (Keytruda) in combination with chemotherapy. "
}
] | 12
|
BioASQ-training12b
| null | null |
6415c9e9690f196b51000018
|
bioasq_factoid
|
factoid
|
Which RNA polymerase II subunit carries RNA cleavage activity?
|
['TFIIS']
|
[
"TFIIS",
"Transcription Factor IIS",
"TFIIS protein",
"TFIIS factor"
] |
['The eukaryotic transcription factor TFIIS enhances elongation and nascent transcript cleavage activities of RNA polymerase II in a stalled elongation complex.', 'The eukaryotic transcription factor TFIIS enhances elongation and nascent transcript cleavage activities of RNA polymerase II in a stalled elongation complex. The transcription factor TFIIS zinc ribbon dipeptide Asp-Glu is critical for stimulation of elongation and RNA cleavage by RNA polymerase II.', 'In contrast, Pol II is fully protected through association with the cleavage stimulatory factor TFIIS, which enables rapid recovery from any depth by RNA cleavage.', 'In contrast, Pol II is fully protected through association with the cleavage stimulatory factor TFIIS, which enables rapid recovery from any depth by RNA cleavage. This mechanism is also used by transcription factor IIS, a factor that can bind Pol II and induce strong RNA cleavage. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12692127",
"http://www.ncbi.nlm.nih.gov/pubmed/9869639",
"http://www.ncbi.nlm.nih.gov/pubmed/21450810",
"http://www.ncbi.nlm.nih.gov/pubmed/26929337",
"http://www.ncbi.nlm.nih.gov/pubmed/8636112",
"http://www.ncbi.nlm.nih.gov/pubmed/17535246",
"http://www.ncbi.nlm.nih.gov/pubmed/7678416",
"http://www.ncbi.nlm.nih.gov/pubmed/8599945",
"http://www.ncbi.nlm.nih.gov/pubmed/8876173",
"http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"http://www.ncbi.nlm.nih.gov/pubmed/21454497",
"http://www.ncbi.nlm.nih.gov/pubmed/22396529"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26929337",
"endSection": "abstract",
"offsetInBeginSection": 851,
"offsetInEndSection": 1014,
"text": "In contrast, Pol II is fully protected through association with the cleavage stimulatory factor TFIIS, which enables rapid recovery from any depth by RNA cleavage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21454497",
"endSection": "abstract",
"offsetInBeginSection": 697,
"offsetInEndSection": 816,
"text": "This mechanism is also used by transcription factor IIS, a factor that can bind Pol II and induce strong RNA cleavage. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8636112",
"endSection": "abstract",
"offsetInBeginSection": 979,
"offsetInEndSection": 1100,
"text": " This mutant enzyme can respond to SII for transcriptional read-through and carry out SII-activated nascent RNA cleavage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8876173",
"endSection": "abstract",
"offsetInBeginSection": 674,
"offsetInEndSection": 1101,
"text": " In vitro, in the absence of TFIIS, the purified wt polymerase and the two mutant polymerases showed similar specific activity in polymerization, readthrough at intrinsic transcriptional arrest sites and nascent RNA cleavage. In contrast to the wt polymerase, both mutant polymerases were not stimulated by the addition of a 3-fold molar excess of TFIIS in assays of promoter-independent transcription, readthrough or cleavage."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8876173",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "In vitro characterization of mutant yeast RNA polymerase II with reduced binding for elongation factor TFIIS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "The transcription factor TFIIS zinc ribbon dipeptide Asp-Glu is critical for stimulation of elongation and RNA cleavage by RNA polymerase II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "The eukaryotic transcription factor TFIIS enhances elongation and nascent transcript cleavage activities of RNA polymerase II in a stalled elongation complex."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 396,
"text": "By site-directed mutagenesis, we have demonstrated that invariant residues Asp-261 and Glu-262 of the nucleic acid-binding TFIIS Zn ribbon are critical for stimulation of both elongation and RNA cleavage activities of RNA polymerase II. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12692127",
"endSection": "abstract",
"offsetInBeginSection": 349,
"offsetInEndSection": 454,
"text": "Highly purified yeast RNA polymerase II is able to perform transcript hydrolysis in the absence of TFIIS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 0,
"text": "The eukaryotic transcription factor TFIIS enhances elongation and nascent transcript cleavage activities of RNA polymerase II in a stalled elongation complex."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 395,
"text": "By site-directed mutagenesis, we have demonstrated that invariant residues Asp-261 and Glu-262 of the nucleic acid-binding TFIIS Zn ribbon are critical for stimulation of both elongation and RNA cleavage activities of RNA polymerase II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17535246",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "The transcription elongation factor S-II, also designated TFIIS, stimulates the nascent transcript cleavage activity intrinsic to RNA polymerase II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 659,
"offsetInEndSection": 884,
"text": "The RNA polymerase II itself may contain a Zn ribbon, in as much as the polymerase's 15-kDa subunit contains a sequence that aligns well with the TFIIS Zn ribbon sequence, including a similarly placed pair of acidic residues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7678416",
"endSection": "abstract",
"offsetInBeginSection": 868,
"offsetInEndSection": 1164,
"text": "Involvement of the vaccinia RNA polymerase subunit rpo30 in the transcript-shortening reaction is suggested based on sequence similarity of rpo30 to mammalian protein SII (TFIIS), an extrinsic transcription factor required for nascent RNA cleavage by RNA polymerase II (Reines, D. (1991) J. Biol."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9869639",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The RNA cleavage activity of RNA polymerase III is mediated by an essential TFIIS-like subunit and is important for transcription termination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22396529",
"endSection": "abstract",
"offsetInBeginSection": 560,
"offsetInEndSection": 869,
"text": "In the resulting model of Pol I, the C-terminal ribbon (C-ribbon) domain of A12.2 reaches the active site via the polymerase pore, like the C-ribbon of the Pol II cleavage factor TFIIS, explaining why the intrinsic RNA cleavage activity of Pol I is strong, in contrast to the weak cleavage activity of Pol II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21450810",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 454,
"text": "The amino and carboxyl regions of C11 are homologous to domains of the pol II subunit Rpb9p, and the pol II elongation and RNA cleavage factor, TFIIS, respectively."
}
] | 11
|
BioASQ-training11b
| null | null |
5a4df811966455904c00000e
|
bioasq_factoid
|
yesno
|
Do bacteria release extracellular vesicles?
|
['yes']
|
[
"yes"
] |
['Yes, Bacterial extracellular vesicles (EVs) are bilayered lipid membrane structures, bearing integral proteins and able to carry diverse cargo outside the cell to distant sites.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33264437",
"http://www.ncbi.nlm.nih.gov/pubmed/31633842",
"http://www.ncbi.nlm.nih.gov/pubmed/31776460"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31633842",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Bacterial extracellular vesicles (EVs) are bilayered lipid membrane structures, bearing integral proteins and able to carry diverse cargo outside the cell to distant sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31776460",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 287,
"text": "Knowledge of the structure, molecular cargo and function of bacterial extracellular vesicles (BEVs) is primarily obtained from bacteria cultured in laboratory conditions. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33264437",
"endSection": "abstract",
"offsetInBeginSection": 367,
"offsetInEndSection": 406,
"text": "bacteria derived-extracellular vesicles"
}
] | 11
|
BioASQ-training11b
| null | null |
603213ea1cb411341a000131
|
bioasq_yesno
|
yesno
|
Is proton beam therapy used for treatment of craniopharyngioma?
|
['yes']
|
[
"yes"
] |
['Yes, proton beam therapy is used for treatment of craniopharyngioma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27556661",
"http://www.ncbi.nlm.nih.gov/pubmed/29404243",
"http://www.ncbi.nlm.nih.gov/pubmed/32086697",
"http://www.ncbi.nlm.nih.gov/pubmed/34078637",
"http://www.ncbi.nlm.nih.gov/pubmed/29520496",
"http://www.ncbi.nlm.nih.gov/pubmed/25260976",
"http://www.ncbi.nlm.nih.gov/pubmed/32387488",
"http://www.ncbi.nlm.nih.gov/pubmed/31860822",
"http://www.ncbi.nlm.nih.gov/pubmed/32129277",
"http://www.ncbi.nlm.nih.gov/pubmed/30257123",
"http://www.ncbi.nlm.nih.gov/pubmed/25052561",
"http://www.ncbi.nlm.nih.gov/pubmed/16580494",
"http://www.ncbi.nlm.nih.gov/pubmed/16630407",
"http://www.ncbi.nlm.nih.gov/pubmed/29459099",
"http://www.ncbi.nlm.nih.gov/pubmed/24222710",
"http://www.ncbi.nlm.nih.gov/pubmed/25487038",
"http://www.ncbi.nlm.nih.gov/pubmed/30108004",
"http://www.ncbi.nlm.nih.gov/pubmed/34049281",
"http://www.ncbi.nlm.nih.gov/pubmed/26295365",
"http://www.ncbi.nlm.nih.gov/pubmed/29932288"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31860822",
"endSection": "abstract",
"offsetInBeginSection": 1465,
"offsetInEndSection": 1602,
"text": " The majority of children had adjuvant therapy comprising proton beam therapy (18/59; 30.5%) or conventional radiotherapy (16/59; 27.1%)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29459099",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Proton Therapy for Craniopharyngioma - An Early Report from a Single European Centre."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29459099",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "AIMS: Proton beam therapy (PBT) is being increasingly used for craniopharyngioma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29459099",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 328,
"text": "MATERIALS AND METHODS: Between August 2013 and July 2016, 18 patients with craniopharyngiomas were treated with 54Â Cobalt Gray Equivalent (CGE) in 30 fractions over 6 weeks at our centre."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29459099",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1261,
"text": "CONCLUSIONS: Our early results are encouraging and comparable with the limited literature on PBT for craniopharyngioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29520496",
"endSection": "abstract",
"offsetInBeginSection": 1902,
"offsetInEndSection": 2048,
"text": "All of the other patients underwent proton-beam radiotherapy with no documented tumor growth (median follow-up: 20 months; range 5.1-29.9Â months)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29404243",
"endSection": "abstract",
"offsetInBeginSection": 1673,
"offsetInEndSection": 2110,
"text": "Where aggressive subtotal resection is achieved, patients should be closely followed, with radiation initiated at the time of progression or recurrence-ideally via proton beam therapy, although three-dimensional conformal radiotherapy, intensity-modulated radiotherapy, and stereotactic radiosurgery are very appropriate in a range of circumstances, governed by access, patient age, disease architecture, and character of the recurrence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29932288",
"endSection": "abstract",
"offsetInBeginSection": 254,
"offsetInEndSection": 661,
"text": " This study examined parental distress in a sample of families of patients with Cp treated with proton beam therapy to identify factors for targeting psychological intervention.PROCEDURE: Prior to (n = 96) and 1 year after (n = 73) proton therapy, parents of children diagnosed with Cp (9.81 ± 4.42 years at baseline; 49% male) completed a self-report measure of distress, the Brief Symptom Inventory (BSI)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30108004",
"endSection": "abstract",
"offsetInBeginSection": 626,
"offsetInEndSection": 736,
"text": "Diagnoses included medulloblastoma, craniopharyngioma, ependymoma, glial tumors, germ cell tumors, and others."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30257123",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1327,
"text": "Initial experience with proton beam therapy in childhood-onset craniopharyngioma patients shows promising results in terms of more protective radiological treatment. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24222710",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Monte Carlo simulations were used to assess secondary neutron doses received by patients treated with proton therapy for ocular melanoma and craniopharyngioma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24222710",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Secondary neutron doses in proton therapy treatments of ocular melanoma and craniopharyngioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29459099",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "AIMS: Proton beam therapy (PBT) is being increasingly used for craniopharyngioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27556661",
"endSection": "abstract",
"offsetInBeginSection": 593,
"offsetInEndSection": 789,
"text": "LTS: Published reports suggest a benefit to proton beam therapy for use in tumors of the skull base, including craniopharyngiomas, chordomas, skull-base sarcomas, and unresectable meningiomas.CONC"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34078637",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 349,
"text": "In recent years, proton therapy (PT), with its physical properties of heavy ion beam, that is, Prague peak phenomenon, has been more frequently used in patients with craniopharyngioma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25052561",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Proton beam therapy versus conformal photon radiation therapy for childhood craniopharyngioma: multi-institutional analysis of outcomes, cyst dynamics, and toxicity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25052561",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "PURPOSE: We compared proton beam therapy (PBT) with intensity modulated radiation therapy (IMRT) for pediatric craniopharyngioma in terms of disease control, cyst dynamics, and toxicity."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34078637",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Proton therapy for craniopharyngioma in adults: a protocol for systematic review and meta-analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32129277",
"endSection": "abstract",
"offsetInBeginSection": 376,
"offsetInEndSection": 584,
"text": "We hereby report a case of a 7-year-old boy with a craniopharyngioma which had been subtotally resected and was subsequently treated with modern pencil beam proton therapy under high-precision image guidance."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32387488",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Pencil beam scanning proton therapy for the treatment of craniopharyngioma complicated with radiation-induced cerebral vasculopathies: A dosimetric and linear energy transfer (LET) evaluation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30257123",
"endSection": "abstract",
"offsetInBeginSection": 1164,
"offsetInEndSection": 1328,
"text": "tial experience with proton beam therapy in childhood-onset craniopharyngioma patients shows promising results in terms of more protective radiological treatment. R"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25052561",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "PURPOSE: We compared proton beam therapy (PBT) with intensity modulated radiation therapy (IMRT) for pediatric craniopharyngioma in terms of disease control, cyst dynamics, and toxic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32387488",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 275,
"text": "BACKGROUND AND PURPOSE: This study analyses the dosimetric and dose averaged Linear Energy transfer (LETd) correlation in paediatric craniopharyngioma (CP) patients with and without radiation-induced cerebral vasculopathies (RICVs) treated with pencil beam scanning (PBS) pro"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34049281",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 293,
"text": "OBJECTIVE: The authors compared survival and multiple comorbidities in children diagnosed with craniopharyngioma who underwent gross-total resection (GTR) versus subtotal resection (STR) with radiation therapy (RT), either intensity-modulated radiation therapy (IMRT) or proton beam therapy (P"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29459099",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Proton Therapy for Craniopharyngioma - An Early Report from a Single European Centre"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34078637",
"endSection": "abstract",
"offsetInBeginSection": 477,
"offsetInEndSection": 571,
"text": "s. Some studies have shown that PT has advantages in the treatment of craniopharyngioma in adu"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26295365",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Postoperative cerebral glucose metabolism in pediatric patients receiving proton therapy for craniopharyngioma"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25487038",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Clinical equipoise: Protons and the child with craniopharyngioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27556661",
"endSection": "abstract",
"offsetInBeginSection": 198,
"offsetInEndSection": 819,
"text": "skull base. More public attention has been given to proton beam therapy due to the increasing number of centers now in operation or in the planning stages for offering this treatment option.METHODS: We reviewed the physical properties of protons and the clinical studies performed to justify their use in the management of skull-base tumors and determine the benefits of proton beam therapy.RESULTS: Published reports suggest a benefit to proton beam therapy for use in tumors of the skull base, including craniopharyngiomas, chordomas, skull-base sarcomas, and unresectable meningiomas.CONCLUSIONS: Use of proton beam th"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16580494",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 336,
"text": "PURPOSE: We report the results of the early cohort of patients treated for craniopharyngioma with combined proton-photon irradiation at the Massachusetts General Hospital and the Harvard Cyclotron Laboratory.METHODS AND MATERIALS: Between 1981 and 1988, 15 patients with craniopharyngioma were treated in part or entirely with fractiona"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16630407",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "UNLABELLED: This retrospective preliminary review evaluated the efficacy and toxicity of fractionated proton radiotherapy in the management of pediatric craniopharyngioma.METHODS: Sixteen patients, aged 7-34 years, were treated with p"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32086697",
"endSection": "abstract",
"offsetInBeginSection": 323,
"offsetInEndSection": 571,
"text": "population. We evaluated the outcomes of all adult craniopharyngioma patients treated at our institution using proton therapy to report outcomes for disease control, treatment-related toxicity, and tumor response.METHODS: We analyzed 14 adult patie"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25260976",
"endSection": "abstract",
"offsetInBeginSection": 176,
"offsetInEndSection": 471,
"text": "Proton radiation has been used safely and effectively for medulloblastoma, primitive neuro-ectodermal tumors, craniopharyngioma, ependymoma, germ cell intracranial tumors, low-grade glioma, retinoblastoma, rhabdomyosarcoma and other soft tissue sarcomas, Ewing's sarcoma and other bone sarcomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34078637",
"endSection": "abstract",
"offsetInBeginSection": 638,
"offsetInEndSection": 1041,
"text": "ontroversial. The purpose of this study was to evaluate the efficacy and safety of PT for craniopharyngioma in adults.METHODS AND ANALYSIS: We will search six databases (MEDLINE, EMBASE, Web of Science, the Cochrane Library, Amed, Scopus), clinical research registration websites and grey literature, aiming to identify randomised controlled trials (RCTs) on PT for craniopharyngioma in adults between 1"
}
] | 11
|
BioASQ-training11b
| null | null |
601c4ff61cb411341a000022
|
bioasq_yesno
|
yesno
|
Are there transposon-free regions in mammalian genomes?
|
['yes']
|
[
"yes"
] |
['Yes. Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length. The majority of human TFRs correlate with orthologous TFRs in the mouse, despite the fact that most transposons are lineage specific. Many human TFRs also overlap with orthologous TFRs in the marsupial opossum, indicating that these regions have remained refractory to transposon insertion for long evolutionary periods. Over 90% of the bases covered by TFRs are noncoding, much of which is not highly conserved. Most TFRs are not associated with unusual nucleotide composition, but are significantly associated with genes encoding developmental regulators, suggesting that they represent extended regions of regulatory information that are largely unable to tolerate insertions, a conclusion difficult to reconcile with current conceptions of gene regulation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"http://www.ncbi.nlm.nih.gov/pubmed/21515576"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 963,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length. The majority of human TFRs correlate with orthologous TFRs in the mouse, despite the fact that most transposons are lineage specific. Many human TFRs also overlap with orthologous TFRs in the marsupial opossum, indicating that these regions have remained refractory to transposon insertion for long evolutionary periods. Over 90% of the bases covered by TFRs are noncoding, much of which is not highly conserved. Most TFRs are not associated with unusual nucleotide composition, but are significantly associated with genes encoding developmental regulators, suggesting that they represent extended regions of regulatory information that are largely unable to tolerate insertions, a conclusion difficult to reconcile with current conceptions of gene regulation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21515576",
"endSection": "abstract",
"offsetInBeginSection": 952,
"offsetInEndSection": 1131,
"text": "All three elements insert only rarely within many Polycomb-regulated regions, a property that may contribute to the origin of \"transposon-free regions\" (TFRs) in metazoan genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21515576",
"endSection": "abstract",
"offsetInBeginSection": 952,
"offsetInEndSection": 1131,
"text": "All three elements insert only rarely within many Polycomb-regulated regions, a property that may contribute to the origin of \"transposon-free regions\" (TFRs) in metazoan genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"endSection": "abstract",
"offsetInBeginSection": 276,
"offsetInEndSection": 562,
"text": "RESULTS: Here we report that transposon-free regions (TFRs) are prominent genomic features of amphibian and fish lineages, and that many have been maintained throughout vertebrate evolution, although most transposon-derived sequences have entered these lineages after their divergence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21515576",
"endSection": "abstract",
"offsetInBeginSection": 778,
"offsetInEndSection": 958,
"text": "All three elements insert only rarely within many Polycomb-regulated regions, a property that may contribute to the origin of \"transposon-free regions\" (TFRs) in metazoan genomes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"endSection": "abstract",
"offsetInBeginSection": 276,
"offsetInEndSection": 562,
"text": "RESULTS: Here we report that transposon-free regions (TFRs) are prominent genomic features of amphibian and fish lineages, and that many have been maintained throughout vertebrate evolution, although most transposon-derived sequences have entered these lineages after their divergence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21515576",
"endSection": "abstract",
"offsetInBeginSection": 778,
"offsetInEndSection": 958,
"text": "All three elements insert only rarely within many Polycomb-regulated regions, a property that may contribute to the origin of \"transposon-free regions\" (TFRs) in metazoan genomes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"endSection": "abstract",
"offsetInBeginSection": 276,
"offsetInEndSection": 562,
"text": "RESULTS: Here we report that transposon-free regions (TFRs) are prominent genomic features of amphibian and fish lineages, and that many have been maintained throughout vertebrate evolution, although most transposon-derived sequences have entered these lineages after their divergence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21515576",
"endSection": "abstract",
"offsetInBeginSection": 778,
"offsetInEndSection": 958,
"text": "All three elements insert only rarely within many Polycomb-regulated regions, a property that may contribute to the origin of \"transposon-free regions\" (TFRs) in metazoan genomes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"endSection": "abstract",
"offsetInBeginSection": 276,
"offsetInEndSection": 562,
"text": "RESULTS: Here we report that transposon-free regions (TFRs) are prominent genomic features of amphibian and fish lineages, and that many have been maintained throughout vertebrate evolution, although most transposon-derived sequences have entered these lineages after their divergence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21515576",
"endSection": "abstract",
"offsetInBeginSection": 778,
"offsetInEndSection": 958,
"text": "All three elements insert only rarely within many Polycomb-regulated regions, a property that may contribute to the origin of \"transposon-free regions\" (TFRs) in metazoan genomes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"endSection": "abstract",
"offsetInBeginSection": 276,
"offsetInEndSection": 562,
"text": "RESULTS: Here we report that transposon-free regions (TFRs) are prominent genomic features of amphibian and fish lineages, and that many have been maintained throughout vertebrate evolution, although most transposon-derived sequences have entered these lineages after their divergence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21515576",
"endSection": "abstract",
"offsetInBeginSection": 778,
"offsetInEndSection": 958,
"text": "All three elements insert only rarely within many Polycomb-regulated regions, a property that may contribute to the origin of \"transposon-free regions\" (TFRs) in metazoan genomes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 542,
"text": "Here we report that transposon-free regions (TFRs) are prominent genomic features of amphibian and fish lineages, and that many have been maintained throughout vertebrate evolution, although most transposon-derived sequences have entered these lineages after their divergence."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 542,
"text": "Here we report that transposon-free regions (TFRs) are prominent genomic features of amphibian and fish lineages, and that many have been maintained throughout vertebrate evolution, although most transposon-derived sequences have entered these lineages after their divergence."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 542,
"text": "Here we report that transposon-free regions (TFRs) are prominent genomic features of amphibian and fish lineages, and that many have been maintained throughout vertebrate evolution, although most transposon-derived sequences have entered these lineages after their divergence."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Transposon-free regions in mammalian genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16365385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Despite the presence of over 3 million transposons separated on average by approximately 500 bp, the human and mouse genomes each contain almost 1000 transposon-free regions (TFRs) over 10 kb in length."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18093339",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 542,
"text": "Here we report that transposon-free regions (TFRs) are prominent genomic features of amphibian and fish lineages, and that many have been maintained throughout vertebrate evolution, although most transposon-derived sequences have entered these lineages after their divergence."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
56c44ce83aaba2a675000001
|
bioasq_yesno
|
yesno
|
Is nucleosome eviction ATP-dependent?
|
['yes']
|
[
"yes"
] |
Yes, nucleosome eviction and chromatin remodelling depends on ATP
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24068556",
"http://www.ncbi.nlm.nih.gov/pubmed/24008565",
"http://www.ncbi.nlm.nih.gov/pubmed/23460895",
"http://www.ncbi.nlm.nih.gov/pubmed/22177115",
"http://www.ncbi.nlm.nih.gov/pubmed/20513433",
"http://www.ncbi.nlm.nih.gov/pubmed/19933844",
"http://www.ncbi.nlm.nih.gov/pubmed/19470761",
"http://www.ncbi.nlm.nih.gov/pubmed/19029894",
"http://www.ncbi.nlm.nih.gov/pubmed/17235287"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068556",
"endSection": "abstract",
"offsetInBeginSection": 33,
"offsetInEndSection": 166,
"text": "ATP-dependent chromatin remodeling and nucleosome-depleted 'barriers' co-operate to determine the kinetics of nucleosome organization"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24008565",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 275,
"text": "ATP-dependent nucleosome-remodeling factors endow chromatin with structural flexibility by promoting assembly or disruption of nucleosomes and the exchange of histone variants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23460895",
"endSection": "abstract",
"offsetInBeginSection": 948,
"offsetInEndSection": 1164,
"text": "remodeling takes place in an ATP-independent manner. Binding of distamycin to the linker and nucleosomal DNA culminates in eviction of the linker histone and the formation of a population of off-centered nucleosomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22177115",
"endSection": "abstract",
"offsetInBeginSection": 574,
"offsetInEndSection": 735,
"text": "which promotes histone deposition onto DNA, and a novel activity, which prevents nucleosome eviction but not remodeling mediated by the ATP-dependent RSC complex"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20513433",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 134,
"text": "ATP-dependent chromatin remodeling complex SWI/SNF regulates transcription and has been implicated in promoter nucleosome eviction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19933844",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 122,
"text": "ATP-dependent nucleosome-remodeling enzyme involved in transcription, replication, and the DNA damage response"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19933844",
"endSection": "abstract",
"offsetInBeginSection": 1361,
"offsetInEndSection": 1430,
"text": "Iec1-Ino80 complex promotes transcription through nucleosome eviction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19933844",
"endSection": "abstract",
"offsetInBeginSection": 237,
"offsetInEndSection": 323,
"text": "Ino80 complex from fission yeast mediates ATP-dependent nucleosome remodeling in vitro"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19470761",
"endSection": "abstract",
"offsetInBeginSection": 969,
"offsetInEndSection": 1153,
"text": "reconstitution of nucleosome disassembly using the ATP-dependent chromatin remodeler Rsc and Vps75 revealed that these proteins can cooperate to remove H2A/H2B dimers from nucleosomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19029894",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 106,
"text": "TP-dependent chromatin-remodeling complexes, such as RSC, can reposition, evict or restructure nucleosome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17235287",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 87,
"text": "TP-dependent chromatin remodeling complexes play a critical role in chromatin dynamics"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17235287",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 418,
"text": " activity of SWI/SNF to histone eviction in trans from gene promoters."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009707",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000255",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0000786",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0006337"
] |
[] |
532ff558d6d3ac6a34000037
|
bioasq_yesno
|
yesno
|
Was erythropoietin effective for optic neuritis in the TONE trial?
|
['no']
|
[
"no"
] |
['No. Erythropoietin as an adjunct to corticosteroids conveyed neither functional nor structural neuroprotection in the visual pathways after optic neuritis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34800417"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34800417",
"endSection": "abstract",
"offsetInBeginSection": 3172,
"offsetInEndSection": 3340,
"text": "INTERPRETATION: Erythropoietin as an adjunct to corticosteroids conveyed neither functional nor structural neuroprotection in the visual pathways after optic neuritis. "
}
] | 12
|
BioASQ-training12b
| null | null |
6402c868201352f04a00000b
|
bioasq_yesno
|
factoid
|
What disease is treated with BIVV001?
|
['Hemophilia A']
|
[
"Hemophilia A",
"Factor VIII deficiency",
"Classic hemophilia",
"A hemophilia",
"Hemophilia A disorder"
] |
['BIVV001 fusion protein has been developed as Factor VIII replacement therapy for hemophilia A']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"http://www.ncbi.nlm.nih.gov/pubmed/32905674"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "BIVV001, a new class of factor VIII replacement for hemophilia A that is independent of von Willebrand factor in primates and mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 756,
"text": "We have developed a new class of FVIII replacement, rFVIIIFc-VWF-XTEN (BIVV001), that is physically decoupled from endogenous VWF and has enhanced pharmacokinetic properties compared with all previous FVIII products"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1557,
"text": "BIVV001 is the first rFVIII with the potential to significantly change the treatment paradigm for severe hemophilia A by providing optimal protection against all bleed types, with less frequent doses. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32905674",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "BIVV001 Fusion Protein as Factor VIII Replacement Therapy for Hemophilia A."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32905674",
"endSection": "abstract",
"offsetInBeginSection": 301,
"offsetInEndSection": 533,
"text": ". BIVV001 (rFVIIIFc-VWF-XTEN) is a novel fusion protein designed to overcome this half-life ceiling and maintain high sustained factor VIII activity levels. Data are lacking on the safety and pharmacokinetics of single-dose BIVV001."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32905674",
"endSection": "abstract",
"offsetInBeginSection": 2003,
"offsetInEndSection": 2392,
"text": "CONCLUSIONS: In a small, early-phase study involving men with severe hemophilia A, a single intravenous injection of BIVV001 resulted in high sustained factor VIII activity levels, with a half-life that was up to four times the half-life associated with recombinant factor VIII, an increase that could signal a new class of factor VIII replacement therapy with a weekly treatment interval."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32905674",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "BIVV001 Fusion Protein as Factor VIII Replacement Therapy for Hemophilia A"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1556,
"text": "BIVV001 is the first rFVIII with the potential to significantly change the treatment paradigm for severe hemophilia A by providing optimal protection against all bleed types, with less frequent doses."
}
] | 11
|
BioASQ-training11b
| null | null |
6020af2e1cb411341a000084
|
bioasq_factoid
|
yesno
|
Has ORMD-0801 been tested in patients?
|
['yes']
|
[
"yes"
] |
['Yes, ORMD-0801 has been tested in patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23593142"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23593142",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Glucose-reducing effect of the ORMD-0801 oral insulin preparation in patients with uncontrolled type 1 diabetes: a pilot study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23593142",
"endSection": "abstract",
"offsetInBeginSection": 393,
"offsetInEndSection": 606,
"text": "In efforts to provide patients with a more compliable treatment method, Oramed Pharmaceuticals tested the capacity of its oral insulin capsule (ORMD-0801, 8 mg insulin) in addressing this resistant clinical state."
}
] | 11
|
BioASQ-training11b
| null | null |
5e763645c6a8763d2300000d
|
bioasq_yesno
|
yesno
|
Has Denosumab (Prolia) been approved by FDA?
|
['yes']
|
[
"yes"
] |
Yes, Denosumab was approved by the FDA in 2010.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24316116",
"http://www.ncbi.nlm.nih.gov/pubmed/24308016",
"http://www.ncbi.nlm.nih.gov/pubmed/24126422",
"http://www.ncbi.nlm.nih.gov/pubmed/24114694",
"http://www.ncbi.nlm.nih.gov/pubmed/23956508",
"http://www.ncbi.nlm.nih.gov/pubmed/23759273",
"http://www.ncbi.nlm.nih.gov/pubmed/23757624",
"http://www.ncbi.nlm.nih.gov/pubmed/23652187",
"http://www.ncbi.nlm.nih.gov/pubmed/23367751",
"http://www.ncbi.nlm.nih.gov/pubmed/22716221",
"http://www.ncbi.nlm.nih.gov/pubmed/22826702",
"http://www.ncbi.nlm.nih.gov/pubmed/22540167",
"http://www.ncbi.nlm.nih.gov/pubmed/22074657",
"http://www.ncbi.nlm.nih.gov/pubmed/21942303",
"http://www.ncbi.nlm.nih.gov/pubmed/21785279",
"http://www.ncbi.nlm.nih.gov/pubmed/21470540",
"http://www.ncbi.nlm.nih.gov/pubmed/21208140",
"http://www.ncbi.nlm.nih.gov/pubmed/21170699",
"http://www.ncbi.nlm.nih.gov/pubmed/21129866",
"http://www.ncbi.nlm.nih.gov/pubmed/21113693",
"http://www.ncbi.nlm.nih.gov/pubmed/20811384"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24316116",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 177,
"text": "Denosumab is a RANK-ligand antibody that was approved by the FDA in 2010 for the prevention of skeletal fractures in patients with bone metastases from solid tumors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24316116",
"endSection": "abstract",
"offsetInBeginSection": 776,
"offsetInEndSection": 1261,
"text": " The authors present the imaging findings and technical report of an attempted percutaneous vertebroplasty in the only patient found to be actively under treatment with denosumab after a retrospective review of the databank of patients with pathological fractures referred to the Department Radiology of the Ohio State University for percutaneous vertebroplasty (a total sample of 20 patients) since the FDA approval of denosumab (November 2010) until June of 2013 (a 30-month period)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24308016",
"endSection": "abstract",
"offsetInBeginSection": 601,
"offsetInEndSection": 769,
"text": "On the basis of this data, the FDA approved denosumab for the treatment of patients whose GCTB is unresectable, or when surgery is likely to result in severe morbidity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24126422",
"endSection": "abstract",
"offsetInBeginSection": 485,
"offsetInEndSection": 816,
"text": "Denosumab (Prolia®) is a fully human monoclonal antibody for RANKL, which selectively inhibits osteoclastogenesis, being recently approved for the treatment of postmenopausal osteoporosis in women at a high or increased risk of fracture by the FDA in the United Sates and by the European Medicines Agency in Europe since June 2010."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24114694",
"endSection": "abstract",
"offsetInBeginSection": 782,
"offsetInEndSection": 999,
"text": "Recent phase II clinical trials with denosumab in skeletally mature adolescents over age 12 years and adults with GCTB, have shown both safety and efficacy, leading to its accelerated US FDA approval on 13 June 2013. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23956508",
"endSection": "abstract",
"offsetInBeginSection": 746,
"offsetInEndSection": 1016,
"text": "Zoledronic acid (ZA), an intravenously administered bisphosphonate, and Denosumab, a subcutaneously administered inhibitor of nuclear factor B ligand (RANKL), have already been approved by Food and Drug Administration (FDA) for their use in treatment of bone metastases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23759273",
"endSection": "abstract",
"offsetInBeginSection": 736,
"offsetInEndSection": 970,
"text": "These results led to the approval of denosumab by the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA), for the prevention of SREs in adults with bone metastases from solid tumors, including breast cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23757624",
"endSection": "abstract",
"offsetInBeginSection": 1070,
"offsetInEndSection": 1210,
"text": "Alendronate, risedronate, zoledronic acid, denosumab, and teriparatide are Food and Drug Administration (FDA)-approved therapeutic options. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23652187",
"endSection": "abstract",
"offsetInBeginSection": 997,
"offsetInEndSection": 1196,
"text": "Several of these therapies have recently been approved by the FDA to treat bone cancer pain (bisphosphonates, denosumab) and others are currently being evaluated in human clinical trials (tanezumab)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23367751",
"endSection": "abstract",
"offsetInBeginSection": 892,
"offsetInEndSection": 1086,
"text": "A fourth agent, denosumab (bone targeted therapy) was also recently approved by the FDA for patients with bone metastasis after showing a reduction in the occurrence of skeletal-related events. "
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22716221",
"endSection": "abstract",
"offsetInBeginSection": 530,
"offsetInEndSection": 968,
"text": "AHRQ published an updated review in March 2012 that summarized the benefits and risks of osteoporosis medications in treatment and prevention of osteoporosis, including bisphosphonates (aledronate, risedronate, ibandronate, zoledronic acid), parathyroid hormone, teriparatide, calcitonin, estrogens (for prevention in postmenopausal women), selective estrogen receptor modulators (raloxifene), and denosumab(approved by the FDA in 2010). "
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22826702",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 1029,
"text": "Four new drugs have received U.S. Food and Drug Administration (FDA)-approval in 2010 and 2011: sipuleucel-T, an immunotherapeutic agent; cabazitaxel, a novel microtubule inhibitor; abiraterone acetate, a new androgen biosynthesis inhibitor; and denosumab, a bone-targeting agent. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22540167",
"endSection": "abstract",
"offsetInBeginSection": 170,
"offsetInEndSection": 326,
"text": "Recently, the US FDA and the EMA approved denosumab (a fully human monoclonal antibody) to treat skeletal-related events in bone-metastatic prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22074657",
"endSection": "abstract",
"offsetInBeginSection": 1023,
"offsetInEndSection": 1260,
"text": "In addition to these new and emerging therapeutic agents, denosumab was approved for the prevention of skeletal complications in patients with bone metastases due to solid tumor malignancies, providing an alternative to zoledronic acid. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21942303",
"endSection": "abstract",
"offsetInBeginSection": 686,
"offsetInEndSection": 798,
"text": "Recently, denosumab was FDA-approved for prevention of SREs in patients with bone metastases from solid tumors. "
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/21785279",
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"offsetInEndSection": 604,
"text": "In the 2010s to date, an additional 3 antibodies (denosumab, belimumab, ipilimumab) have been approved and one antibody-drug conjugate (brentuximab vedotin) is undergoing regulatory review and may be approved in the US by August 30, 2011."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/21470540",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 562,
"text": "We also review the evidence supporting the FDA's approval of denosumab (bone-targeted therapy) as a treatment option for men with CRPC and bony metastases. "
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/21208140",
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"offsetInBeginSection": 368,
"offsetInEndSection": 546,
"text": " It has been approved for clinical use by the FDA in the US and by the European Medicines Agency in Europe since June 2010 (trade name Prolia(â„¢), Amgen, Thousand Oaks, CA, USA). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21170699",
"endSection": "abstract",
"offsetInBeginSection": 147,
"offsetInEndSection": 363,
"text": "The fully human monoclonal antibody denosumab (Prolia(®)) has been recently approved by the European Medical Agency (EMEA) and the Food and Drug Administration (FDA) for the treatment of postmenopausal osteoporosis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21129866",
"endSection": "abstract",
"offsetInBeginSection": 1321,
"offsetInEndSection": 1400,
"text": "Raloxifene and denosumab are only FDA approved for postmenopausal osteoporosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21113693",
"endSection": "abstract",
"offsetInBeginSection": 708,
"offsetInEndSection": 936,
"text": "The new antiresorptive drug, denosumab, although FDA-approved only for postmenopausal women, has been shown in a study of men on ADT to increase bone density in spine, hip, and forearm and decrease vertebral fractures on x-ray. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20811384",
"endSection": "abstract",
"offsetInBeginSection": 519,
"offsetInEndSection": 665,
"text": " Since then, an additional six human mAbs have received FDA approval: panitumumab, golimumab, canakinumab, ustekinumab, ofatumumab and denosumab. "
}
] | 5
|
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4268082"
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] |
52bf1db603868f1b06000011
|
bioasq_yesno
|
factoid
|
What is another name for AZD0530?
|
['Saracatinib']
|
[
"Saracatinib",
"AZD0530",
"BMS-345541",
"Saracatinib (AZD0530)",
"Saracatinib (BMS-345541)"
] |
['AZD0530 is also known as saracatinib.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23144237"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23144237",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Antitumor activity of saracatinib (AZD0530), a c-Src/Abl kinase inhibitor, alone or in combination with chemotherapeutic agents in gastric cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23144237",
"endSection": "abstract",
"offsetInBeginSection": 459,
"offsetInEndSection": 655,
"text": "We evaluated the antitumor effect of a c-Src/Abl kinase inhibitor, saracatinib (AZD0530), alone or combined with chemotherapeutic agents in gastric cancer cell lines and a NCI-N87 xenograft model."
}
] | 11
|
BioASQ-training11b
| null | null |
5e540c866d0a277941000052
|
bioasq_factoid
|
yesno
|
Can RG7112 inhibit MDM2?
|
['yes']
|
[
"yes"
] |
['Yes, RG7112 is a small molecule MDM2 antagonist.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24309210",
"http://www.ncbi.nlm.nih.gov/pubmed/23400593",
"http://www.ncbi.nlm.nih.gov/pubmed/23084521",
"http://www.ncbi.nlm.nih.gov/pubmed/22753001",
"http://www.ncbi.nlm.nih.gov/pubmed/24900694",
"http://www.ncbi.nlm.nih.gov/pubmed/24869939",
"http://www.ncbi.nlm.nih.gov/pubmed/23808545",
"http://www.ncbi.nlm.nih.gov/pubmed/24812409",
"http://www.ncbi.nlm.nih.gov/pubmed/21391905",
"http://www.ncbi.nlm.nih.gov/pubmed/25082860"
] |
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"text": "To assess the influence of the p53 regulatory pathway further, we studied the effect of RG7112, a small molecule MDM2 antagonist that activates p53 by preventing its interaction with MDM2, on normal megakaryocytopoiesis and platelet production."
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"text": "RG7112 (2g) is the first clinical small-molecule MDM2 inhibitor designed to occupy the p53-binding pocket of MDM2."
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"text": "We report a proof-of-mechanism study of RG7112, a small-molecule MDM2 antagonist, in patients with chemotherapy-naive primary or relapsed well-differentiated or dedifferentiated MDM2-amplified liposarcoma who were eligible for resection."
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"text": "RG7112 is a selective inhibitor of p53-MDM2 binding that frees p53 from negative control, activating the p53 pathway in cancer cells leading to cell cycle arrest and apoptosis."
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"text": "The effects of RG7112 and Peg-IFNα 2a on MPN progenitor cells were dependent on blocking p53-MDM2 interactions and activating the p53 pathway, thereby increasing MPN CD34(+) cell apoptosis"
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"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23808545",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 401,
"text": "However, the hydrophobic protein-protein interaction surface represents a significant challenge for the development of small-molecule inhibitors with desirable pharmacological profiles. RG7112 was the first small-molecule p53-MDM2 inhibitor in clinical development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22753001",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Initial testing of the MDM2 inhibitor RG7112 by the Pediatric Preclinical Testing Program."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24869939",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 866,
"text": "Treatment with low doses of RG7112, an orally available small-molecule inhibitor of p53-MDM2, both alone and combined with pegylated interferon α 2a (Peg-IFNα 2a), significantly decreased MPN colony-forming unit-granulocyte macrophage and burst-forming unit-erythroid numbers and preferentially eliminated the total number of JAKV617F(+) MPN hematopoietic progenitor cells. The effects of RG7112 and Peg-IFNα 2a on MPN progenitor cells were dependent on blocking p53-MDM2 interactions and activating the p53 pathway, thereby increasing MPN CD34(+) cell apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22753001",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 372,
"text": "RG7112 is a selective inhibitor of p53-MDM2 binding that frees p53 from negative control, activating the p53 pathway in cancer cells leading to cell cycle arrest and apoptosis. RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (PPTP) due to the relatively low incidence of p53 mutations in pediatric cancers compared with adult malignancies."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24309210",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Activation of p53 by the MDM2 inhibitor RG7112 impairs thrombopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23808545",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 401,
"text": "However, the hydrophobic protein-protein interaction surface represents a significant challenge for the development of small-molecule inhibitors with desirable pharmacological profiles. RG7112 was the first small-molecule p53-MDM2 inhibitor in clinical development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24900694",
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"text": "Discovery of RG7112: A Small-Molecule MDM2 Inhibitor in Clinical Development."
},
{
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"text": "Treatment with low doses of RG7112, an orally available small-molecule inhibitor of p53-MDM2, both alone and combined with pegylated interferon α 2a (Peg-IFNα 2a), significantly decreased MPN colony-forming unit-granulocyte macrophage and burst-forming unit-erythroid numbers and preferentially eliminated the total number of JAKV617F(+) MPN hematopoietic progenitor cells. The effects of RG7112 and Peg-IFNα 2a on MPN progenitor cells were dependent on blocking p53-MDM2 interactions and activating the p53 pathway, thereby increasing MPN CD34(+) cell apoptosis."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24900694",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 807,
"text": "RG7112 (2g) is the first clinical small-molecule MDM2 inhibitor designed to occupy the p53-binding pocket of MDM2. In cancer cells expressing wild-type p53, RG7112 stabilizes p53 and activates the p53 pathway, leading to cell cycle arrest, apoptosis, and inhibition or regression of human tumor xenografts."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24869939",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 866,
"text": "Treatment with low doses of RG7112, an orally available small-molecule inhibitor of p53-MDM2, both alone and combined with pegylated interferon α 2a (Peg-IFNα 2a), significantly decreased MPN colony-forming unit-granulocyte macrophage and burst-forming unit-erythroid numbers and preferentially eliminated the total number of JAKV617F(+) MPN hematopoietic progenitor cells. The effects of RG7112 and Peg-IFNα 2a on MPN progenitor cells were dependent on blocking p53-MDM2 interactions and activating the p53 pathway, thereby increasing MPN CD34(+) cell apoptosis."
},
{
"beginSection": "title",
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"endSection": "title",
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"offsetInEndSection": 70,
"text": "Activation of p53 by the MDM2 inhibitor RG7112 impairs thrombopoiesis."
},
{
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"endSection": "title",
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"text": "Discovery of RG7112: A Small-Molecule MDM2 Inhibitor in Clinical Development."
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"text": "Initial testing of the MDM2 inhibitor RG7112 by the Pediatric Preclinical Testing Program."
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"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 401,
"text": "However, the hydrophobic protein-protein interaction surface represents a significant challenge for the development of small-molecule inhibitors with desirable pharmacological profiles. RG7112 was the first small-molecule p53-MDM2 inhibitor in clinical development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24900694",
"endSection": "abstract",
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"offsetInEndSection": 807,
"text": "RG7112 (2g) is the first clinical small-molecule MDM2 inhibitor designed to occupy the p53-binding pocket of MDM2. In cancer cells expressing wild-type p53, RG7112 stabilizes p53 and activates the p53 pathway, leading to cell cycle arrest, apoptosis, and inhibition or regression of human tumor xenografts."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22753001",
"endSection": "abstract",
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"offsetInEndSection": 372,
"text": "RG7112 is a selective inhibitor of p53-MDM2 binding that frees p53 from negative control, activating the p53 pathway in cancer cells leading to cell cycle arrest and apoptosis. RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (PPTP) due to the relatively low incidence of p53 mutations in pediatric cancers compared with adult malignancies."
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"text": "Activation of p53 by the MDM2 inhibitor RG7112 impairs thrombopoiesis."
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"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 401,
"text": "However, the hydrophobic protein-protein interaction surface represents a significant challenge for the development of small-molecule inhibitors with desirable pharmacological profiles. RG7112 was the first small-molecule p53-MDM2 inhibitor in clinical development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24900694",
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"text": "Discovery of RG7112: A Small-Molecule MDM2 Inhibitor in Clinical Development."
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"text": "Initial testing of the MDM2 inhibitor RG7112 by the Pediatric Preclinical Testing Program."
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"text": "Treatment with low doses of RG7112, an orally available small-molecule inhibitor of p53-MDM2, both alone and combined with pegylated interferon α 2a (Peg-IFNα 2a), significantly decreased MPN colony-forming unit-granulocyte macrophage and burst-forming unit-erythroid numbers and preferentially eliminated the total number of JAKV617F(+) MPN hematopoietic progenitor cells. The effects of RG7112 and Peg-IFNα 2a on MPN progenitor cells were dependent on blocking p53-MDM2 interactions and activating the p53 pathway, thereby increasing MPN CD34(+) cell apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24900694",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 807,
"text": "RG7112 (2g) is the first clinical small-molecule MDM2 inhibitor designed to occupy the p53-binding pocket of MDM2. In cancer cells expressing wild-type p53, RG7112 stabilizes p53 and activates the p53 pathway, leading to cell cycle arrest, apoptosis, and inhibition or regression of human tumor xenografts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22753001",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 372,
"text": "RG7112 is a selective inhibitor of p53-MDM2 binding that frees p53 from negative control, activating the p53 pathway in cancer cells leading to cell cycle arrest and apoptosis. RG7112 was selected for evaluation by the Pediatric Preclinical Testing Program (PPTP) due to the relatively low incidence of p53 mutations in pediatric cancers compared with adult malignancies."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24869939",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 866,
"text": "Treatment with low doses of RG7112, an orally available small-molecule inhibitor of p53-MDM2, both alone and combined with pegylated interferon α 2a (Peg-IFNα 2a), significantly decreased MPN colony-forming unit-granulocyte macrophage and burst-forming unit-erythroid numbers and preferentially eliminated the total number of JAKV617F(+) MPN hematopoietic progenitor cells. The effects of RG7112 and Peg-IFNα 2a on MPN progenitor cells were dependent on blocking p53-MDM2 interactions and activating the p53 pathway, thereby increasing MPN CD34(+) cell apoptosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22753001",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Initial testing of the MDM2 inhibitor RG7112 by the Pediatric Preclinical Testing Program."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24309210",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Activation of p53 by the MDM2 inhibitor RG7112 impairs thrombopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24900694",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 807,
"text": "RG7112 (2g) is the first clinical small-molecule MDM2 inhibitor designed to occupy the p53-binding pocket of MDM2. In cancer cells expressing wild-type p53, RG7112 stabilizes p53 and activates the p53 pathway, leading to cell cycle arrest, apoptosis, and inhibition or regression of human tumor xenografts."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24900694",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Discovery of RG7112: A Small-Molecule MDM2 Inhibitor in Clinical Development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23808545",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 401,
"text": "However, the hydrophobic protein-protein interaction surface represents a significant challenge for the development of small-molecule inhibitors with desirable pharmacological profiles. RG7112 was the first small-molecule p53-MDM2 inhibitor in clinical development."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/MDM2_MOUSE",
"http://www.uniprot.org/uniprot/MDM2_MESAU",
"http://www.uniprot.org/uniprot/MDM2_HUMAN",
"http://www.uniprot.org/uniprot/MDM2_XENLA",
"http://www.uniprot.org/uniprot/MDM2_FELCA",
"http://www.uniprot.org/uniprot/MDM2_DANRE",
"http://www.uniprot.org/uniprot/MDM2_CANLF"
] |
[] |
56ed08062ac5ed1459000005
|
bioasq_yesno
|
factoid
|
What disease is associated with Anticitrullinated peptide antibodies (ACPAs)?
|
['rheumatoid arthritis']
|
[
"rheumatoid arthritis",
"RA",
"chronic inflammatory arthritis",
"rheumatoid disease",
"rheumatoid joint disease"
] |
['nticitrullinated protein antibodies (ACPAs) are serological biomarkers associated with early, rapidly progressing rheumatoid arthritis (RA)', 'Anticitrullinated peptide antibodies (ACPAs) are associated with rheumatoid arthritis.', 'Anticitrullinated peptide antibodies (ACPAs) have been shown to be associated with rheumatoid arthritis', 'The aim of this study was to evaluate the presence of autoantibodies to cyclic citrullinated synthetic peptides (ACPAs) in the sputum of patients with long-standing rheumatoid arthritis.', 'Anticitrullinated protein antibodies are found in patients with rheumatoid arthritis']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32079664",
"http://www.ncbi.nlm.nih.gov/pubmed/16188943",
"http://www.ncbi.nlm.nih.gov/pubmed/22661643",
"http://www.ncbi.nlm.nih.gov/pubmed/27696777",
"http://www.ncbi.nlm.nih.gov/pubmed/31565241",
"http://www.ncbi.nlm.nih.gov/pubmed/29290168",
"http://www.ncbi.nlm.nih.gov/pubmed/30297575",
"http://www.ncbi.nlm.nih.gov/pubmed/28826660",
"http://www.ncbi.nlm.nih.gov/pubmed/29200020",
"http://www.ncbi.nlm.nih.gov/pubmed/24206219",
"http://www.ncbi.nlm.nih.gov/pubmed/27348081",
"http://www.ncbi.nlm.nih.gov/pubmed/23440041",
"http://www.ncbi.nlm.nih.gov/pubmed/27755123",
"http://www.ncbi.nlm.nih.gov/pubmed/25120260",
"http://www.ncbi.nlm.nih.gov/pubmed/24429169",
"http://www.ncbi.nlm.nih.gov/pubmed/25997035",
"http://www.ncbi.nlm.nih.gov/pubmed/26613769",
"http://www.ncbi.nlm.nih.gov/pubmed/25819755",
"http://www.ncbi.nlm.nih.gov/pubmed/18270852",
"http://www.ncbi.nlm.nih.gov/pubmed/23716070"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29200020",
"endSection": "title",
"offsetInBeginSection": 6,
"offsetInEndSection": 95,
"text": " Anticitrullinated Protein Antibodies in Patients With Long-standing Rheumatoid Arthritis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29200020",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 196,
"text": "The aim of this study was to evaluate the presence of autoantibodies to cyclic citrullinated synthetic peptides (ACPAs) in the sputum of patients with long-standing rheumatoid arthritis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29290168",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 153,
"text": "nticitrullinated protein antibodies (ACPAs) are serological biomarkers associated with early, rapidly progressing rheumatoid arthritis (RA),"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27755123",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Anticitrullinated protein antibodies: origin and role in the pathogenesis of rheumatoid arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27755123",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 168,
"text": "This article reviews recent literature on the origin and pathogenic role of anticitrullinated protein antibodies (ACPAs) in rheumatoid arthritis (RA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22661643",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 368,
"text": "OBJECTIVES: To increase understanding of the aetiology and pathogenesis of rheumatoid arthritis (RA), genetic and environmental risk factors for RA subsets, defined by the presence or absence of different anticitrullinated protein/peptide antibodies (ACPAs) targeting citrullinated peptides from α-enolase, vimentin, fibrinogen and collagen type II, were investigated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23716070",
"endSection": "abstract",
"offsetInBeginSection": 122,
"offsetInEndSection": 285,
"text": "Citrullinated proteins are observed in RA lung tissues; however, the association of specific anticitrullinated peptide antibodies (ACPA) with ILD in RA is unknown."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23716070",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Association of fine specificity and repertoire expansion of anticitrullinated peptide antibodies with rheumatoid arthritis associated interstitial lung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26613769",
"endSection": "abstract",
"offsetInBeginSection": 194,
"offsetInEndSection": 485,
"text": "This longitudinal study investigated (1) progression from CSA to clinically detectable arthritis and (2) associations of clinical factors, serological factors (among which are anticitrullinated peptide antibodies (ACPAs)) and MRI-detected subclinical inflammation with arthritis development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32079664",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 328,
"text": "Anticitrullinated peptide antibodies (ACPAs) are arguably the most likely candidate biomarker to screen for RA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24206219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Anticitrullinated protein antibodies (ACPAs) constitute a class of autoantibodies found in 60-70% of patients with rheumatoid arthritis (RA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29290168",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "BACKGROUND: Anticitrullinated protein antibodies (ACPAs) are serological biomarkers associated with early, rapidly progressing rheumatoid arthritis (RA), including more severe disease and joint damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23440041",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "Antibodies targeting citrullinated proteins (ACPAs [anticitrullinated protein antibodies]) are commonly found in patients with rheumatoid arthritis (RA), strongly associate with distinct HLA-DR alleles, and predict a more aggressive disease course as compared with seronegative patients. Still, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16188943",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "OBJECTIVES: Anticitrullinated protein/peptide antibodies (ACPA) have an excellent diagnostic performance for rheumatoid arthriti"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18270852",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Anticitrullinated protein/peptide antibodies (ACPA) are highly specific for rheumatoid arthritis (RA). They"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24206219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Anticitrullinated protein antibodies (ACPAs) constitute a class of autoantibodies found in 60-70% of patients with rheumatoid arthritis (RA). The m"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30297575",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Background: Anti-citrullinated peptides antibodies (ACPA) are specific for rheumatoid arthritis and have been implicated in disease patho"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25997035",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Anticitrullinated peptide/protein antibodies (ACPA), which are highly specific for rheumatoid arthritis (RA), may be found in some patients with other systemic autoimmune diseases. The c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23716070",
"endSection": "abstract",
"offsetInBeginSection": 122,
"offsetInEndSection": 286,
"text": "Citrullinated proteins are observed in RA lung tissues; however, the association of specific anticitrullinated peptide antibodies (ACPA) with ILD in RA is unknown.M"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25120260",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "Anti-citrullinated protein/peptide antibodies (ACPAs) are detected in rheumatoid arthritis (RA) sera and because of their strict association with the disease are considered marker antibodies, probably endowed with pathogenic potential."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28826660",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "OBJECTIVES: Anti-citrullinated protein/peptide antibodies (ACPA) represent an important tool for the diagnosis of rheumatoid arthritis (RA) and the presence of multiple ACPA specificities is highly correlated with the evolution"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24429169",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "OBJECTIVE: Anticitrullinated protein/peptide antibodies (ACPA) are implicated in rheumatoid arthritis (RA) pathogenesis and linked to the shared ep"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25997035",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Anticitrullinated peptide/protein antibodies (ACPA), which are highly specific for rheumatoid arthritis (RA), may be found in some patients with other systemic autoimmune diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27348081",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Rheumatoid arthritis (RA) is an autoimmune connective tissue disease, associated with the presence of anti-citrullinated protein antibodies (ACPA)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31565241",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Antibodies against citrullinated peptides are associated with clinical and radiological outcomes in patients with early rheumatoid arthritis: a prospective longitudinal inception cohort study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25997035",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "In antisynthetase syndrome, ACPA are associated with severe and erosive arthritis: an overlapping rheumatoid arthritis and antisynthetase syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31565241",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Introduction: Anticitrullinated peptide antibody (ACPA) responses for 22 citrullinated peptides in patients with early rheumatoid arthritis (RA) were analysed and related to radiological and clinical outcome during the first 2 years in a prospective inc"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25819755",
"endSection": "abstract",
"offsetInBeginSection": 107,
"offsetInEndSection": 225,
"text": "Recent studies have revealed that periodontal disease (PD) is closely associated with RA and production of ACPA in RA."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27696777",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Association of Anti-Citrullinated Peptide Antibodies With Coronary Artery Calcification in Rheumatoid Arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25819755",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Anti-citrullinated peptide antibody (ACPA) is a highly specific autoantibody to rheumatoid arthritis (RA)."
}
] | 11
|
BioASQ-training11b
| null | null |
5e6e9a2fc6a8763d23000007
|
bioasq_factoid
|
factoid
|
Which is the most important prognosis sub-classification in Chronic Lymphocytic Leukemia?
|
['The mutational status of the IGHV genes.']
|
[
"IGHV genes",
"Immunoglobulin heavy chain variable region genes",
"Immunoglobulin heavy variable genes",
"Immunoglobulin heavy chain variable genes",
"IGHV"
] |
['The mutational status of the immunoglobulin heavy variable (IGHV) genes, defines two subsets: mutated and unmutated CLL. Unmutated CLL patients show a shorter progression-free and overall survival than mutated CLL patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23468975",
"http://www.ncbi.nlm.nih.gov/pubmed/22560084",
"http://www.ncbi.nlm.nih.gov/pubmed/20353875",
"http://www.ncbi.nlm.nih.gov/pubmed/20090781",
"http://www.ncbi.nlm.nih.gov/pubmed/19500131",
"http://www.ncbi.nlm.nih.gov/pubmed/19127482",
"http://www.ncbi.nlm.nih.gov/pubmed/17786276",
"http://www.ncbi.nlm.nih.gov/pubmed/16825496",
"http://www.ncbi.nlm.nih.gov/pubmed/16014569",
"http://www.ncbi.nlm.nih.gov/pubmed/16083281"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22560084",
"endSection": "sections.0",
"offsetInBeginSection": 621,
"offsetInEndSection": 879,
"text": "One of the most reliable prognostic markers in chronic lymphocytic leukemia (CLL) is the mutational status of immunoglobulin heavy variable (IGHV) genes, which defines 2 subsets, mutated CLL (M-CLL) and unmutated CLL (U-CLL), with different clinical courses."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20090781",
"endSection": "sections.0",
"offsetInBeginSection": 119,
"offsetInEndSection": 268,
"text": "Mutational status of the immunoglobulin heavy chain variable regions (IGHVs) of CLL cells offers useful prognostic information for high-risk patients"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20090781",
"endSection": "sections.0",
"offsetInBeginSection": 270,
"offsetInEndSection": 496,
"text": "but time and economical costs originally prevented it from being routinely used in a clinical setting. Instead, alternative markers of IGHV status, such as zeta-associated protein (ZAP70) or messenger RNA levels are often used"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19127482",
"endSection": "sections.0",
"offsetInBeginSection": 109,
"offsetInEndSection": 282,
"text": "Patients with unmutated IgV(H) gene show a shorter progression-free and overall survival than patients with immunoglobulin heavy chain variable regions (IgV(H)) gene mutated"
}
] | 5
|
BioASQ-training5b
| null | null |
51739df58ed59a060a00001c
|
bioasq_factoid
|
factoid
|
Which receptor is targeted by telcagepant?
|
[['calcitonin gene-related peptide']]
|
[
"calcitonin gene-related peptide",
"CGRP",
"calcitonin gene-related peptide alpha",
"calcitonin gene-related peptide beta",
"CGRP alpha",
"CGRP beta"
] |
['Telcagepant (MK-0974) is a novel calcitonin gene-related peptide (CGRP) receptor antagonist currently undergoing clinical trials for migraine.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23975906",
"http://www.ncbi.nlm.nih.gov/pubmed/23798725",
"http://www.ncbi.nlm.nih.gov/pubmed/23196486",
"http://www.ncbi.nlm.nih.gov/pubmed/22816019",
"http://www.ncbi.nlm.nih.gov/pubmed/22512641",
"http://www.ncbi.nlm.nih.gov/pubmed/22278333",
"http://www.ncbi.nlm.nih.gov/pubmed/22221076",
"http://www.ncbi.nlm.nih.gov/pubmed/22090312",
"http://www.ncbi.nlm.nih.gov/pubmed/21631478",
"http://www.ncbi.nlm.nih.gov/pubmed/21480950",
"http://www.ncbi.nlm.nih.gov/pubmed/21457238",
"http://www.ncbi.nlm.nih.gov/pubmed/21383046",
"http://www.ncbi.nlm.nih.gov/pubmed/21350792",
"http://www.ncbi.nlm.nih.gov/pubmed/21221171",
"http://www.ncbi.nlm.nih.gov/pubmed/21110235",
"http://www.ncbi.nlm.nih.gov/pubmed/21070230",
"http://www.ncbi.nlm.nih.gov/pubmed/21070229",
"http://www.ncbi.nlm.nih.gov/pubmed/21054362",
"http://www.ncbi.nlm.nih.gov/pubmed/20974601",
"http://www.ncbi.nlm.nih.gov/pubmed/20954694",
"http://www.ncbi.nlm.nih.gov/pubmed/20937606",
"http://www.ncbi.nlm.nih.gov/pubmed/20855369",
"http://www.ncbi.nlm.nih.gov/pubmed/20826335",
"http://www.ncbi.nlm.nih.gov/pubmed/20573757",
"http://www.ncbi.nlm.nih.gov/pubmed/20433208",
"http://www.ncbi.nlm.nih.gov/pubmed/20416945",
"http://www.ncbi.nlm.nih.gov/pubmed/20188075",
"http://www.ncbi.nlm.nih.gov/pubmed/20173082",
"http://www.ncbi.nlm.nih.gov/pubmed/20164785",
"http://www.ncbi.nlm.nih.gov/pubmed/20120204",
"http://www.ncbi.nlm.nih.gov/pubmed/20099900",
"http://www.ncbi.nlm.nih.gov/pubmed/20078608",
"http://www.ncbi.nlm.nih.gov/pubmed/23480465",
"http://www.ncbi.nlm.nih.gov/pubmed/19939188",
"http://www.ncbi.nlm.nih.gov/pubmed/19914210",
"http://www.ncbi.nlm.nih.gov/pubmed/19796656",
"http://www.ncbi.nlm.nih.gov/pubmed/19795182",
"http://www.ncbi.nlm.nih.gov/pubmed/19779958",
"http://www.ncbi.nlm.nih.gov/pubmed/19770473",
"http://www.ncbi.nlm.nih.gov/pubmed/19737844",
"http://www.ncbi.nlm.nih.gov/pubmed/19579177",
"http://www.ncbi.nlm.nih.gov/pubmed/19551474",
"http://www.ncbi.nlm.nih.gov/pubmed/19469188",
"http://www.ncbi.nlm.nih.gov/pubmed/19346171",
"http://www.ncbi.nlm.nih.gov/pubmed/19219746",
"http://www.ncbi.nlm.nih.gov/pubmed/19157980",
"http://www.ncbi.nlm.nih.gov/pubmed/19084002",
"http://www.ncbi.nlm.nih.gov/pubmed/18991732",
"http://www.ncbi.nlm.nih.gov/pubmed/19036425",
"http://www.ncbi.nlm.nih.gov/pubmed/18808506",
"http://www.ncbi.nlm.nih.gov/pubmed/18799366",
"http://www.ncbi.nlm.nih.gov/pubmed/18590336",
"http://www.ncbi.nlm.nih.gov/pubmed/18217201",
"http://www.ncbi.nlm.nih.gov/pubmed/18039958",
"http://www.ncbi.nlm.nih.gov/pubmed/17929795",
"http://www.ncbi.nlm.nih.gov/pubmed/17914062",
"http://www.ncbi.nlm.nih.gov/pubmed/25107879"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23975906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "In vivo quantification of calcitonin gene-related peptide receptor occupancy by telcagepant in rhesus monkey and human brain using the positron emission tomography tracer [11C]MK-4232."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23798725",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Lack of hemodynamic interaction between CGRP-receptor antagonist telcagepant (MK-0974) and sumatriptan: results from a randomized study in patients with migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23196486",
"endSection": "abstract",
"offsetInBeginSection": 684,
"offsetInEndSection": 963,
"text": "Olcegepant is the first selective CGRP receptor antagonist of proven efficacy in migraine. Olcegepant could only be administered intravenously and never taken beyond Phase II. Telcagepant is orally available and several completed Phase III trials have revealed positive results. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22816019",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Telcagepant (MK-0974) is a novel calcitonin gene-related peptide (CGRP) receptor antagonist currently undergoing clinical trials for migraine (http://www.merck.com/research/pipeline/home.html)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22512641",
"endSection": "abstract",
"offsetInBeginSection": 599,
"offsetInEndSection": 765,
"text": "Four chemically unrelated CGRP receptor (CGRP-R) antagonists (olcegepant, telcagepant, MK-3207 and BI 44370 TA) have displayed efficacy in the treatment of migraine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22278333",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Telcagepant is a calcitonin gene-related peptide (CGRP) receptor antagonist being evaluated for acute migraine treatment. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22221076",
"endSection": "abstract",
"offsetInBeginSection": 106,
"offsetInEndSection": 328,
"text": "BACKGROUND: Calcitonin gene-related peptide receptor antagonists, such as telcagepant, may be useful for acute migraine treatment in patients with cardiovascular disease, a population for whom triptans are contraindicated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22090312",
"endSection": "abstract",
"offsetInBeginSection": 493,
"offsetInEndSection": 683,
"text": "The calcitonin gene-related peptide (CGRP) receptor antagonists (gepants)-olcegepant (BIBN 4096 BS), telcagepant (MK-0974), MK3207, and BI 44370 TA-are effective in treating acute migraine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21631478",
"endSection": "abstract",
"offsetInBeginSection": 314,
"offsetInEndSection": 438,
"text": "Telcagepant, a calcitonin gene-related peptide receptor antagonist, is being developed for the acute treatment of migraine. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21480950",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The potent calcitonin gene-related peptide receptor antagonist, telcagepant, does not affect nitroglycerin-induced vasodilation in healthy men."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21480950",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "AIMS: To assess the effect of the calcitonin gene-related peptide (CGRP) receptor antagonist, telcagepant, on the haemodynamic response to sublingual nitroglycerin (NTG). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21457238",
"endSection": "abstract",
"offsetInBeginSection": 158,
"offsetInEndSection": 307,
"text": "BACKGROUND: Telcagepant is an oral calcitonin gene-related peptide receptor antagonist which is being evaluated for the acute treatment of migraine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21383046",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "BACKGROUND: The calcitonin gene-related peptide (CGRP) receptor antagonists olcegepant and telcagepant are very potent drugs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21383046",
"endSection": "abstract",
"offsetInBeginSection": 841,
"offsetInEndSection": 995,
"text": "CONCLUSION: The apparently high doses of CGRP receptor antagonists, olcegepant and telcagepant needed for anti-migraine effect are not so high after all. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21350792",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Dose-response curves for headaches relief and adverse events (AEs) are presented for five triptans: sumatriptan, zolmitriptan, naratriptan, almotriptan, and frovatriptan, and the CGRP antagonist telcagepant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21221171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "INTRODUCTION: Telcagepant (MK-0974) is a novel, orally active and selective CGRP receptor antagonist being investigated for acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21110235",
"endSection": "abstract",
"offsetInBeginSection": 1175,
"offsetInEndSection": 1469,
"text": "Calcitonin gene-related peptide (CGRP) receptor antagonists are another promising nonvasoconstrictor approach to treating acute migraine. Olcegepant (BIBN4096BS) and telcagepant (MK-0974) have been shown to be safe and effective in phase I, II, and (for telcagepant) phase III clinical trials. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21070230",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 263,
"text": "Background.- Telcagepant is a calcitonin gene-related peptide (CGRP) receptor antagonist being investigated for the acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21070229",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "In 3 randomized clinical trials (n = 1585) the calcitonin gene-related peptide antagonist telcagepant 300 mg orally had an incidence of adverse events similar to placebo when used in the acute treatment of migraine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21054362",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 246,
"text": "BACKGROUND: Telcagepant is an oral calcitonin gene-related peptide receptor antagonist with acute antimigraine efficacy comparable to oral triptans"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20974601",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "METHODS: This study evaluated the calcitonin gene-related peptide (CGRP) receptor antagonist telcagepant (tablet formulation) for treatment of a migraine attack and across four attacks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20954694",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "A highly efficient, asymmetric synthesis of telcagepant (1), a CGRP receptor antagonist for the treatment of migraine, is described"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20954694",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Asymmetric synthesis of telcagepant, a CGRP receptor antagonist for the treatment of migraine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20937606",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Sustained pain freedom and no adverse events as an endpoint in clinical trials of acute migraine treatments: application to patient-level data from a trial of the CGRP receptor antagonist, telcagepant, and zolmitriptan."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20937606",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 623,
"text": "METHODS: The aim of this study was to evaluate new composite efficacy-plus-tolerability endpoints based on a post-hoc analysis of patient-level data from a previous randomized, placebo-controlled trial of the calcitonin gene-related peptide (CGRP) receptor antagonist, telcagepant, and zolmitriptan in the acute treatment of migraine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20855369",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Effect of the calcitonin gene-related peptide (CGRP) receptor antagonist telcagepant in human cranial arteries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20855369",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 375,
"text": "MATERIALS AND METHODS: We investigated the effect of the CGRP receptor antagonist, telcagepant, on CGRP-induced cranial vasodilatation in human isolated cerebral and middle meningeal arteries. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20855369",
"endSection": "abstract",
"offsetInBeginSection": 1102,
"offsetInEndSection": 1328,
"text": "CONCLUSIONS: Our findings provide morphological and functional data on the presence of CGRP receptors in cerebral and meningeal arteries, which illustrates a possible site of action of telcagepant in the treatment of migraine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20573757",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "Characterization of the calcitonin gene-related peptide receptor antagonist telcagepant (MK-0974) in human isolated coronary arteries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20573757",
"endSection": "abstract",
"offsetInBeginSection": 287,
"offsetInEndSection": 585,
"text": "We therefore investigated the effects of the antimigraine CGRP receptor antagonist telcagepant (MK-0974) [N-[(3R,6S)-6-(2,3-difluorophenyl)-2-oxo-1-(2,2,2-trifluoroethyl)azepan-3-yl]-4-(2-oxo-2,3-dihydro-1H-imidazo[4,5-b]pyridine-1-yl)piperidine-1-carboxamide] on human isolated coronary arteries. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20573757",
"endSection": "abstract",
"offsetInBeginSection": 1861,
"offsetInEndSection": 2060,
"text": "These findings in vitro support the cardiovascular safety of CGRP receptor antagonists and suggest that telcagepant is unlikely to induce coronary side effects under normal cardiovascular conditions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20433208",
"endSection": "abstract",
"offsetInBeginSection": 1115,
"offsetInEndSection": 1482,
"text": "Towards this end, the non-peptide CGRP receptor antagonists olcegepant and telcagepant have been shown to be effective in the acute treatment of migraine. While telcagepant is being pursued as a frontline abortive migraine drug in a phase III clinical trial, an oral formulation of a novel CGRP receptor antagonist, BI 44370, is currently in phase II clinical trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20416945",
"endSection": "abstract",
"offsetInBeginSection": 229,
"offsetInEndSection": 340,
"text": "Telcagepant represents a new class of antimigraine drug-the calcitonin gene-related peptide receptor blockers. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20188075",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 634,
"text": "The CGRP receptor antagonists telcagepant and olcegepant (BIBN4096BS) have demonstrated clinical efficacy in the treatment of migraine and there is now a need to better understand how these molecules interact with the receptor. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20173082",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Single- and multiple-dose pharmacokinetics and tolerability of telcagepant, an oral calcitonin gene-related peptide receptor antagonist, in adults."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20173082",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Telcagepant is a novel, orally active, and selective calcitonin gene-related peptide receptor antagonist being developed for acute treatment of migraine with and without aura. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20164785",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Studies were conducted in human isolated coronary arteries to explore the vascular effects of the calcitonin gene-related peptide (CGRP) receptor antagonist telcagepant and to compare its coronary vasoconstrictive potential to that of zolmitriptan. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20120204",
"endSection": "abstract",
"offsetInBeginSection": 662,
"offsetInEndSection": 848,
"text": "Intravenous BIBN4096BS (olcegepant) and oral MK-0974 (telcagepant), two CGRP-receptor antagonists, were safe and effective in the treatment of migraine attacks in Phase I and II trials. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19346171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Telcagepant (MK-0974) is a novel oral calcitonin gene-related peptide (CGRP) receptor antagonist and is currently under clinical development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23975906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "In vivo quantification of calcitonin gene-related peptide receptor occupancy by telcagepant in rhesus monkey and human brain using the positron emission tomography tracer [11C]MK-4232."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23798725",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Lack of hemodynamic interaction between CGRP-receptor antagonist telcagepant (MK-0974) and sumatriptan: results from a randomized study in patients with migraine."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
55032efde9bde69634000035
|
bioasq_factoid
|
factoid
|
Are male or female persons more prone to autoimmunity?
|
['Female']
|
[
"Female",
"Woman",
"Girl",
"Feminine",
"Lady",
"Dame",
"She",
"Her"
] |
['Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases.', 'Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases. Most recently, sex chromosome abnormalities and skewed X chromosome inactivation have been suggested as novel players, particularly in later-onset diseases.', 'Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases. Examples of this autoimmune dimorphism include (but are not limited to) lupus, rheumatoid arthritis and multiple sclerosis with the two former more prevalent in females than males and the latter more severe during pregnancy. Most recently, sex chromosome abnormalities and skewed X chromosome inactivation have been suggested as novel players, particularly in later-onset diseases.', 'females', 'Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases. Sex hormone expression is altered among patients with autoimmune disease, and this variation of expression contributes to immune dysregulation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17108242",
"http://www.ncbi.nlm.nih.gov/pubmed/25956531",
"http://www.ncbi.nlm.nih.gov/pubmed/30394940",
"http://www.ncbi.nlm.nih.gov/pubmed/18603021",
"http://www.ncbi.nlm.nih.gov/pubmed/508371",
"http://www.ncbi.nlm.nih.gov/pubmed/1958563",
"http://www.ncbi.nlm.nih.gov/pubmed/22155196",
"http://www.ncbi.nlm.nih.gov/pubmed/16549717"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/508371",
"endSection": "abstract",
"offsetInBeginSection": 594,
"offsetInEndSection": 683,
"text": " Estrogens cause a marked acceleration of autoimmunity and a reduction in thymus weight. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/508371",
"endSection": "abstract",
"offsetInBeginSection": 719,
"offsetInEndSection": 1042,
"text": "we found that a number of problems or variables arise in studying sex hormone effects, including: 1) X-linked genes, 2) metabolism of testosterone to estrogens, 3) dose of hormone, 4) age at which administration is initiated, 5) differential effects of sex hormones on different autoantibodies and various immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1958563",
"endSection": "abstract",
"offsetInBeginSection": 721,
"offsetInEndSection": 945,
"text": "Examples of this autoimmune dimorphism include (but are not limited to) lupus, rheumatoid arthritis and multiple sclerosis with the two former more prevalent in females than males and the latter more severe during pregnancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17108242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16549717",
"endSection": "abstract",
"offsetInBeginSection": 376,
"offsetInEndSection": 635,
"text": "Sex hormones have definitive roles in lymphocyte maturation, activation, and synthesis of antibodies and cytokines. Sex hormone expression is altered among patients with autoimmune disease, and this variation of expression contributes to immune dysregulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16549717",
"endSection": "abstract",
"offsetInBeginSection": 1329,
"offsetInEndSection": 1561,
"text": "ex hormones affect the function of the mammalian immune system, and sex hormone expression is different in patients with systemic lupus erythematosus than in healthy subjects. Sex hormones play a role in the genesis of autoimmunity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18603021",
"endSection": "abstract",
"offsetInBeginSection": 720,
"offsetInEndSection": 876,
"text": "Most recently, sex chromosome abnormalities and skewed X chromosome inactivation have been suggested as novel players, particularly in later-onset diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22155196",
"endSection": "abstract",
"offsetInBeginSection": 1452,
"offsetInEndSection": 1679,
"text": "As a result we may hypothesize that more than one mechanism may contribute to the female susceptibility to tolerance breakdown while the possibility that unknown factors may indeed protect men from AID should not be overlooked."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25956531",
"endSection": "abstract",
"offsetInBeginSection": 430,
"offsetInEndSection": 651,
"text": " The gut microbiome, which impacts the innate and adaptive branches of immunity, not only influences the development of autoimmune disorders but may interact with sex-hormones to modulate disease progression and sex-bias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394940",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 545,
"text": "Recent studies investigating the origins of sex bias in autoimmune disease have revealed an extensive and interconnected network of genetic, hormonal, microbial, and environmental influences. Investigation of sex hormones has moved beyond profiling the effects of hormones on activity and prevalence of immune cell types to defining the specific immunity-related genes driving these changes"
}
] | 11
|
BioASQ-training11b
| null | null |
5cebf83ea49efeb44c00000a
|
bioasq_factoid
|
factoid
|
In which cell organelle is the SAF-A protein localized?
|
['the nucleus']
|
[
"the nucleus",
"cell nucleus",
"nuclear envelope",
"nuclear membrane",
"nuclear structure",
"nuclear region"
] |
['saf-a/hnrnp u is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region dna', 'SAF-A/hnRNP U is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region DNA (MAR) and RNA as a component of hnRNPs. Scaffold attachment factor A (SAF-A) participates in the regulation of gene expression by organizing chromatin into transcriptionally active domains and by interacting directly with RNA polymerase II.', 'Scaffold attachment factor B (SAF-B) is a nuclear matrix-associated protein. It is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region DNA (MAR) and RNA as a component of hnRNPs.', 'TheSAF-A protein is localized to the nuclear matrix', 'SAF-A/hnRNP U is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region DNA (MAR) and RNA as a component of hnRNPs. ', 'The SAF-A protein localizes to the nucleus where it promotes ribosome biogenesis', 'SAF-A is localized to the nucleus where it promotes ribosomal RNA (rRNA) transcription thereby stimulating cell growth.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/10933876",
"http://www.ncbi.nlm.nih.gov/pubmed/19556781",
"http://www.ncbi.nlm.nih.gov/pubmed/22162999"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19556781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "SAF-A/hnRNP U is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region DNA (MAR) and RNA as a component of hnRNPs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162999",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 212,
"text": "Scaffold attachment factor A (SAF-A) participates in the regulation of gene expression by organizing chromatin into transcriptionally active domains and by interacting directly with RNA polymerase II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162999",
"endSection": "abstract",
"offsetInBeginSection": 877,
"offsetInEndSection": 1074,
"text": "Functional analyses reveal that dual depletion of SAF-A and BRG1 abolishes global transcription by RNA polymerase II, while the nucleolar RNA polymerase I transcription machinery remains unaffected"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10933876",
"endSection": "abstract",
"offsetInBeginSection": 698,
"offsetInEndSection": 916,
"text": "Using this domain as a probe, we performed a yeast two-hybrid screening and we found that scaffold attachment factor B (SAF-B), a nuclear matrix-associated protein, exhibits protein-protein interaction to this region. "
}
] | 11
|
BioASQ-training11b
| null | null |
5d35e7ddb3a638076300000e
|
bioasq_factoid
|
factoid
|
What is the function of the gene MDA5?
|
['Sensing of non-self RNAs, especially viral RNA']
|
[
"Sensing of non-self RNAs, especially viral RNA",
"Recognition of foreign RNAs",
"Detection of non-self RNA",
"Viral RNA sensing",
"Non-self RNA detection",
"Viral RNA recognition"
] |
['Melanoma differentiation-associated gene 5 (MDA5) is a pattern recognition receptor that recognizes cytoplasmic viral double-stranded RNA (dsRNA) and initiates rapid innate antiviral responses. MDA5 forms a filament-like multimer along the dsRNA leading to oligomerization, which in turn activates the adaptor protein mitochondrial antiviral signaling protein (MAVS) to provide a signal platform for the induction of type I interferon (IFN) and proinflammatory cytokines. The conformational switch of MDA5 causes antiviral defense, but excessive activation of the MDA5-MAVS pathway may result in autoimmune diseases.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28530548",
"http://www.ncbi.nlm.nih.gov/pubmed/29117565",
"http://www.ncbi.nlm.nih.gov/pubmed/28250012",
"http://www.ncbi.nlm.nih.gov/pubmed/29069650",
"http://www.ncbi.nlm.nih.gov/pubmed/28374903"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28250012",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "Sensing of viral RNA by the cytosolic receptors RIG-I and melanoma differentiation-associated gene 5 (MDA5) leads to innate antiviral response. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28530548",
"endSection": "abstract",
"offsetInBeginSection": 407,
"offsetInEndSection": 647,
"text": "The host innate immune response to RNA virus infection primarily involves pathogen-sensing toll-like receptors (TLRs) TLR3 and TLR7 and retinoic acid-inducible gene I-like receptor RIG-I and melanoma differentiation associated gene 5 (MDA5)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28374903",
"endSection": "abstract",
"offsetInBeginSection": 652,
"offsetInEndSection": 748,
"text": "RNA PRRs are comprised of TLR3, TLR7, TLR8, RIG-I, MDA5, NLRP3, NOD2, and some other minorities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29069650",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 616,
"text": "Melanoma differentiation-associated gene 5 (MDA5) is a pattern recognition receptor that recognizes cytoplasmic viral double-stranded RNA (dsRNA) and initiates rapid innate antiviral responses. MDA5 forms a filament-like multimer along the dsRNA leading to oligomerization, which in turn activates the adaptor protein mitochondrial antiviral signaling protein (MAVS) to provide a signal platform for the induction of type I interferon (IFN) and proinflammatory cytokines. The conformational switch of MDA5 causes antiviral defense, but excessive activation of the MDA5-MAVS pathway may result in autoimmune diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29117565",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "Retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), including melanoma differentiation-associated gene 5 (MDA5) and RIG-I, are crucial for host recognition of non-self RNAs, especially viral RNA. "
}
] | 11
|
BioASQ-training11b
| null | null |
5a88370c61bb38fb24000014
|
bioasq_factoid
|
yesno
|
Is depression associated with poor prognosis of brain tumor patients?
|
['yes']
|
[
"yes"
] |
['Yes. In brain tumor patients depression is associated with shorter survival and worse functional outcomes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/16304988",
"http://www.ncbi.nlm.nih.gov/pubmed/16960653",
"http://www.ncbi.nlm.nih.gov/pubmed/15918939",
"http://www.ncbi.nlm.nih.gov/pubmed/15072475"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16304988",
"endSection": "sections.0",
"offsetInBeginSection": 583,
"offsetInEndSection": 819,
"text": "Before surgery 27 patients (35%) had BDI scores indicating the presence of depression. These scores were significantly higher in patients with a history of depression (p = 0.017) and in those with a lower functional outcome (p = 0.015)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16304988",
"endSection": "sections.0",
"offsetInBeginSection": 949,
"offsetInEndSection": 1128,
"text": "A lower functional status (KPS score < or = 70) in patients was significantly associated with high depression scores at the 3-month (p = 0.000) and 1-year (p = 0.005) assessments."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16960653",
"endSection": "sections.0",
"offsetInBeginSection": 782,
"offsetInEndSection": 964,
"text": "At all follow-ups, depressed low-grade glioma patients had a significantly shorter survival time, 3.3-5.8 years, compared to non-depressed low-grade glioma patients, 10.0-11.7 years."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16960653",
"endSection": "sections.0",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1223,
"text": "The results suggest that depression and decreased QOL among low-grade glioma patients is related to shorter survival at long-term follow-up."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15918939",
"endSection": "sections.0",
"offsetInBeginSection": 11,
"offsetInEndSection": 143,
"text": "The adverse impact of depression in relation to survival among cancer patients is currently a subject of great interest in research."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15918939",
"endSection": "sections.0",
"offsetInBeginSection": 1193,
"offsetInEndSection": 1388,
"text": "In the subgroup of patients with low-grade gliomas, depressive patients had a significantly shorter survival time compared with nondepressive subjects (P = 0.031, Kaplan-Meier survival analysis)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15918939",
"endSection": "sections.0",
"offsetInBeginSection": 1731,
"offsetInEndSection": 1848,
"text": "Preoperative depression seemed to be a significant prognostic factor for worse survival in low-grade glioma patients."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15072475",
"endSection": "sections.0",
"offsetInBeginSection": 1075,
"offsetInEndSection": 1244,
"text": "Major depressive disorder was marginally associated with outcomes, while surgical interventions and radiotherapy did not show strong associations with test performances."
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001932",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011379",
"http://www.disease-ontology.org/api/metadata/DOID:1319",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003863",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016019",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017063"
] | null |
514cc8dcd24251bc05000066
|
bioasq_yesno
|
factoid
|
What part of the body is associated with Cauda equina
|
['spine']
|
[
"spine",
"vertebral column",
"backbone",
"spinal column",
"spinal cord",
"spinal vertebrae"
] |
['The cauda equina is the sack of nerve roots (nerves that leave the spinal cord between spaces in the bones of the spine to connect to other parts of the body) at the lower end of the spinal cord.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26442520",
"http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"http://www.ncbi.nlm.nih.gov/pubmed/22254963",
"http://www.ncbi.nlm.nih.gov/pubmed/27753733",
"http://www.ncbi.nlm.nih.gov/pubmed/3356808",
"http://www.ncbi.nlm.nih.gov/pubmed/22996855",
"http://www.ncbi.nlm.nih.gov/pubmed/3806684",
"http://www.ncbi.nlm.nih.gov/pubmed/32541159",
"http://www.ncbi.nlm.nih.gov/pubmed/33261250",
"http://www.ncbi.nlm.nih.gov/pubmed/23101243",
"http://www.ncbi.nlm.nih.gov/pubmed/11311464",
"http://www.ncbi.nlm.nih.gov/pubmed/18664636",
"http://www.ncbi.nlm.nih.gov/pubmed/10797973",
"http://www.ncbi.nlm.nih.gov/pubmed/34321945",
"http://www.ncbi.nlm.nih.gov/pubmed/22764663"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33261250",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 346,
"text": "the right pedicle of L4, moved inside the vertebral canal (bridging the cauda equina) stopping just in front of the body of S2. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23101243",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 124,
"text": "Thermoesthesia-and-algesthesia status in the dermatomes of cauda equina roots in patients with lumbar spine osteochondrosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23101243",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Thermoesthesia-and-algesthesia disorders have been registered in the dermatomes of cauda equina roots of patients with lumbar spine osteochondrosis in all the cases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22764663",
"endSection": "abstract",
"offsetInBeginSection": 581,
"offsetInEndSection": 722,
"text": " Magnetic resonance images of the lumbar spine showed an intradural cystic lesion displacing and compressing the lower cord and cauda equina."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22996855",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Cauda equina syndrome is a well described state of neurologic compromise due to lumbosacral root compression."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22996855",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Acute cauda equina syndrome secondary to a lumbar synovial cyst"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 296,
"text": "INTRODUCTION: Schwannoma is a relatively common benign spinal cord and/or cauda equina tumor; however, giant cauda equina schwannoma with extensive scalloping of the lumbar vertebral body is a rare pathology, and the treatment strategy, including the use of surgical procedures, is controversial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 509,
"text": "In this report, we present a rare case of a giant lumbar schwannoma of the cauda equina with extremely large scalloping of the vertebral body, and we discuss the surgical strategy we used to treat this pathology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3356808",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 791,
"text": "In contrast, the caudal cord of Rana is reduced to a filum terminale consisting of little more than an ependymal tube; spinal nerves to all caudal myotomes leave the cord in the sacral region and reach their motor targets via a cauda equina and caudal plexus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3806684",
"endSection": "abstract",
"offsetInBeginSection": 662,
"offsetInEndSection": 791,
"text": "The spinal cords of other teleosts, the sun-fish and angler, also are abbreviated and possess a filum terminale and cauda equina."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10797973",
"endSection": "abstract",
"offsetInBeginSection": 993,
"offsetInEndSection": 1126,
"text": "Penetrating spinal cord injury with foreign body included or myelography stop or showing cauda equina syndrome should be operated on."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27753733",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Cauda Equina Conduction Time Determined by F-Waves in Normal Subjects and Patients With Neurogenic Intermittent Claudication Caused by Lumbar Spinal Stenosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22254963",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 259,
"text": "After spinal cord injury, electrical stimulation of the roots inside the spinal column at the level of the cauda equina is a safe and effective way to regain some degree of control over lower body function, e.g. bladder and bowel management and leg movement. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32541159",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Malignant spinal cord compression(MSCC)is defined as a compression of the spinal cord or cauda equina with neuropathy caused by tumor spreading to the vertebral body. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26442520",
"endSection": "abstract",
"offsetInBeginSection": 37,
"offsetInEndSection": 187,
"text": "nction of the cauda equina, the collection of ventral and dorsal lumbar, sacral and coccygeal nerve roots that surround the filum terminale. This most"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "INTRODUCTION: Schwannoma is a relatively common benign spinal cord and/or cauda equina tumor; however, giant cauda equina schwannoma with extensive scalloping of the lumbar vertebral body is a rare pathology, and the treatment strategy, including the use of surgical procedures, is controversial"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18664636",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Cauda equina syndrome is a relatively uncommon condition typically associated with a large, space-occupying lesion within the canal of the lumbosacral spine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26442520",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Cauda equina syndrome refers to dysfunction of the cauda equina, the collection of ventral and dorsal lumbar, sacral and coccygeal nerve roots that surround the filum terminale."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11311464",
"endSection": "abstract",
"offsetInBeginSection": 1320,
"offsetInEndSection": 1510,
"text": "The involvement of intrinsic spinal cord neurons in the compression-induced cauda equina syndrome includes anterograde, retrograde and transneuronal degeneration in the lumbosacral segments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11311464",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Single or double-level compression of the lumbosacral nerve roots located in the dural sac results in a polyradicular symptomatology clinically diagnosed as cauda equina syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34321945",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 470,
"text": "The cauda equina is an anatomic structure located in the lower part of the spinal canal consisting of multiple lumbar and sacral nerve roots."
}
] | 11
|
BioASQ-training11b
| null | null |
6238a0033a8413c6530000b8
|
bioasq_factoid
|
factoid
|
What is the role of cytidine deaminase in healthy cells?
|
['deamination of deoxycytidines']
|
[
"deamination of deoxycytidines",
"deoxycytidine deamination",
"deoxycytidine deaminase reaction",
"deamination of dC",
"deamination of 2'-deoxycytidine"
] |
['Activation-induced cytidine deaminase (AID) catalyses the deamination of deoxycytidines to deoxyuracils within immunoglobulin genes to induce somatic hypermutation and class-switch recombination.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34819671",
"http://www.ncbi.nlm.nih.gov/pubmed/34819670",
"http://www.ncbi.nlm.nih.gov/pubmed/32729075",
"http://www.ncbi.nlm.nih.gov/pubmed/34528388",
"http://www.ncbi.nlm.nih.gov/pubmed/32729074"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32729074",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "The AID/APOBEC family of enzymes are cytidine deaminases that act upon DNA and RNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32729075",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "APOBEC1 is a member of the AID/APOBECs, a group of deaminases responsible for the editing of C>U in both DNA and RNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34528388",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 281,
"text": "The human genome contains 11 APOBEC (apolipoprotein B mRNA editing catalytic polypeptide-like) cytidine deaminases classified into four families. These proteins function mainly in innate antiviral immunity and can also restrict endogenous retrotransposable element multiplication. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34819670",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "Activation-induced cytidine deaminase (AID) catalyses the deamination of deoxycytidines to deoxyuracils within immunoglobulin genes to induce somatic hypermutation and class-switch recombination"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34819671",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 411,
"text": "Efficient humoral responses rely on DNA damage, mutagenesis and error-prone DNA repair. Diversification of B cell receptors through somatic hypermutation and class-switch recombination are initiated by cytidine deamination in DNA mediated by activation-induced cytidine deaminase (AID)1 and by the subsequent excision of the resulting uracils by uracil DNA glycosylase (UNG) and by mismatch repair proteins1-3. "
}
] | 11
|
BioASQ-training11b
| null | null |
6217d8973a8413c653000020
|
bioasq_factoid
|
factoid
|
Which disease is caused by repeat expansion in VWA1?
|
['Recessive hereditary motor neuropathy']
|
[
"Recessive hereditary motor neuropathy",
"Hereditary motor neuropathy type 1A",
"HMN type 1A",
"Recessive hereditary motor neuron disease",
"Recessive hereditary motor neuronopathy"
] |
['An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33559681"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33559681",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33559681",
"endSection": "abstract",
"offsetInBeginSection": 2510,
"offsetInEndSection": 3068,
"text": "In summary, we estimate that biallelic variants in VWA1 may be responsible for up to 1% of unexplained hereditary motor neuropathy cases in Europeans. The detailed clinical characterization provided here will facilitate targeted testing on suitable patient cohorts. This novel disease gene may have previously evaded detection because of high GC content, consequential low coverage and computational difficulties associated with robustly detecting repeat-expansions. Reviewing previously unsolved exomes using lower QC filters may generate further diagnoses."
}
] | 11
|
BioASQ-training11b
| null | null |
61f86c03882a024a10000044
|
bioasq_factoid
|
yesno
|
Has FTY720 been considered for the treatment of stroke?
|
['yes']
|
[
"yes"
] |
['Yes, FTY720 is a strong candidate for stroke treatment.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31785606"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31785606",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "FTY720 (Fingolimod) Ameliorates Brain Injury through Multiple Mechanisms and is a Strong Candidate for Stroke Treatment"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31785606",
"endSection": "abstract",
"offsetInBeginSection": 1192,
"offsetInEndSection": 1691,
"text": "Many researchers have recognized the positive effects of FTY720 and launched basic and clinical experiments to test the use of this agent against stroke. Although the mechanism of FTY720 has not been fully elucidated, its efficacy against cerebral stroke is becoming clear, not only in animal models, but also in ischemic stroke patients through clinical trials. In this article, we review the data obtained from laboratory findings and preliminary clinical trials using FTY720 for stroke treatment."
}
] | 11
|
BioASQ-training11b
| null | null |
605265ee94d57fd87900000d
|
bioasq_yesno
|
factoid
|
What is the process that generates multiple transcripts from the same gene?
|
['Alternative splicing', 'Alternative splicing (AS)']
|
[
"Alternative splicing",
"Alternative splicing (AS)",
"AS",
"Alternative RNA splicing",
"Variable splicing",
"Differential splicing"
] |
['The process that generates multiple transcripts from the same gene is called alternative splicing (AS). AS is a post-transcriptional regulatory mechanism that allows for the production of different mRNA isoforms from a single gene. This process can increase proteome diversity and regulate mRNA levels, which is important for expanding proteomic complexity and functional diversity in higher eukaryotes. In plants, AS may also serve as a buffer against stress-responsive transcriptomes to reduce the metabolic cost of translating all AS transcripts. While the contribution of AS to proteome complexity remains elusive in plants, it is clear that this process plays an important role in regulating gene expression and generating protein isoforms with distinct functions.', 'Alternative splicing generates multiple transcripts and potentially more than one protein from the same gene. It markedly enhances the coding capacity of the genome and can increase protein diversity which plays a crucial role in controlling development and stress responses.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18369186",
"http://www.ncbi.nlm.nih.gov/pubmed/30014301",
"http://www.ncbi.nlm.nih.gov/pubmed/2788825",
"http://www.ncbi.nlm.nih.gov/pubmed/16611169",
"http://www.ncbi.nlm.nih.gov/pubmed/28064309",
"http://www.ncbi.nlm.nih.gov/pubmed/20815140",
"http://www.ncbi.nlm.nih.gov/pubmed/30852095",
"http://www.ncbi.nlm.nih.gov/pubmed/33406240",
"http://www.ncbi.nlm.nih.gov/pubmed/34383135",
"http://www.ncbi.nlm.nih.gov/pubmed/35269461",
"http://www.ncbi.nlm.nih.gov/pubmed/26273603",
"http://www.ncbi.nlm.nih.gov/pubmed/21896509",
"http://www.ncbi.nlm.nih.gov/pubmed/18088312",
"http://www.ncbi.nlm.nih.gov/pubmed/16054339",
"http://www.ncbi.nlm.nih.gov/pubmed/24369421",
"http://www.ncbi.nlm.nih.gov/pubmed/32811430",
"http://www.ncbi.nlm.nih.gov/pubmed/22811948",
"http://www.ncbi.nlm.nih.gov/pubmed/22961303",
"http://www.ncbi.nlm.nih.gov/pubmed/18817741",
"http://www.ncbi.nlm.nih.gov/pubmed/31921258",
"http://www.ncbi.nlm.nih.gov/pubmed/35821097",
"http://www.ncbi.nlm.nih.gov/pubmed/26327458",
"http://www.ncbi.nlm.nih.gov/pubmed/32484809",
"http://www.ncbi.nlm.nih.gov/pubmed/34440445",
"http://www.ncbi.nlm.nih.gov/pubmed/33629774",
"http://www.ncbi.nlm.nih.gov/pubmed/28402429",
"http://www.ncbi.nlm.nih.gov/pubmed/25577379",
"http://www.ncbi.nlm.nih.gov/pubmed/25577391",
"http://www.ncbi.nlm.nih.gov/pubmed/29074233",
"http://www.ncbi.nlm.nih.gov/pubmed/35327956",
"http://www.ncbi.nlm.nih.gov/pubmed/28273663",
"http://www.ncbi.nlm.nih.gov/pubmed/35339647"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30852095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Alternative splicing (AS) generates multiple transcripts from the same gene, however, AS contribution to proteome complexity remains elusive in plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30852095",
"endSection": "abstract",
"offsetInBeginSection": 306,
"offsetInEndSection": 522,
"text": "We propose that plants employ AS not only to potentially increasing proteomic complexity, but also to buffer against the stress-responsive transcriptome to reduce the metabolic cost of translating all AS transcripts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29074233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Alternative splicing, which generates multiple transcripts from the same gene, is an important modulator of gene expression that can increase proteome diversity and regulate mRNA levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22961303",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Alternative splicing, which generates multiple transcripts from the same gene and potentially different protein isoforms, is a key posttranscriptional regulatory mechanism for expanding proteomic diversity and functional complexity in higher eukaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24369421",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Alternative splicing (AS), in higher eukaryotes, is one of the mechanisms of post-transcriptional regulation that generate multiple transcripts from the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26273603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 245,
"text": "Over the past decade, alternative splicing has been progressively recognized as a major mechanism regulating gene expression patterns in different tissues and disease states through the generation of multiple mRNAs from the same gene transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35269461",
"endSection": "abstract",
"offsetInBeginSection": 317,
"offsetInEndSection": 497,
"text": "Alternative splicing is a physiological process by which cells generate several transcripts from one single gene and may in turn give rise to different proteins from the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16054339",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 490,
"text": "However, as well as conventional splicing, several genes have the inherent capacity to undergo alternative splicing, thus allowing synthesis of multiple gene transcripts, perhaps with different functional properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18088312",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Alternative splicing (AS) increases the proteomic and functional capacity of genomes through the generation of alternative mRNA transcripts from the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25577391",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 226,
"text": "Indeed, through AS individual gene loci can generate multiple RNAs from the same pre-mRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26327458",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Alternative splicing is an important biological process in the generation of multiple functional transcripts from the same genomic sequences."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33406240",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Alternative splicing generates multiple transcript and protein isoforms from a single gene and controls transcript intracellular localization and stability by coupling to mRNA export and nonsense-mediated mRNA decay (NMD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31921258",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Alternative Splicing (AS) is a mechanism that generates different mature transcripts from precursor mRNAs (pre-mRNAs) of the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16611169",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Alternative splicing is a widespread mechanism in mammals that generates several mRNAs from one gene, thereby creating genetic diversity of the genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34440445",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Alternative pre-mRNA splicing plays a very important role in expanding protein diversity as it generates numerous transcripts from a single protein-coding gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32484809",
"endSection": "abstract",
"offsetInBeginSection": 378,
"offsetInEndSection": 534,
"text": " This task is complicated due to the complexity of alternative splicing - a mechanism by which the same gene may generate multiple distinct RNA transcripts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28064309",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Alternative splicing of pre-mRNA is one of the main mechanisms regulating gene expression that generates multiple transcripts from one gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28402429",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Alternative splicing generates multiple transcript and protein isoforms from the same gene and thus is important in gene expression regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34383135",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Alternative splicing is a widespread phenomenon, which generates multiple isoforms of the gene product."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18817741",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Alternative splicing of messenger RNA (mRNA) precursors generates multiple transcripts from a single primary transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32811430",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 223,
"text": "Among eukaryotic organisms, alternative splicing is an important process that can generate multiple transcripts from one same precursor messenger RNA, which greatly increase transcriptome and proteome diversity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21896509",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 156,
"text": " Alternative splicing (AS) is a pre-mRNA maturation process leading to the expression of multiple mRNA variants from the same primary transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33629774",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 375,
"text": "Alternative splicing (AS) is a process that produces various mRNA splicing isoforms via different splicing patterns of mRNA precursors (pre-mRNAs). AS is the primary mechanism for increasing the types and quantities of proteins to improve biodiversity and influence multiple biological processes, including chromatin modification, signal transduction, and protein expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35821097",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 274,
"text": "Alternative splicing generates multiple transcripts from a single gene, enriching the diversity of proteins and phenotypic traits."
}
] | 12
|
BioASQ-training12b
| null | null |
6428da74690f196b51000052
|
bioasq_factoid
|
factoid
|
Which cyclin- dependent kinase inhibitor is regulated by Bmi-1?
|
['p16INK4']
|
[
"p16INK4",
"p16",
"p16INK4a",
"CDKN2A",
"cyclin-dependent kinase inhibitor 2A"
] |
p16INK4 (also known as CDKN2A)
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20661663",
"http://www.ncbi.nlm.nih.gov/pubmed/20591222",
"http://www.ncbi.nlm.nih.gov/pubmed/20551323",
"http://www.ncbi.nlm.nih.gov/pubmed/19321450",
"http://www.ncbi.nlm.nih.gov/pubmed/18371338",
"http://www.ncbi.nlm.nih.gov/pubmed/18371328",
"http://www.ncbi.nlm.nih.gov/pubmed/18275833",
"http://www.ncbi.nlm.nih.gov/pubmed/17989730",
"http://www.ncbi.nlm.nih.gov/pubmed/17651940",
"http://www.ncbi.nlm.nih.gov/pubmed/17145810",
"http://www.ncbi.nlm.nih.gov/pubmed/17102614",
"http://www.ncbi.nlm.nih.gov/pubmed/16537449",
"http://www.ncbi.nlm.nih.gov/pubmed/16157028",
"http://www.ncbi.nlm.nih.gov/pubmed/16155021",
"http://www.ncbi.nlm.nih.gov/pubmed/14982841",
"http://www.ncbi.nlm.nih.gov/pubmed/14574365",
"http://www.ncbi.nlm.nih.gov/pubmed/12714971",
"http://www.ncbi.nlm.nih.gov/pubmed/12482990",
"http://www.ncbi.nlm.nih.gov/pubmed/9923679",
"http://www.ncbi.nlm.nih.gov/pubmed/21928107",
"http://www.ncbi.nlm.nih.gov/pubmed/18346113",
"http://www.ncbi.nlm.nih.gov/pubmed/21496667",
"http://www.ncbi.nlm.nih.gov/pubmed/21164364",
"http://www.ncbi.nlm.nih.gov/pubmed/19907431",
"http://www.ncbi.nlm.nih.gov/pubmed/19390085",
"http://www.ncbi.nlm.nih.gov/pubmed/19389366",
"http://www.ncbi.nlm.nih.gov/pubmed/17597110",
"http://www.ncbi.nlm.nih.gov/pubmed/17233832",
"http://www.ncbi.nlm.nih.gov/pubmed/16869752",
"http://www.ncbi.nlm.nih.gov/pubmed/16778197",
"http://www.ncbi.nlm.nih.gov/pubmed/15964994",
"http://www.ncbi.nlm.nih.gov/pubmed/15892997",
"http://www.ncbi.nlm.nih.gov/pubmed/14732230",
"http://www.ncbi.nlm.nih.gov/pubmed/14536079",
"http://www.ncbi.nlm.nih.gov/pubmed/11355949"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20661663",
"endSection": "abstract",
"offsetInBeginSection": 663,
"offsetInEndSection": 748,
"text": "the knockdown of BMI-1 expression could lead to significant up-regulation of p16INK4a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20591222",
"endSection": "abstract",
"offsetInBeginSection": 1621,
"offsetInEndSection": 1694,
"text": "In EC9706 cells transfected by Bmi-1 siRNA, the expression levels of p16 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20551323",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 392,
"text": "One important pathway regulated by Bmi-1 is that involving two cyclin-dependent kinase inhibitors, p16(Ink4a) and p19(Arf)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19321450",
"endSection": "abstract",
"offsetInBeginSection": 643,
"offsetInEndSection": 814,
"text": "We also observe that ROS-induced up-regulation of p16(Ink4a) occurs correlatively with ERK1/2-dependent down-regulation and subsequent dissociation from chromatin of Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371338",
"endSection": "abstract",
"offsetInBeginSection": 51,
"offsetInEndSection": 214,
"text": "Bmi-1 is important for postnatal, but not embryonic, neural stem cell (NSC) self-renewal and have identified the cell-cycle inhibitors p16/p19 as molecular targets"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371328",
"endSection": "abstract",
"offsetInBeginSection": 180,
"offsetInEndSection": 307,
"text": "Bmi-1 function in stem cells during development that, surprisingly, seems to involve regulation of the cell-cycle inhibitor p21"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371338",
"endSection": "abstract",
"offsetInBeginSection": 823,
"offsetInEndSection": 892,
"text": "Our data therefore implicate p21 as an important Bmi-1 target in NSCs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18275833",
"endSection": "abstract",
"offsetInBeginSection": 628,
"offsetInEndSection": 663,
"text": "Bmi-1-mediated repression of Cdkn2A"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17989730",
"endSection": "abstract",
"offsetInBeginSection": 798,
"offsetInEndSection": 894,
"text": "decreased expression of proliferating cell nuclear antigen and Bmi-1; upregulation of p16(INK4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17651940",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 701,
"text": "BMI-1 promotes self-renewal of stem cells largely by interfering with two central cellular tumor suppressor pathways, p16(Ink4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17145810",
"endSection": "abstract",
"offsetInBeginSection": 104,
"offsetInEndSection": 327,
"text": "p16INK4a and p14ARF tumor suppressors, human telomerase reverse transcriptase (h-TERT), and oncoprotein c-Myc have been implicated in the regulation of the cell cycle and proliferation mediated by PcG proteins, mainly Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17102614",
"endSection": "abstract",
"offsetInBeginSection": 395,
"offsetInEndSection": 492,
"text": "involving the polycomb group repressor Bmi-1 and the cyclin-dependent kinase inhibitor p16(INK4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16537449",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 596,
"text": "increased frequency to a telomere-independent senescent state mediated by the cyclin-dependent kinase inhibitor p16(INK4a). p16(INK4a) expression was regulated by the Polycomb group repressor Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157028",
"endSection": "abstract",
"offsetInBeginSection": 1445,
"offsetInEndSection": 1549,
"text": "The antisense Bmi-1 gene can inhibit the growth of K562 cell and upgrade expression of p16 in K562 cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16155021",
"endSection": "abstract",
"offsetInBeginSection": 912,
"offsetInEndSection": 989,
"text": "overexpression of BMI-1, a transcriptional repressor of the p16(INK4a) locus,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14982841",
"endSection": "abstract",
"offsetInBeginSection": 800,
"offsetInEndSection": 874,
"text": "experimental model systems indicate that p16 is a downstream target of Bmi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14574365",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 777,
"text": "In the absence of Bmi-1, the cyclin-dependent kinase inhibitor gene p16Ink4a is upregulated in neural stem cells, reducing the rate of proliferation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12714971",
"endSection": "abstract",
"offsetInBeginSection": 686,
"offsetInEndSection": 935,
"text": "A gene expression analysis revealed that the expression of stem cell associated genes, cell survival genes, transcription factors, and genes modulating proliferation including p16Ink4a and p19Arf was altered in bone marrow cells of the Bmi-1-/- mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12482990",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 106,
"text": "polycomb protein Bmi-1 represses the INK4a locus, which encodes the tumor suppressors p16 and p14(ARF)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9923679",
"endSection": "title",
"offsetInBeginSection": 17,
"offsetInEndSection": 110,
"text": "Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9923679",
"endSection": "abstract",
"offsetInBeginSection": 777,
"offsetInEndSection": 912,
"text": "in bmi-1-deficient lymphocytes, the expression of the tumour suppressors p16 and p19Arf, which are encoded by ink4a, is raised markedly"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21928107",
"endSection": "abstract",
"offsetInBeginSection": 1493,
"offsetInEndSection": 1526,
"text": "BMI-1-mediated INK4a/ARF pathway "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18346113",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 320,
"text": " expression of the polycomb protein BMI-1 and its downstream targets p16(Ink4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21496667",
"endSection": "abstract",
"offsetInBeginSection": 905,
"offsetInEndSection": 1029,
"text": "reduced expression of Bmi-1, OC, DSP, and BSP compared with rapidly proliferating cells, whereas p16(INK4A) level increased."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21164364",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 52,
"text": "16Ink4a suppression of lung adenocarcinoma by Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21164364",
"endSection": "abstract",
"offsetInBeginSection": 1386,
"offsetInEndSection": 1460,
"text": "The suppression of p16Ink4a occurred in parallel with an increase in Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19907431",
"endSection": "abstract",
"offsetInBeginSection": 1224,
"offsetInEndSection": 1282,
"text": "Bmi-1 overexpression reduced p16(INK4a) promoter activity "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19390085",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 35,
"text": "mi-1 regulates the Ink4a/Arf locus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19390085",
"endSection": "abstract",
"offsetInBeginSection": 212,
"offsetInEndSection": 291,
"text": "derepression of the Ink4a/Arf locus is associated with decreased Bmi-1 binding,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19389366",
"endSection": "abstract",
"offsetInBeginSection": 1029,
"offsetInEndSection": 1152,
"text": "pronounced effects of Bmi-1 over-expression in culture were largely attributable to the attenuated induction of p16(Ink4a) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17597110",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 443,
"text": "BMI-1 is a transcriptional repressor of the Ink4a/Arf locus encoding p16(ink4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17233832",
"endSection": "abstract",
"offsetInBeginSection": 387,
"offsetInEndSection": 442,
"text": "introduction of Bmi-1 can inhibit p16(INK4a) expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16869752",
"endSection": "abstract",
"offsetInBeginSection": 635,
"offsetInEndSection": 718,
"text": "Bmi-1 promotes stem cell self-renewal partly by repressing the expression of Ink4a "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16778197",
"endSection": "abstract",
"offsetInBeginSection": 917,
"offsetInEndSection": 1060,
"text": "Overexpression of Bmi-1 in NPECs led to the induction of human telomerase reverse transcriptase activity and reduction of p16(INK4a) expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15964994",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 742,
"text": "Bmi-1 thus prevents the premature senescence of neural stem cells by repressing Ink4a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15892997",
"endSection": "abstract",
"offsetInBeginSection": 355,
"offsetInEndSection": 442,
"text": "overexpression of the polycomb-group gene BMI-1 might also down-regulate p16 expression"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14732230",
"endSection": "title",
"offsetInBeginSection": 4,
"offsetInEndSection": 113,
"text": "Bmi-1 oncoprotein is overexpressed in human colorectal cancer and correlates with the reduced p16INK4a/p14ARF"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14732230",
"endSection": "abstract",
"offsetInBeginSection": 809,
"offsetInEndSection": 925,
"text": "modulation of Bmi-1 protein might be involved in human colorectal carcinogenesis by repressing the INK4a/ARF protein"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14536079",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 29,
"text": "mi-1 regulation of INK4A-ARF"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14536079",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 428,
"text": "expression of BMI-1, a lymphoid oncogene whose product functions as a transcriptional repressor of the INK4A-ARF tumor suppressor locu"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11355949",
"endSection": "title",
"offsetInBeginSection": 4,
"offsetInEndSection": 126,
"text": "bmi-1 oncoprotein is differentially expressed in non-small cell lung cancer and correlates with INK4A-ARF locus expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11355949",
"endSection": "abstract",
"offsetInBeginSection": 419,
"offsetInEndSection": 495,
"text": "bmi-1 overexpression induces immortalization due to repression of p16/p19ARF"
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D050756",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019941",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0004861",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0045736",
"http://www.uniprot.org/uniprot/CD2A1_MONDO"
] |
[] |
533abc76d6d3ac6a34000064
|
bioasq_factoid
|
yesno
|
Down's syndrome occurs when an individual has an extra copy or part of a copy of chromosome 21, yes or no?
|
['yes']
|
[
"yes"
] |
['Yes, Downs syndrome is caused by a duplication or all or part of chromosome 21.', 'Down syndrome (DS), trisomy 21, is caused by increased dose of genes present on human chromosome 21 (HSA21). ', 'Down syndrome (DS; trisomy 21) is the most common survivable disorder due to aneuploidy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26391045",
"http://www.ncbi.nlm.nih.gov/pubmed/19636252",
"http://www.ncbi.nlm.nih.gov/pubmed/26243569",
"http://www.ncbi.nlm.nih.gov/pubmed/9800738",
"http://www.ncbi.nlm.nih.gov/pubmed/27245382",
"http://www.ncbi.nlm.nih.gov/pubmed/2143053",
"http://www.ncbi.nlm.nih.gov/pubmed/3036686",
"http://www.ncbi.nlm.nih.gov/pubmed/9050924",
"http://www.ncbi.nlm.nih.gov/pubmed/23394617",
"http://www.ncbi.nlm.nih.gov/pubmed/18801168",
"http://www.ncbi.nlm.nih.gov/pubmed/27931082",
"http://www.ncbi.nlm.nih.gov/pubmed/11371509",
"http://www.ncbi.nlm.nih.gov/pubmed/26300975",
"http://www.ncbi.nlm.nih.gov/pubmed/18056702",
"http://www.ncbi.nlm.nih.gov/pubmed/21081842",
"http://www.ncbi.nlm.nih.gov/pubmed/19212162",
"http://www.ncbi.nlm.nih.gov/pubmed/25862935",
"http://www.ncbi.nlm.nih.gov/pubmed/24980541",
"http://www.ncbi.nlm.nih.gov/pubmed/2880544",
"http://www.ncbi.nlm.nih.gov/pubmed/15176487",
"http://www.ncbi.nlm.nih.gov/pubmed/25706610",
"http://www.ncbi.nlm.nih.gov/pubmed/25738006",
"http://www.ncbi.nlm.nih.gov/pubmed/23686780",
"http://www.ncbi.nlm.nih.gov/pubmed/28342823",
"http://www.ncbi.nlm.nih.gov/pubmed/24210986",
"http://www.ncbi.nlm.nih.gov/pubmed/7532356"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27931082",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "Down syndrome (DS; trisomy 21) is the most common survivable disorder due to aneuploidy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28342823",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Down syndrome (DS), trisomy 21, is caused by increased dose of genes present on human chromosome 21 (HSA21)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27245382",
"endSection": "abstract",
"offsetInBeginSection": 97,
"offsetInEndSection": 207,
"text": "Down syndrome, or Trisomy 21, is the most frequently occurring chromosomal abnormality in live-born children. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26391045",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 55,
"text": "Down syndrome (DS), caused by trisomy of chromosome 21,"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3036686",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Submicroscopic duplication of chromosome 21 and trisomy 21 phenotype (Down syndrome)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19636252",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Trisomy 21 or Down syndrome is a chromosomal disorder resulting from the presence of all or part of an extra Chromosome 21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19212162",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Down syndrome is a genetic disorder, occurring when an individual has all or part of an extra copy of chromosome 21."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25738006",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Downs syndrome (DS) occurs due to an extra copy of chromosome 21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26243569",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Down syndrome, which arises in individuals carrying an extra copy of chromosome 21, is associated with a greatly increased risk of early-onset Alzheimer disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24980541",
"endSection": "abstract",
"offsetInBeginSection": 518,
"offsetInEndSection": 769,
"text": "Aneuploidy refers to the presence of an extra copy of a specific chromosome, or trisomy, as seen in Down's syndrome (trisomy 21), or the absence of a single chromosome, or monosomy, as seen in Turner syndrome (a single X chromosome in females: 45, X)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21081842",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "Down syndrome (DS) or Trisomy 21 (Ts21) is caused by the presence of an extra copy of all or part of human chromosome 21 (Hsa21) and is the most frequent survivable congenital chromosomal abnormality."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2143053",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "Down syndrome (DS) is a major cause of mental retardation and heart disease. Although it is usually caused by the presence of an extra chromosome 21, a subset of the diagnostic features may be caused by the presence of only band 21q22."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7532356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 55,
"text": "Down syndrome is usually caused by complete trisomy 21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056702",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Down syndrome, the most frequent genetic disorder, is characterized by an extra copy of all or part of chromosome 21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23394617",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 190,
"text": "Down syndrome (DS), caused by an extra copy of chromosome 21, affects 1 in 750 live births and is characterized by cognitive impairment and a constellation of congenital defects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25706610",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Down syndrome (DS) results from one extra copy of human chromosome 21 and leads to several alterations including intellectual disabilities and locomotor defects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9050924",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Down's syndrome results from the production of three copies of chromosome 21 within a cell. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25738006",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Downs syndrome (DS) occurs due to an extra copy of chromosome 21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11371509",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Trisomy 21 (Ts21) is the most common live-born human aneuploidy; it results in a constellation of features known as Down's syndrome (DS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25862935",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 98,
"text": "Down syndrome comprises multiple malformations and is due to trisomy of chromosome 21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24210986",
"endSection": "abstract",
"offsetInBeginSection": 161,
"offsetInEndSection": 292,
"text": "n 1959, J. Lejeune, M. Gautier, and R. Turpin demonstrated that the children with Down syndrome had an extra copy of chromosome 21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23686780",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 112,
"text": "To develop a reliable and specific method for rapid prenatal diagnosis of Trisomy 21 (Down syndrome)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26300975",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 126,
"text": "Trisomy 21 Down syndrome is the most common genetic cause for congenital malformations and intellectual disability"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18801168",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 154,
"text": "Down syndrome, characterized by an extra chromosome 21 is the most common genetic cause for congenital malformations and learning disability. "
}
] | 11
|
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D004314",
"https://meshb.nlm.nih.gov/record/ui?ui=D056915",
"https://meshb.nlm.nih.gov/record/ui?ui=D000076103",
"https://meshb.nlm.nih.gov/record/ui?ui=D002891"
] | null |
5a76016683b0d9ea6600000d
|
bioasq_yesno
|
yesno
|
Can Connexin hemi channels be used for drug delivery?
|
['yes']
|
[
"yes"
] |
['Yes, Connexin hemi channels can be used for drug delivery.', 'Yes, Connexin hemi channels can be used for drug delivery due to their permeability to small molecules and macromolecules.', 'Yes, Connexin hemi channels can be used for drug delivery due to their ability to create transitory plasma membrane permeability changes, allowing for the non-selective passage of molecules up to 1,000 Da.', 'Yes, Cx43 channels are highly permeable to small molecules and macromolecules, making them attractive targets for delivering drugs directly into the cytoplasm.', 'Yes, Connexin hemi channels have been proposed as a potential route for drug delivery due to their ability to form open channels in the cell membrane, allowing for the passage of molecules, including drugs, into and out of the cell.', 'Yes,, Connexin hemichannels can be used for drug delivery.', 'yes, pore forming channels such as connexin can potentiially be used as a drug delivery system.', 'Yes, Connexin hemi-channels can be employed for drug delivery.', 'Yes, Connexin hemichannels can be used for drug delivery, as shown by the delivery of polymeric macromolecules via gap junctions.', 'yes, Connexin hemichannels, due to their permeability to small molecules and macromolecules, can be utilized for delivering drugs directly into the cytoplasm.', 'Yes, Connexin hemichannels can be utilized for drug delivery.', 'Yes, Connexin hemichannels can be used for drug delivery due to their ability to allow the passage of molecules up to 1,000 Da.', 'Yes, connexin hemichannels can be used as a conduit for the delivery of therapeutic agents into cells', 'Yes, Connexin hemi channels can be used for drug delivery due to their high permeability to small molecules and macromolecules, allowing for direct delivery of drugs into the cytoplasm.', 'Yes, Connexin hemichannels can be used for drug delivery due to their ability to allow for the non-selective passage of molecules up to 1,000 Da.', 'Yes, the permeability of Cx43 channels to small molecules and macromolecules makes them highly attractive targets for delivering drugs directly into the cytoplasm.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29861876",
"http://www.ncbi.nlm.nih.gov/pubmed/30472182",
"http://www.ncbi.nlm.nih.gov/pubmed/35263989"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30472182",
"endSection": "abstract",
"offsetInBeginSection": 763,
"offsetInEndSection": 920,
"text": "he permeability of Cx43 channels to small molecules and macromolecules makes them highly attractive targets for delivering drugs directly into the cytoplasm."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30472182",
"endSection": "abstract",
"offsetInBeginSection": 921,
"offsetInEndSection": 1011,
"text": "Cancer cells overexpressing Cx43 may be more permeable and sensitive to chemotherapeutics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29861876",
"endSection": "abstract",
"offsetInBeginSection": 1213,
"offsetInEndSection": 1434,
"text": "n this context, certain channels lead to transitory plasma membrane permeability changes, such as pannexin, connexin hemmichannels, TRPV1-4 and P2×7, which allow for the non-selective passage of molecules up to 1,000 Da. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35263989",
"endSection": "abstract",
"offsetInBeginSection": 1428,
"offsetInEndSection": 1679,
"text": "Collectively, these results reveal that polymeric macromolecules can be delivered to cells via gap junctions, suggesting that the gap junction route may be useful for the delivery of polymeric therapeutic molecules, such as nucleic acids and peptides."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35263989",
"endSection": "abstract",
"offsetInBeginSection": 176,
"offsetInEndSection": 422,
"text": "Gap junction channels, composed of connexin proteins, provide a mechanism for direct transfer of small molecules across membranes, and recent evidence suggests that the transfer of larger, polymer-like molecules such as microRNAs may be possible."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30472182",
"endSection": "abstract",
"offsetInBeginSection": 762,
"offsetInEndSection": 920,
"text": "The permeability of Cx43 channels to small molecules and macromolecules makes them highly attractive targets for delivering drugs directly into the cytoplasm."
}
] | 13
|
BioASQ-training13b
| null | null |
660712a1fdcbea915f000003
|
bioasq_yesno
|
factoid
|
What is the cause of a STAG3 truncating variant?
|
['Primary ovarian insufficiency', 'POI']
|
[
"Primary ovarian insufficiency",
"POI",
"Premature ovarian failure",
"Premature ovarian insufficiency",
"Ovarian insufficiency",
"Ovarian failure"
] |
['Linkage analysis identified a locus on chromosome 7 where exome sequencing successfully identified a homozygous two base pair duplication (c.1947_48dupCT), leading to a truncated protein p.(Y650Sfs*22) in the STAG3 gene, confirming it as the cause of POI in this family', 'Primary ovarian insufficiency (POI) is a distressing cause of infertility in young women. POI is heterogeneous with only a few causative genes having been discovered so far. Linkage analysis identified a locus on chromosome 7 where exome sequencing successfully identified a homozygous two base pair duplication (c.1947_48dupCT), leading to a truncated protein p.(Y650Sfs*22) in the STAG3 gene, confirming it as the cause of POI in this family.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27836978",
"http://www.ncbi.nlm.nih.gov/pubmed/26059840",
"http://www.ncbi.nlm.nih.gov/pubmed/30006057"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26059840",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "STAG3 truncating variant as the cause of primary ovarian insufficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26059840",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1233,
"text": "Primary ovarian insufficiency (POI) is a distressing cause of infertility in young women. POI is heterogeneous with only a few causative genes having been discovered so far. Our objective was to determine the genetic cause of POI in a consanguineous Lebanese family with two affected sisters presenting with primary amenorrhoea and an absence of any pubertal development. Multipoint parametric linkage analysis was performed. Whole-exome sequencing was done on the proband. Linkage analysis identified a locus on chromosome 7 where exome sequencing successfully identified a homozygous two base pair duplication (c.1947_48dupCT), leading to a truncated protein p.(Y650Sfs*22) in the STAG3 gene, confirming it as the cause of POI in this family. Exome sequencing combined with linkage analyses offers a powerful tool to efficiently find novel genetic causes of rare, heterogeneous disorders, even in small single families. This is only the second report of a STAG3 variant; the first STAG3 variant was recently described in a phenotypically similar family with extreme POI. Identification of an additional family highlights the importance of STAG3 in POI pathogenesis and suggests it should be evaluated in families affected with POI."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26059840",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "STAG3 truncating variant as the cause of primary ovarian insufficiency.Primary ovarian insufficiency (POI) is a distressing cause of infertility in young women. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30006057",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Two rare loss-of-function variants in the STAG3 gene leading to primary ovarian insufficiency."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27836978",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "A homozygous NOBOX truncating variant causes defective transcriptional activation and leads to primary ovarian insufficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30006057",
"endSection": "abstract",
"offsetInBeginSection": 1270,
"offsetInEndSection": 1556,
"text": "The parents' DNA was not available to segregate these variants.<br><b>CONCLUSION</b>: Our results suggested that POI is caused by pathogenic compound heterozygous variants in the STAG3 gene, supporting the key role of the STAG3 gene in the etiology of primary ovarian insufficiency.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30006057",
"endSection": "abstract",
"offsetInBeginSection": 1410,
"offsetInEndSection": 1606,
"text": "Our results suggested that POI is caused by pathogenic compound heterozygous variants in the STAG3 gene, supporting the key role of the STAG3 gene in the etiology of primary ovarian insufficiency."
}
] | 11
|
BioASQ-training11b
| null | null |
5c632cc1e842deac6700000f
|
bioasq_factoid
|
yesno
|
Does clinical trial data support the use of minocycline for amyotrophic lateral sclerosis?
|
['no']
|
[
"no"
] |
['No. Available clinical trial data suggest that minocycline does not improve prognosis and functional status, and has a harmful effect on patients with amyotrophic lateral sclerosis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/15159491",
"http://www.ncbi.nlm.nih.gov/pubmed/17980667",
"http://www.ncbi.nlm.nih.gov/pubmed/16193258",
"http://www.ncbi.nlm.nih.gov/pubmed/16638021",
"http://www.ncbi.nlm.nih.gov/pubmed/18802797"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15159491",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Two double-blind, randomized, placebo-controlled feasibility trials of minocycline in ALS were conducted. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16193258",
"endSection": "abstract",
"offsetInBeginSection": 772,
"offsetInEndSection": 918,
"text": "This pilot study shows that minocycline and riluzole can be taken safely together. Further trials are needed to assess efficacy of such treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16638021",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 283,
"text": "It reduces apoptosis in mouse models of Huntington's disease and familial amyotrophic lateral sclerosis (ALS) and is in clinical trial for sporadic ALS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17980667",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Efficacy of minocycline in patients with amyotrophic lateral sclerosis: a phase III randomised trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17980667",
"endSection": "abstract",
"offsetInBeginSection": 947,
"offsetInEndSection": 1514,
"text": "FINDINGS: ALSFRS-R score deterioration was faster in the minocycline group than in the placebo group (-1.30 vs -1.04 units/month, 95% CI for difference -0.44 to -0.08; p=0.005). Patients on minocycline also had non-significant tendencies towards faster decline in FVC (-3.48 vs -3.01, -1.03 to 0.11; p=0.11) and MMT score (-0.30 vs -0.26, -0.08 to 0.01; p=0.11), and greater mortality during the 9-month treatment phase (hazard ratio=1.32, 95% CI 0.83 to 2.10; p=0.23) than did patients on placebo. Quality-of-life scores did not differ between the treatment groups. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17980667",
"endSection": "abstract",
"offsetInBeginSection": 1725,
"offsetInEndSection": 1989,
"text": "INTERPRETATION: Our finding that minocycline has a harmful effect on patients with ALS has implications for trials of minocycline in patients with other neurological disorders, and for how potential neuroprotective agents are screened for use in patients with ALS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18802797",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 265,
"text": "A recent publication of the results of a clinical trial of minocycline in 412 ALS patient has aroused considerable controversy in the ALS scientific community. As on previous occasions, the results obtained in the laboratory are not reproduced in clinical practice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18802797",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "A recent publication of the results of a clinical trial of minocycline in 412 ALS patient has aroused considerable controversy in the ALS scientific community."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17980667",
"endSection": "abstract",
"offsetInBeginSection": 1731,
"offsetInEndSection": 1995,
"text": "INTERPRETATION\n\nOur finding that minocycline has a harmful effect on patients with ALS has implications for trials of minocycline in patients with other neurological disorders, and for how potential neuroprotective agents are screened for use in patients with ALS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18802797",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "A recent publication of the results of a clinical trial of minocycline in 412 ALS patient has aroused considerable controversy in the ALS scientific community"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18802797",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "A recent publication of the results of a clinical trial of minocycline in 412 ALS patient has aroused considerable controversy in the ALS scientific community."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17980667",
"endSection": "abstract",
"offsetInBeginSection": 1697,
"offsetInEndSection": 1945,
"text": "Our finding that minocycline has a harmful effect on patients with ALS has implications for trials of minocycline in patients with other neurological disorders, and for how potential neuroprotective agents are screened for use in patients with ALS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17980667",
"endSection": "abstract",
"offsetInBeginSection": 1096,
"offsetInEndSection": 1416,
"text": "Patients on minocycline also had non-significant tendencies towards faster decline in FVC (-3.48 vs -3.01, -1.03 to 0.11; p=0.11) and MMT score (-0.30 vs -0.26, -0.08 to 0.01; p=0.11), and greater mortality during the 9-month treatment phase (hazard ratio=1.32, 95% CI 0.83 to 2.10; p=0.23) than did patients on placebo."
}
] | 11
|
BioASQ-training11b
| null | null |
5e4b5fd86d0a277941000022
|
bioasq_yesno
|
yesno
|
Is the protein Asporin related to disease?
|
['yes']
|
[
"yes"
] |
['Yes,\nAccumulating evidence demonstrates the involvement of asporin in OA pathogenesis. Asporin has been reported as a tumor suppressor in breast cancer, while asporin-activated invasion has been described in gastric cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25689697",
"http://www.ncbi.nlm.nih.gov/pubmed/27409832",
"http://www.ncbi.nlm.nih.gov/pubmed/28152543",
"http://www.ncbi.nlm.nih.gov/pubmed/27705916"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25689697",
"endSection": "abstract",
"offsetInBeginSection": 307,
"offsetInEndSection": 388,
"text": "Accumulating evidence demonstrates the involvement of asporin in OA pathogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27409832",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Asporin has been reported as a tumor suppressor in breast cancer, while asporin-activated invasion has been described in gastric cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27705916",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Asporin has been implicated as an oncogene in various types of human cancers; "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27705916",
"endSection": "abstract",
"offsetInBeginSection": 1264,
"offsetInEndSection": 1425,
"text": " These results suggested that asporin promoted the tumor growth and metastasis of CRC, and it could be a potential therapeutic target for CRC patients in future."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28152543",
"endSection": "abstract",
"offsetInBeginSection": 1975,
"offsetInEndSection": 2118,
"text": "Our results suggest that ASPN is a stromally expressed biomarker that correlates with disease progression, and is observed in reactive stroma. "
}
] | 11
|
BioASQ-training11b
| null | null |
5c8ab614d558e5f23200000d
|
bioasq_yesno
|
factoid
|
What does RUNX1T1 stand for?
|
['runt-related transcription factor 1']
|
[
"runt-related transcription factor 1",
"RUNX1",
"AML1",
"CBFA2",
"runt domain transcription factor 1",
"runt-related transcription factor alpha",
"runt-related transcription factor 1 alpha"
] |
['RUNX1T1 stands for runt-related transcription factor 1.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32589708"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32589708",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 96,
"text": "Runt-related transcription factor 1 (RUNX1T1) isoforms are involved in adipogenesis."
}
] | 11
|
BioASQ-training11b
| null | null |
62265b4a3a8413c653000083
|
bioasq_factoid
|
yesno
|
Is Mical an oxidoreductase?
|
['yes']
|
[
"yes"
] |
['Yes,\nMICAL is an oxidoreductase']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31949908",
"http://www.ncbi.nlm.nih.gov/pubmed/12700098",
"http://www.ncbi.nlm.nih.gov/pubmed/27223600",
"http://www.ncbi.nlm.nih.gov/pubmed/33671465"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33671465",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 497,
"text": "the MICALs, which are flavoprotein monooxygenase/hydroxylase enzymes that associate with flavin adenine dinucleotide (FAD) and use the co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH) in Redox reactions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31949908",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 26,
"text": "MICAL is an oxidoreductase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27223600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "We have recently identified a new family of multidomain oxidoreductase (redox) enzymes, the MICALs,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12700098",
"endSection": "abstract",
"offsetInBeginSection": 1552,
"offsetInEndSection": 1576,
"text": "the oxidoreductase MICAL"
}
] | 11
|
BioASQ-training11b
| null | null |
62515021e764a53204000018
|
bioasq_yesno
|
yesno
|
Are there any R packages that help with visualizing data on spirals?
|
['yes']
|
[
"yes"
] |
['Yes. Spiralize is an R package for visualizing data on spirals.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34849585"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34849585",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "spiralize: an R package for Visualizing Data on Spirals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34849585",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 584,
"text": "Spiral layout has two major advantages for data visualization. First, it is able to visualize data with long axes, which greatly improves the resolution of visualization. Second, it is efficient for time series data to reveal periodic patterns. Here we present the R package spiralize that provides a general solution for visualizing data on spirals. spiralize implements numerous graphics functions so that self-defined high-level graphics can be easily implemented by users. The flexibility and power of spiralize are demonstrated by five examples from real-world datasets."
}
] | 11
|
BioASQ-training11b
| null | null |
621e62c33a8413c653000050
|
bioasq_yesno
|
yesno
|
Are neurexins localized at pre-synapses?
|
['yes']
|
[
"yes"
] |
['Yes, neurexins are localized at pre-synapses.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28154140",
"http://www.ncbi.nlm.nih.gov/pubmed/28643105",
"http://www.ncbi.nlm.nih.gov/pubmed/27664583",
"http://www.ncbi.nlm.nih.gov/pubmed/27725662"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27664583",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Neurexins and neuroligins are two distinct families of single-pass transmembrane proteins localized at pre- and postsynapses, respectively. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27725662",
"endSection": "abstract",
"offsetInBeginSection": 66,
"offsetInEndSection": 87,
"text": "presynaptic neurexins"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28154140",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 307,
"text": "best-characterized transsynaptic interactions are formed by presynaptic neurexins, which bind to diverse postsynaptic ligands."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28643105",
"endSection": "abstract",
"offsetInBeginSection": 435,
"offsetInEndSection": 455,
"text": "presynaptic neurexin"
}
] | 11
|
BioASQ-training11b
| null | null |
5a8866958cb19eca6b000003
|
bioasq_yesno
|
factoid
|
Which biological process takes place in nuclear speckles?
|
['mRNA processing', 'mRNA splicing']
|
[
"mRNA processing",
"mRNA splicing",
"messenger RNA processing",
"messenger RNA splicing",
"RNA processing",
"RNA splicing"
] |
['Speckles are subnuclear structures that are enriched in pre-messenger RNA splicing factors and are located in the interchromatin regions of the nucleoplasm of mammalian cells. They serve as splicing factor storage sites and play important roles in regulation of pre-mRNA splicing.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12923522",
"http://www.ncbi.nlm.nih.gov/pubmed/12826600",
"http://www.ncbi.nlm.nih.gov/pubmed/12002677",
"http://www.ncbi.nlm.nih.gov/pubmed/29496966",
"http://www.ncbi.nlm.nih.gov/pubmed/23934081",
"http://www.ncbi.nlm.nih.gov/pubmed/27239700",
"http://www.ncbi.nlm.nih.gov/pubmed/30032211",
"http://www.ncbi.nlm.nih.gov/pubmed/29773831",
"http://www.ncbi.nlm.nih.gov/pubmed/30194269"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23934081",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 295,
"text": "Here we demonstrate that mRNAs containing ALREX-promoting elements are trafficked through nuclear speckles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23934081",
"endSection": "abstract",
"offsetInBeginSection": 734,
"offsetInEndSection": 893,
"text": "Finally, we demonstrate that mRNAs lacking a poly(A)-tail are not efficiently exported by the ALREX pathway and show enhanced association with nuclear speckles"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12002677",
"endSection": "abstract",
"offsetInBeginSection": 138,
"offsetInEndSection": 521,
"text": " In a previous study (Melcák et al., 2001), it has been shown that the pre-spliceosomal assembly on microinjected splicing-competent precursor mRNA takes place in the speckles, and it has been suggested that the targeting of RNA into speckes consists of two interdependent steps, namely the diffusion process, followed by the energy-dependent translocation of RNA into the speckles. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12826600",
"endSection": "abstract",
"offsetInBeginSection": 250,
"offsetInEndSection": 445,
"text": "Nuclear speckles, a unique nuclear subcompartment, accumulate a family of proteins, namely, serine- and arginine-rich (SR) proteins. They play important roles in regulation of pre-mRNA splicing. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29496966",
"endSection": "abstract",
"offsetInBeginSection": 233,
"offsetInEndSection": 332,
"text": " Here we show that C3G localizes to SC35-positive nuclear speckles and regulates splicing activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29496966",
"endSection": "abstract",
"offsetInBeginSection": 1247,
"offsetInEndSection": 1385,
"text": "Our results identify C3G and Rap1 as novel components of nuclear speckles and a role for C3G in regulating cellular RNA splicing activity."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29773831",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "DNAJC17 is localized in nuclear speckles and interacts with splicing machinery components."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30032211",
"endSection": "abstract",
"offsetInBeginSection": 470,
"offsetInEndSection": 552,
"text": "These results suggest that exosomal mRNA degradation mostly occurs outside of NSs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30194269",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "Nuclear speckles (NSs) serve as splicing factor storage sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12923522",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Speckles are subnuclear structures that are enriched in pre-messenger RNA splicing factors and are located in the interchromatin regions of the nucleoplasm of mammalian cells."
}
] | 11
|
BioASQ-training11b
| null | null |
5c74266a7c78d694710000a2
|
bioasq_factoid
|
factoid
|
Which was the first adeno-associated virus vector gene therapy product approved in the United States?
|
['Luxturna']
|
[
"Luxturna",
"voretigene neparvovec",
"voretigene neparvovec-rzyl",
"LUXTURNA"
] |
['The first adeno-associated virus vector gene therapy product in the United States was Luxturna.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30089698"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30089698",
"endSection": "abstract",
"offsetInBeginSection": 1755,
"offsetInEndSection": 2009,
"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 |
5c897555d558e5f232000009
|
bioasq_factoid
|
yesno
|
Does prolactinoma increase osteoporosis risk?
|
['yes']
|
[
"yes"
] |
['Yes, prolactinomas increase risk of osteoporosis. Prolactinomas also cause hypogonadism, infertility, and tumor mass effects.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26319389",
"http://www.ncbi.nlm.nih.gov/pubmed/22553947",
"http://www.ncbi.nlm.nih.gov/pubmed/27446618",
"http://www.ncbi.nlm.nih.gov/pubmed/20205855",
"http://www.ncbi.nlm.nih.gov/pubmed/26243714",
"http://www.ncbi.nlm.nih.gov/pubmed/17578827",
"http://www.ncbi.nlm.nih.gov/pubmed/25472533",
"http://www.ncbi.nlm.nih.gov/pubmed/15816365",
"http://www.ncbi.nlm.nih.gov/pubmed/21479837",
"http://www.ncbi.nlm.nih.gov/pubmed/11293923",
"http://www.ncbi.nlm.nih.gov/pubmed/23965473",
"http://www.ncbi.nlm.nih.gov/pubmed/9550540"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27446618",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Prolactinoma: A Massive Effect on Bone Mineral Density in a Young Patient."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27446618",
"endSection": "abstract",
"offsetInBeginSection": 84,
"offsetInEndSection": 456,
"text": "Osteoporosis has been noted to be an issue in postmenopausal women with prolactinomas. This case shows a similar impact on bone health in a young male resulting in low bone mineral density for age based on Z-score. This case report highlights the possible mechanisms for the bone loss in the setting of prolactinoma and the need for assessing bone health in such patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26319389",
"endSection": "abstract",
"offsetInBeginSection": 1013,
"offsetInEndSection": 1181,
"text": " Hyperprolactinaemia related to prolactinoma significantly (more than functional hyperprolactiaemia) increases the risk of osteopenia, osteoporosis and bone fractures. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26243714",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 354,
"text": "Prolactinomas are the most common type of functional pituitary tumor. Effective hyperprolactinemia treatment is of great importance, due to its potential deleterious effects including infertility, gonadal dysfunction and osteoporosis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25472533",
"endSection": "abstract",
"offsetInBeginSection": 212,
"offsetInEndSection": 350,
"text": "Prolactinomas cause hypogonadism, infertility, osteoporosis, and tumor mass effects, and are the most common type of neuroendocrine tumor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23965473",
"endSection": "abstract",
"offsetInBeginSection": 481,
"offsetInEndSection": 733,
"text": "We present a 22-year-old man with multiple osteoporotic fractures associated with prolactinoma despite the use of teriparatide for 18 months. We emphasize and highlight the importance of hyperprolactinemia and fractures caused by high prolactin levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22553947",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "OBJECTIVE: Patients with prolactinoma seem to be at high risk for osteopenia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22553947",
"endSection": "abstract",
"offsetInBeginSection": 601,
"offsetInEndSection": 724,
"text": "RESULTS: Compared to the matched controls, BMD of patients with prolactinoma or craniopharyngioma significantly decreased. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22553947",
"endSection": "abstract",
"offsetInBeginSection": 1079,
"offsetInEndSection": 1310,
"text": "CONCLUSION: In the premenopausal women, patients with prolactinoma or craniopharyngioma are often accompanied with osteopenia or osteoporosis, and disease duration and hypogonadism are the risk factors of bone loss in prolactinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21479837",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 394,
"text": "Data on osteoporotic fractures in hyperprolactinemia are limited. An increased prevalence of radiological vertebral fractures was recently observed in women with prolactin (PRL)-secreting adenoma, whereas it is unknown whether this observation may reflect a more general increased risk of fractures in this disease and whether the prevalence of fractures in males is affected by gonadal status."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20205855",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Prolactinoma presenting as chronic anaemia with osteoporosis: a case report."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20205855",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 374,
"text": "Six years later, he was evaluated and diagnosed with a prolactinoma and resultant osteoporosis. Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without sexual dysfunction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11293923",
"endSection": "abstract",
"offsetInBeginSection": 1145,
"offsetInEndSection": 1327,
"text": "The relative risk for developing osteoporosis in women with prolactinoma was found to be 4.5, indicating that hyperprolactinemia in women is a major risk factor for osteoporosis.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17578827",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "<b>INTRODUCTION</b>: Osteopenia and osteoporosis because of hyperprolactinaemia caused by prolactinoma may be followed by an increased risk of fracture."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22553947",
"endSection": "abstract",
"offsetInBeginSection": 948,
"offsetInEndSection": 1350,
"text": "Univariate and multivariate regression analysis indicated that the bone loss in prolactinomas was significantly correlated to disease duration and hypogonadism.<br><b>CONCLUSION</b>: In the premenopausal women, patients with prolactinoma or craniopharyngioma are often accompanied with osteopenia or osteoporosis, and disease duration and hypogonadism are the risk factors of bone loss in prolactinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26319389",
"endSection": "abstract",
"offsetInBeginSection": 782,
"offsetInEndSection": 873,
"text": "High serum prolactin levels lead to increase of the risk of osteopenia or/and osteoporosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20205855",
"endSection": "abstract",
"offsetInBeginSection": 257,
"offsetInEndSection": 509,
"text": "Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without sexual dysfunction.<br><b>CASE PRESENTATION</b>: We describe the case of a 70-year-old Caucasian man who presented with mild anaemia and tiredness."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22553947",
"endSection": "abstract",
"offsetInBeginSection": 1094,
"offsetInEndSection": 1313,
"text": "In the premenopausal women, patients with prolactinoma or craniopharyngioma are often accompanied with osteopenia or osteoporosis, and disease duration and hypogonadism are the risk factors of bone loss in prolactinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11293923",
"endSection": "abstract",
"offsetInBeginSection": 1145,
"offsetInEndSection": 1323,
"text": "The relative risk for developing osteoporosis in women with prolactinoma was found to be 4.5, indicating that hyperprolactinemia in women is a major risk factor for osteoporosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22553947",
"endSection": "abstract",
"offsetInBeginSection": 1085,
"offsetInEndSection": 1315,
"text": "CONCLUSION In the premenopausal women, patients with prolactinoma or craniopharyngioma are often accompanied with osteopenia or osteoporosis, and disease duration and hypogonadism are the risk factors of bone loss in prolactinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20205855",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 373,
"text": "Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without sexual dysfunction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26319389",
"endSection": "abstract",
"offsetInBeginSection": 1014,
"offsetInEndSection": 1180,
"text": "Hyperprolactinaemia related to prolactinoma significantly (more than functional hyperprolactiaemia) increases the risk of osteopenia, osteoporosis and bone fractures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17578827",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "INTRODUCTION Osteopenia and osteoporosis because of hyperprolactinaemia caused by prolactinoma may be followed by an increased risk of fracture."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15816365",
"endSection": "abstract",
"offsetInBeginSection": 1442,
"offsetInEndSection": 1531,
"text": "In conclusion, men with prolactinoma have high prevalence of osteopenia and osteoporosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9550540",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 54,
"text": "Humans with prolactinoma are at risk for osteoporosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17578827",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Osteopenia and osteoporosis because of hyperprolactinaemia caused by prolactinoma may be followed by an increased risk of fracture."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11293923",
"endSection": "abstract",
"offsetInBeginSection": 1145,
"offsetInEndSection": 1324,
"text": "The relative risk for developing osteoporosis in women with prolactinoma was found to be 4.5, indicating that hyperprolactinemia in women is a major risk factor for osteoporosis.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22553947",
"endSection": "abstract",
"offsetInBeginSection": 1039,
"offsetInEndSection": 1258,
"text": "In the premenopausal women, patients with prolactinoma or craniopharyngioma are often accompanied with osteopenia or osteoporosis, and disease duration and hypogonadism are the risk factors of bone loss in prolactinoma."
}
] | 11
|
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D010024",
"http://www.disease-ontology.org/api/metadata/DOID:5394",
"https://meshb.nlm.nih.gov/record/ui?ui=D015175",
"https://meshb.nlm.nih.gov/record/ui?ui=D012306"
] | null |
5a70d43b99e2c3af26000003
|
bioasq_yesno
|
factoid
|
What is the cause of lactose intolerance?
|
['Lactase deficiency']
|
[
"Lactase deficiency",
"Lactose intolerance",
"Lactose malabsorption",
"Lactase non-persistence",
"Lactase insufficiency"
] |
['Lactose intolerance is a common condition caused by lactase deficiency and may result in symptoms of lactose malabsorption (bloating, flatulence, abdominal discomfort, and change in bowel habits).\nFour clinical subtypes of lactose intolerance may be distinguished, namely lactase deficiency in premature infants, congenital lactase deficiency, adult-type hypolactasia and secondary lactase intolerance.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32048961",
"http://www.ncbi.nlm.nih.gov/pubmed/31802224",
"http://www.ncbi.nlm.nih.gov/pubmed/32443748",
"http://www.ncbi.nlm.nih.gov/pubmed/30617948",
"http://www.ncbi.nlm.nih.gov/pubmed/31904838"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30617948",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 197,
"text": "Lactose intolerance is a common condition caused by lactase deficiency and may result in symptoms of lactose malabsorption (bloating, flatulence, abdominal discomfort, and change in bowel habits). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31802224",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 259,
"text": " Adult lactose intolerance (ALI) significantly alters calcium intake and absorption, and thus may promote osteoporosis. ALI is a recessive condition with a geographical north-south gradient characterised by decreased levels of intestinal lactase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31904838",
"endSection": "abstract",
"offsetInBeginSection": 295,
"offsetInEndSection": 500,
"text": "Considerations include recognizing that a substantial proportion of the world's adult population (65%-70%) exhibits lactase nonpersistence, a reduced ability to metabolize lactose to glucose and galactose."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32048961",
"endSection": "abstract",
"offsetInBeginSection": 755,
"offsetInEndSection": 961,
"text": " Four clinical subtypes of lactose intolerance may be distinguished, namely lactase deficiency in premature infants, congenital lactase deficiency, adult-type hypolactasia and secondary lactase intolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32443748",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 443,
"text": "Lactose intolerance (LI) is characterized by the presence of primarily gastrointestinal clinical signs resulting from colonic fermentation of lactose, the absorption of which is impaired due to a deficiency in the lactase enzyme. These clinical signs can be modified by several factors, including lactose dose, residual lactase expression, concurrent ingestion of other dietary components, gut-transit time, and enteric microbiome composition."
}
] | 11
|
BioASQ-training11b
| null | null |
606b2b1994d57fd87900005c
|
bioasq_factoid
|
yesno
|
Do angiotensin-converting-enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) increase the likelihood of severe COVID-19?
|
['no']
|
[
"no"
] |
['No. Patients receiving angiotensin-converting-enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) should continue treatment with these agents if there is no other reason for discontinuation. Despite speculation that patients with COVID-19 who are receiving these agents may be at increased risk for adverse outcomes, accumulating evidence does not support an association of ACE inhibitors and ARBs with more severe disease. In addition, stopping these agents in some patients can exacerbate comorbid cardiovascular or kidney disease and increase mortality.', 'ACEIs and ARBs were not associated with an increased risk of Covid-19 hospitalization or with hospitalization involving ICU admission, invasive mechanical ventilation, or death.', 'No. ACEIs and ARBs have not been shown to increase the likelihood of severe COVID-19 hospitalization.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33210357",
"http://www.ncbi.nlm.nih.gov/pubmed/32514935",
"http://www.ncbi.nlm.nih.gov/pubmed/32474043",
"http://www.ncbi.nlm.nih.gov/pubmed/33201001",
"http://www.ncbi.nlm.nih.gov/pubmed/33842874",
"http://www.ncbi.nlm.nih.gov/pubmed/34611496",
"http://www.ncbi.nlm.nih.gov/pubmed/33614350",
"http://www.ncbi.nlm.nih.gov/pubmed/33038021",
"http://www.ncbi.nlm.nih.gov/pubmed/34599472",
"http://www.ncbi.nlm.nih.gov/pubmed/32757246",
"http://www.ncbi.nlm.nih.gov/pubmed/33085063",
"http://www.ncbi.nlm.nih.gov/pubmed/32579597",
"http://www.ncbi.nlm.nih.gov/pubmed/33231487",
"http://www.ncbi.nlm.nih.gov/pubmed/32651067",
"http://www.ncbi.nlm.nih.gov/pubmed/33891615",
"http://www.ncbi.nlm.nih.gov/pubmed/32422062",
"http://www.ncbi.nlm.nih.gov/pubmed/32587982",
"http://www.ncbi.nlm.nih.gov/pubmed/32685191",
"http://www.ncbi.nlm.nih.gov/pubmed/32875060",
"http://www.ncbi.nlm.nih.gov/pubmed/33658619",
"http://www.ncbi.nlm.nih.gov/pubmed/33222020",
"http://www.ncbi.nlm.nih.gov/pubmed/33748156",
"http://www.ncbi.nlm.nih.gov/pubmed/32485082",
"http://www.ncbi.nlm.nih.gov/pubmed/33981731",
"http://www.ncbi.nlm.nih.gov/pubmed/32611676",
"http://www.ncbi.nlm.nih.gov/pubmed/32320478",
"http://www.ncbi.nlm.nih.gov/pubmed/32558877",
"http://www.ncbi.nlm.nih.gov/pubmed/32348166",
"http://www.ncbi.nlm.nih.gov/pubmed/32737124",
"http://www.ncbi.nlm.nih.gov/pubmed/33095513",
"http://www.ncbi.nlm.nih.gov/pubmed/32242182",
"http://www.ncbi.nlm.nih.gov/pubmed/33504565",
"http://www.ncbi.nlm.nih.gov/pubmed/34155486",
"http://www.ncbi.nlm.nih.gov/pubmed/32918209",
"http://www.ncbi.nlm.nih.gov/pubmed/32965603"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34611496",
"endSection": "abstract",
"offsetInBeginSection": 1495,
"offsetInEndSection": 1726,
"text": "These findings suggest that the use of ACE-I and ARB is not associated with adverse outcomes and may be associated with improved outcomes in COVID-19, which is immediately relevant to care of the many patients on these medications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34599472",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 181,
"text": "There are theoretical concerns that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) could increase the risk of severe Covid-19."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34599472",
"endSection": "abstract",
"offsetInBeginSection": 1085,
"offsetInEndSection": 1311,
"text": "ACEIs and ARBs were associated with a slight reduction in Covid-19 hospitalization risk compared with treatment with other first-line antihypertensives (OR for ACEIs 0.95, 95% CI 0.92-0.98; OR for ARBs 0.94, 95% CI 0.90-0.97)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34599472",
"endSection": "abstract",
"offsetInBeginSection": 1431,
"offsetInEndSection": 1505,
"text": "There were no meaningful differences in risk for ACEIs compared with ARBs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34599472",
"endSection": "abstract",
"offsetInBeginSection": 1795,
"offsetInEndSection": 1972,
"text": "ACEIs and ARBs were not associated with an increased risk of Covid-19 hospitalization or with hospitalization involving ICU admission, invasive mechanical ventilation, or death."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33222020",
"endSection": "abstract",
"offsetInBeginSection": 1346,
"offsetInEndSection": 1448,
"text": "In patients with HTN and COVID-19, neither ACEi nor ARBs were independently associated with mortality."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33222020",
"endSection": "abstract",
"offsetInBeginSection": 1542,
"offsetInEndSection": 1687,
"text": "Our data confirm Specialty Societal recommendations, suggesting that treatment with ACEIs or ARBs should not be discontinued because of COVID-19."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33095513",
"endSection": "abstract",
"offsetInBeginSection": 1016,
"offsetInEndSection": 1258,
"text": "Random-effects meta-analysis showed ACEI/ARB treatment was significantly associated with a lower risk of mortality in hypertensive COVID-19 patients (odds ratio [OR] = 0.624, 95% confidence interval [CI] = 0.457-0.852, p = .003, I2  = 74.3%)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33095513",
"endSection": "abstract",
"offsetInBeginSection": 1562,
"offsetInEndSection": 1864,
"text": "In addition, the ACEI/ARB treatment was associated with a lower risk of ventilatory support (OR = 0.682, 95% CI = 0.475-1.978, p = .037, I2  = 0.0%). In conclusion, these results suggest that ACEI/ARB medications should not be discontinued for hypertensive patients in the context of COVID-19 pandemic."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34611496",
"endSection": "abstract",
"offsetInBeginSection": 942,
"offsetInEndSection": 1317,
"text": "Use of ACE-I or ARB medications was not associated with increased risk of hospitalization, intensive care unit admission, or death. Compared to patients with charted past medical history, there was a lower risk of hospitalization for patients on ACE-I (odds ratio (OR) 0.43; 95% confidence interval (CI) 0.19-0.97; P = 0.0426) and ARB (OR 0.39; 95% CI 0.17-0.90; P = 0.0270)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33038021",
"endSection": "abstract",
"offsetInBeginSection": 1092,
"offsetInEndSection": 1642,
"text": "The second analysis showed that the use of ACEI and/or ARB did not affect in-hospital mortality (risk ratio [RR] 95% [CI]] = 0.88 [0.64-1.20], p = 0.42). The subgroup analysis by limiting studies of patients with hypertension showed ACEI and/or ARB use was associated with a significant reduction of in-hospital mortality compared with no ACEI or ARB use (RR [CI] = 0.66 [0.49-0.89], p = 0.004). Our analysis demonstrated that ACEI and/or ARB use was associated neither with testing positive rates of COVID-19 nor with mortality of COVID-19 patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33085063",
"endSection": "abstract",
"offsetInBeginSection": 1349,
"offsetInEndSection": 1513,
"text": "ACEIs/ARBs are protective factors against mortality in COVID-19 patients with HTN, and these agents can be considered potential therapeutic options in this disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32242182",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "There has been a lot of speculation that patients with coronavirus disease 2019 (COVID-19) who are receiving angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) may be at increased risk for adverse outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32514935",
"endSection": "abstract",
"offsetInBeginSection": 880,
"offsetInEndSection": 1201,
"text": "Although further research on the influence of blood-pressure-lowering drugs, including those not targeting the renin-angiotensin system, is warranted, there are presently no compelling clinical data showing that ACEIs and ARBs increase the likelihood of contracting COVID-19 or worsen the outcome of SARS-CoV‑2 infections"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32242182",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "There has been a lot of speculation that patients with coronavirus disease 2019 (COVID-19) who are receiving angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) may be at increased risk for adverse outcomes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32965603",
"endSection": "abstract",
"offsetInBeginSection": 1537,
"offsetInEndSection": 1601,
"text": "ACEIs and ARBs do not promote a more severe outcome of COVID-19."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32757246",
"endSection": "abstract",
"offsetInBeginSection": 626,
"offsetInEndSection": 936,
"text": "Meta-analysis showed no significant increase in the risk of COVID-19 infection (odds ratio [OR]: 0.95, 95%CI: 0.89-1.05) in patients receiving ACEI/ARB therapy, and ACEI/ARB therapy was associated with a decreased risk of severe COVID-19 (OR: 0.75, 95%CI: 0.59-0.96) and mortality (OR: 0.52, 95%CI: 0.35-0.79)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32757246",
"endSection": "abstract",
"offsetInBeginSection": 937,
"offsetInEndSection": 1218,
"text": "Subgroup analyses showed among the general population, ACEI/ARB therapy was associated with reduced severe COVID-19 infection (OR: 0.79, 95%CI: 0.60-1.05) and all-cause mortality (OR: 0.31, 95%CI: 0.13-0.75), and COVID-19 infection (OR: 0.85, 95% CI: 0.66-1.08) were not increased."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32757246",
"endSection": "abstract",
"offsetInBeginSection": 1476,
"offsetInEndSection": 1658,
"text": "On the basis of the available evidence, ACEI/ARB therapy should be continued in patients who are at risk for, or have COVID-19, either in general population or hypertension patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32474043",
"endSection": "abstract",
"offsetInBeginSection": 26,
"offsetInEndSection": 271,
"text": "Some studies of hospitalized patients suggested that the risk of death and/or severe illness due to COVID-19 is not associated with the use of angiotensin-converting enzyme inhibitors (ACEIs) and/or angiotensin II receptor type 1 blockers (ARBs)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32320478",
"endSection": "abstract",
"offsetInBeginSection": 1180,
"offsetInEndSection": 1472,
"text": "Available evidence, in particular, data from human studies, does not support the hypothesis that ACEI/ARB use increases ACE2 expression and the risk of complications from COVID-19. We conclude that patients being treated with ACEIs and ARBs should continue their use for approved indications."
}
] | 11
|
BioASQ-training11b
| null | null |
6276d2d956bf9aee6f000002
|
bioasq_yesno
|
yesno
|
Do nematodes contain a CTCF gene?
|
['yes']
|
[
"yes"
] |
['Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes. We suggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans.', 'Insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans . The most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode yeast . Our findings show that C.TCF and possibly chromatin insulation are present in basal nemathews .', 'Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes.', 'We suggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes. The most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode.', 'Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes. We suggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. The most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"http://www.ncbi.nlm.nih.gov/pubmed/17442748",
"http://www.ncbi.nlm.nih.gov/pubmed/29385718"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 1157,
"offsetInEndSection": 1357,
"text": "Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes. We suggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17442748",
"endSection": "abstract",
"offsetInBeginSection": 884,
"offsetInEndSection": 983,
"text": "The most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 966,
"offsetInEndSection": 1147,
"text": " show that three ZF proteins from three basal nematodes cluster together with known CTCF proteins whereas no zinc finger protein of C. elegans and other derived nematodes does so.CO"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 505,
"offsetInEndSection": 659,
"text": "SULTS: While orthologs for other insulator proteins were absent in all 35 analysed nematode species, we find orthologs of CTCF in a subset of nematodes. A"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29385718",
"endSection": "abstract",
"offsetInBeginSection": 785,
"offsetInEndSection": 989,
"text": "of CTCF from several nematodes is paralleled by a loss of two of its interactors, the polycomb repressive complex subunit SuZ12 and the multifunctional transcription factor TYY1. In contrast to earlier st"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1254,
"text": "LUSION: Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes. We "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 1255,
"offsetInEndSection": 1361,
"text": "uggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. We "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 504,
"offsetInEndSection": 658,
"text": "ESULTS: While orthologs for other insulator proteins were absent in all 35 analysed nematode species, we find orthologs of CTCF in a subset of nematodes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 1253,
"offsetInEndSection": 1359,
"text": " suggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. W"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 965,
"offsetInEndSection": 1147,
"text": "e show that three ZF proteins from three basal nematodes cluster together with known CTCF proteins whereas no zinc finger protein of C. elegans and other derived nematodes does so.CO"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 810,
"offsetInEndSection": 964,
"text": "o investigate the pattern of CTCF occurrence in nematodes, we performed phylogenetic analysis with the ZF protein sets of completely sequenced nematodes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 1159,
"offsetInEndSection": 1252,
"text": "r findings show that CTCF and possibly chromatin insulation are present in basal nematodes. W"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 1360,
"offsetInEndSection": 1631,
"text": " propose a switch in the regulation of gene expression during nematode evolution, from the common vertebrate and insect type involving distantly acting regulatory elements and chromatin insulation to a so far poorly characterised mode present in more derived nematodes. H"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 400,
"offsetInEndSection": 504,
"text": "We therefore searched in nematodes for orthologs of proteins that are involved in chromatin insulation.R"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29385718",
"endSection": "abstract",
"offsetInBeginSection": 759,
"offsetInEndSection": 963,
"text": "The unique secondary loss of CTCF from several nematodes is paralleled by a loss of two of its interactors, the polycomb repressive complex subunit SuZ12 and the multifunctional transcription factor TYY1."
}
] | 11
|
BioASQ-training11b
| null | null |
5e9eba150d431b5f73000005
|
bioasq_yesno
|
yesno
|
Is alemtuzumab effective for remission induction in patients diagnosed with T-cell prolymphocytic leukemia?
|
['yes']
|
[
"yes"
] |
Yes, alemtuzumab (anti-CD52, Campath-1H) is effective for remission induction in patients diagnosed with T-cell prolymphocytic leukemia. Alemtuzumab can be administered in combination with other chemotherapeutic agents or as mono-therapy. Response rate to alemtuzumab is more than 90%. Alemtuzumab therapy is associated with improved survival of T-cell prolymphocytic leukemia patients.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"http://www.ncbi.nlm.nih.gov/pubmed/23233647",
"http://www.ncbi.nlm.nih.gov/pubmed/23211022",
"http://www.ncbi.nlm.nih.gov/pubmed/22517037",
"http://www.ncbi.nlm.nih.gov/pubmed/16720203",
"http://www.ncbi.nlm.nih.gov/pubmed/16645226",
"http://www.ncbi.nlm.nih.gov/pubmed/15869731",
"http://www.ncbi.nlm.nih.gov/pubmed/12950233",
"http://www.ncbi.nlm.nih.gov/pubmed/11986948",
"http://www.ncbi.nlm.nih.gov/pubmed/11535503",
"http://www.ncbi.nlm.nih.gov/pubmed/10561018",
"http://www.ncbi.nlm.nih.gov/pubmed/22649104",
"http://www.ncbi.nlm.nih.gov/pubmed/15757437",
"http://www.ncbi.nlm.nih.gov/pubmed/21948296",
"http://www.ncbi.nlm.nih.gov/pubmed/17118783",
"http://www.ncbi.nlm.nih.gov/pubmed/23645660",
"http://www.ncbi.nlm.nih.gov/pubmed/15453953"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Sequential chemoimmunotherapy of fludarabine, mitoxantrone, and cyclophosphamide induction followed by alemtuzumab consolidation is effective in T-cell prolymphocytic leukemia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 318,
"text": "A central need in this historically refractory tumor is the controlled evaluation of multiagent chemotherapy and its combination with the currently most active single agent, alemtuzumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"endSection": "abstract",
"offsetInBeginSection": 1489,
"offsetInEndSection": 1581,
"text": "FMC-A is a safe and efficient protocol in T-PLL, which compares favorably to published data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23233647",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 773,
"text": "Currently, the best treatment for T-PLL is IV alemtuzumab, which has resulted in very high response rates of more than 90% when given as frontline treatment and a significant improvement in survival. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23211022",
"endSection": "abstract",
"offsetInBeginSection": 735,
"offsetInEndSection": 906,
"text": "The patient failed to respond to standard ALL induction chemotherapy, but achieved complete remission following treatment with a fludarabine and alemtuzumab-based regimen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22517037",
"endSection": "abstract",
"offsetInBeginSection": 216,
"offsetInEndSection": 401,
"text": "Here we present a rare case of concurrent T-PLL and Kaposi sarcoma who achieved a complete hematologic and cytogenetic remission after a very short course of treatment with alemtuzumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16720203",
"endSection": "abstract",
"offsetInBeginSection": 1035,
"offsetInEndSection": 1243,
"text": " Recent studies with single-agent alemtuzumab, an anti-CD52 monoclonal antibody, have shown improved response rates and survival in patients with T-cell prolymphocytic leukemia and cutaneous T-cell lymphoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16645226",
"endSection": "abstract",
"offsetInBeginSection": 510,
"offsetInEndSection": 696,
"text": "The CD52 antigen is expressed at high density on the malignant T-cells and therapy with alemtuzumab, a humanized IgG1 antibody that targets this antigen, has produced promising results. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15869731",
"endSection": "abstract",
"offsetInBeginSection": 484,
"offsetInEndSection": 707,
"text": "With the introduction of alemtuzumab, most patients who progressed despite treatment with pentostatin had a major response with a complete remission rate higher than that obtained with pentostatin when used as a first line."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12950233",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 227,
"text": "Alemtuzumab (anti-CD52, Campath-1H) has recently been shown to be effective in the treatment of a range of hematological malignancies, including B-cell chronic lymphocytic leukemia and T-cell prolymphocytic leukemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11986948",
"endSection": "abstract",
"offsetInBeginSection": 179,
"offsetInEndSection": 384,
"text": "Here we report the outcome of two patients with CD4-positive T cell prolymphocytic leukemia treated with CAMPATH-1H. Both patients responded rapidly to treatment and subsequently developed CD4 lymphopenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11535503",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "T-cell prolymphocytic leukemia (T-PLL) is a chemotherapy-resistant malignancy with a median survival of 7.5 months. Preliminary results indicated a high remission induction rate with the human CD52 antibody, CAMPATH-1H. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11535503",
"endSection": "abstract",
"offsetInBeginSection": 472,
"offsetInEndSection": 738,
"text": "CAMPATH-1H (30 mg) was administered intravenously 3 times weekly until maximal response. The overall response rate was 76% with 60% CR and 16% partial remission (PR). These responses were durable with a median disease-free interval of 7 months (range, 4-45 months). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11535503",
"endSection": "abstract",
"offsetInBeginSection": 1444,
"offsetInEndSection": 1570,
"text": "The conclusion is that CAMPATH-1H is an effective therapy in T-PLL, producing remissions in more than two thirds of patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10561018",
"endSection": "abstract",
"offsetInBeginSection": 1097,
"offsetInEndSection": 1343,
"text": "For example, most patients with T-cell prolymphocytic leukemia, including those with large tumor burdens and high peripheral white blood cell counts, will enter complete remission using the antibody CAMPATH-1H without any evidence of tumor lysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"endSection": "abstract",
"offsetInBeginSection": 746,
"offsetInEndSection": 1006,
"text": "Overall response rate to FMC was 68%, comprising 6 complete remissions (all bone-marrow confirmed) and 11 partial remissions. Alemtuzumab consolidation increased the intent-to-treat overall response rate to 92% (12 complete remissions; 11 partial remissions). "
}
] | 5
|
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015461",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012074",
"http://www.biosemantics.org/jochem#4002029"
] |
[] |
530cefaaad0bf1360c000001
|
bioasq_yesno
|
yesno
|
Are Sidekick proteins members of the immunoglobulin superfamily?
|
['yes']
|
[
"yes"
] |
['Yes, sidekick are cell adhesion molecules of the immunoglobulin superfamily.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18216854",
"http://www.ncbi.nlm.nih.gov/pubmed/15703275"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18216854",
"endSection": "abstract",
"offsetInBeginSection": 523,
"offsetInEndSection": 708,
"text": "Here we show that four closely related immunoglobulin superfamily (IgSF) adhesion molecules--Dscam (Down's syndrome cell adhesion molecule), DscamL (refs 6-9), Sidekick-1 and Sidekick-2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15703275",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Sidekick-1, a cell adhesion molecule of the immunoglobulin superfamily, is up-regulated in glomerular podocytes in the collapsing glomerulopathy of HIV-associated nephropathy (HIVAN)."
}
] | 5
|
BioASQ-training5b
|
[] |
[] |
5709e947cf1c32585100001d
|
bioasq_yesno
|
yesno
|
Does silencing of SRRM4 promote microexon inclusion?
|
['no']
|
[
"no"
] |
['No, silencing of SRRM4 does not promote microexon inclusion.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33207694"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33207694",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "SRRM4 Expands the Repertoire of Circular RNAs by Regulating Microexon Inclusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33207694",
"endSection": "abstract",
"offsetInBeginSection": 1272,
"offsetInEndSection": 1572,
"text": "Overexpressing SRRM4, known for regulating ME inclusion in mRNAs critical for neural differentiation, in human HEK293 cells resulted in the biogenesis of over 2000 novel ME-circRNAs, including ME-circEIF4G3, and changes in the abundance of many canonical circRNAs, including circSETDB2 and circLBRA. "
}
] | 12
|
BioASQ-training12b
| null | null |
63f9cdb033942b094c000012
|
bioasq_yesno
|
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