Dataset Viewer
type
stringclasses 1
value | question
stringlengths 20
192
| answer
stringclasses 6
values | golden_answers
sequencelengths 1
1
| ideal_answer
stringlengths 3
20.8k
| documents
sequencelengths 1
96
| snippets
listlengths 0
126
| asq_challenge
int64 3
13
| folder_name
stringclasses 7
values | concepts
sequencelengths 0
97
⌀ | triples
listlengths 0
3.75k
⌀ | id
stringlengths 24
24
| __index_level_0__
int64 0
1.46k
|
|---|---|---|---|---|---|---|---|---|---|---|---|---|
yesno | Should Lubeluzole be used for treatment of ischemic stroke? | ['no'] | [
"no"
]
| ['No. Lubeluzole failed to consistently show an efficacy in the treatment of acute stroke and should not be used.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29550817",
"http://www.ncbi.nlm.nih.gov/pubmed/28939972",
"http://www.ncbi.nlm.nih.gov/pubmed/8553408",
"http://www.ncbi.nlm.nih.gov/pubmed/11869612",
"http://www.ncbi.nlm.nih.gov/pubmed/11062273",
"http://www.ncbi.nlm.nih.gov/pubmed/12038658",
"http://www.ncbi.nlm.nih.gov/pubmed/9412611",
"http://www.ncbi.nlm.nih.gov/pubmed/9619701"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28939972",
"endSection": "abstract",
"offsetInBeginSection": 729,
"offsetInEndSection": 870,
"text": "Lubeluzole showed promising neuroprotective effects in animal stroke models, but failed to show benefits in acute ischemic stroke in humans. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29550817",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 311,
"text": "However, clinical research on lubeluzole is now at a standstill, since lubeluzole seems to be associated with the acquired long QT syndrome and ventricular arrhythmias. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12038658",
"endSection": "abstract",
"offsetInBeginSection": 302,
"offsetInEndSection": 696,
"text": "Ten classes of neuroprotective agents have reached phase III efficacy trials but have shown mixed results. They included calcium channel antagonists, NMDA receptor antagonists, lubeluzole, CDP-choline, the free radical scavenger tirilazad and ebselen, enlimomab, GABA agonist clomethiazole, the sodium channel antagonist fosphenytoin, magnesium, glycine site antagonist GV150526 and piracetam. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11062273",
"endSection": "abstract",
"offsetInBeginSection": 2385,
"offsetInEndSection": 2484,
"text": "CONCLUSIONS: This study failed to show an efficacy of lubeluzole in the treatment of acute stroke. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11062273",
"endSection": "abstract",
"offsetInBeginSection": 1816,
"offsetInEndSection": 2125,
"text": "Overall, of all treated patients, 401 (22.5%) died: 203 (22.5%) in the lubeluzole group and 198 (22.4%) with placebo. Of all subjects treated, 853 (95%) on lubeluzole and 826 (93%) on placebo reported an adverse event during their treatment period or within the next 2 days after discontinuation of treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9412611",
"endSection": "abstract",
"offsetInBeginSection": 1760,
"offsetInEndSection": 1976,
"text": "CONCLUSIONS: Treatment with lubeluzole within 6 hours of the onset of ischemic stroke had a nonsignificant effect on mortality and resulted in improved clinical outcome compared with placebo, with no safety concerns."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9412611",
"endSection": "abstract",
"offsetInBeginSection": 1088,
"offsetInEndSection": 1700,
"text": "RESULTS: The overall mortality rate at 12 weeks for lubeluzole-treated patients was 20.7% compared to 25.2% for placebo-treated patients (NS). Controlling for relevant covariates, the degree of neurological recovery (NIHSS) at week 12 significantly favored lubeluzole over placebo (P = .033). Lubeluzole treatment similarly resulted in significantly greater improvements in functional status (Barthel Index) (P = .038) and overall disability (Rankin Scale) (P = .034) after 12 weeks. A global test statistic confirmed that lubeluzole-treated patients had a more favorable clinical outcome at 12 weeks (P = .041)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8553408",
"endSection": "abstract",
"offsetInBeginSection": 1922,
"offsetInEndSection": 2121,
"text": "CONCLUSIONS: In patients with acute ischemic stroke, the dosage regimen of 7.5 mg over 1 hour followed by 10 mg/d of intravenous lubeluzole is safe and statistically significantly reduced mortality. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9412611",
"endSection": "abstract",
"offsetInBeginSection": 1766,
"offsetInEndSection": 1982,
"text": "CONCLUSIONS\n\nTreatment with lubeluzole within 6 hours of the onset of ischemic stroke had a nonsignificant effect on mortality and resulted in improved clinical outcome compared with placebo, with no safety concerns."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11869612",
"endSection": "abstract",
"offsetInBeginSection": 2301,
"offsetInEndSection": 2594,
"text": "CONCLUSIONS: Lubeluzole, given in the acute phase of ischaemic stroke, is not associated with a significant reduction of death or dependency at the end of scheduled follow-up period but seems to be associated with a significant increase of heart-conduction disorders (Q-T prolonged >450 msec)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9412611",
"endSection": "abstract",
"offsetInBeginSection": 1721,
"offsetInEndSection": 1924,
"text": "Treatment with lubeluzole within 6 hours of the onset of ischemic stroke had a nonsignificant effect on mortality and resulted in improved clinical outcome compared with placebo, with no safety concerns."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9619701",
"endSection": "abstract",
"offsetInBeginSection": 1963,
"offsetInEndSection": 2123,
"text": "In the overall study population, treatment with intravenous lubeluzole within 6 h of the onset of ischaemic stroke did not affect mortality or clinical outcome."
}
]
| 11 | BioASQ-training11b | null | null | 5e44caaf48dab47f26000024 | 0 |
yesno | Are integrins part of the extracellular matrix? | ['yes'] | [
"yes"
]
| ['Yes, \tintegrins are a central family of extracellular matrix receptors.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26029690",
"http://www.ncbi.nlm.nih.gov/pubmed/26067407",
"http://www.ncbi.nlm.nih.gov/pubmed/26096733",
"http://www.ncbi.nlm.nih.gov/pubmed/26089687",
"http://www.ncbi.nlm.nih.gov/pubmed/25605337",
"http://www.ncbi.nlm.nih.gov/pubmed/25759527",
"http://www.ncbi.nlm.nih.gov/pubmed/25460334",
"http://www.ncbi.nlm.nih.gov/pubmed/24965068",
"http://www.ncbi.nlm.nih.gov/pubmed/25220424",
"http://www.ncbi.nlm.nih.gov/pubmed/25631868",
"http://www.ncbi.nlm.nih.gov/pubmed/25886986"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26029690",
"endSection": "abstract",
"offsetInBeginSection": 314,
"offsetInEndSection": 451,
"text": "Several constituents of the ECM provide adhesive cues, which serve as binding sites for cell trans-membrane receptors, such as integrins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26067407",
"endSection": "abstract",
"offsetInBeginSection": 1026,
"offsetInEndSection": 1129,
"text": "We also determined that blocking β1integrins, the major class of receptors for all ECM proteins tested,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26096733",
"endSection": "abstract",
"offsetInBeginSection": 135,
"offsetInEndSection": 298,
"text": "Here, we elucidate a cross-scale mechanism for tissue assembly and ECM remodeling involving Cadherin 2, the ECM protein Fibronectin, and its receptor Integrin α5. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089687",
"endSection": "abstract",
"offsetInBeginSection": 410,
"offsetInEndSection": 604,
"text": "due to the diverse functions and variable expression of proteoglycans, matrix proteins, and integrins, it is rather difficult to identify a comprehensive therapeutic target among ECM components."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25605337",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Integrin-dependent cell-extracellular matrix (ECM) adhesion is a determinant of spindle orientation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25759527",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "The extracellular matrix component periostin is a secreted protein that functions as both a cell attachment protein and an autocrine or paracrine factor that signals through the cell adhesion molecule integrins αvβ3 and αvβ5. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25460334",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "Integrin receptors connect the extracellular matrix to the cell cytoskeleton to provide essential forces and signals. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24965068",
"endSection": "abstract",
"offsetInBeginSection": 690,
"offsetInEndSection": 839,
"text": " the integrin, talin, and actin filament form a linear complex of which both ends are typically anchored to the extracellular matrices via integrins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25886986",
"endSection": "abstract",
"offsetInBeginSection": 179,
"offsetInEndSection": 338,
"text": "Integrins, a central family of cellular ECM receptors, have been implicated in these processes but their specific role in ES cell self-renewal remains unclear."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25631868",
"endSection": "abstract",
"offsetInBeginSection": 259,
"offsetInEndSection": 446,
"text": "Attachment to the extracellular matrix is mediated by a complex of adhesion proteins, including integrins, signaling molecules, actin and actin-binding proteins, and scaffolding proteins."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25220424",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Beta 1 integrin binding plays a role in the constant traction force generation in response to varying stiffness for cells grown on mature cardiac extracellular matrix."
}
]
| 5 | BioASQ-training5b | []
| []
| 56e83a2342442bac75000001 | 1 |
yesno | Is Baloxavir effective for influenza? | ['yes'] | [
"yes"
]
| ['Yes. Baloxavir is approved for influenza A or B virus infections.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30395523",
"http://www.ncbi.nlm.nih.gov/pubmed/30316915",
"http://www.ncbi.nlm.nih.gov/pubmed/29623652",
"http://www.ncbi.nlm.nih.gov/pubmed/30184455",
"http://www.ncbi.nlm.nih.gov/pubmed/30476172",
"http://www.ncbi.nlm.nih.gov/pubmed/30396860",
"http://www.ncbi.nlm.nih.gov/pubmed/30203386",
"http://www.ncbi.nlm.nih.gov/pubmed/29941893"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29623652",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 358,
"text": "Baloxavir marboxil (Xofluza™; baloxavir) is an oral cap-dependent endonuclease inhibitor that has been developed by Roche and Shionogi. The drug blocks influenza virus proliferation by inhibiting the initiation of mRNA synthesis. In February 2018, baloxavir received its first global approval in Japan for the treatment of influenza A or B virus infections. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29623652",
"endSection": "abstract",
"offsetInBeginSection": 448,
"offsetInEndSection": 595,
"text": "This article summarized the milestones in the development of baloxavir leading to this first global approval for influenza A or B virus infections."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29941893",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "Baloxavir acid (BXA), derived from the prodrug baloxavir marboxil (BXM), potently and selectively inhibits the cap-dependent endonuclease within the polymerase PA subunit of influenza A and B viruses."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29941893",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Characterization of influenza virus variants induced by treatment with the endonuclease inhibitor baloxavir marboxil."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30184455",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Baloxavir Marboxil for Uncomplicated Influenza in Adults and Adolescents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30184455",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 248,
"text": "BACKGROUND: Baloxavir marboxil is a selective inhibitor of influenza cap-dependent endonuclease. It has shown therapeutic activity in preclinical models of influenza A and B virus infections, including strains resistant to current antiviral agents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30184455",
"endSection": "abstract",
"offsetInBeginSection": 1917,
"offsetInEndSection": 2209,
"text": "CONCLUSIONS: Single-dose baloxavir was without evident safety concerns, was superior to placebo in alleviating influenza symptoms, and was superior to both oseltamivir and placebo in reducing the viral load 1 day after initiation of the trial regimen in patients with uncomplicated influenza."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30396860",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 469,
"text": "A single oral dose of baloxavir is usually well tolerated; it hastens alleviation of influenza symptoms and shortens the duration of viral shedding."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30396860",
"endSection": "abstract",
"offsetInBeginSection": 69,
"offsetInEndSection": 156,
"text": "Japan was the first country to approve baloxavir marboxil as a treatment for influenza."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29623652",
"endSection": "abstract",
"offsetInBeginSection": 448,
"offsetInEndSection": 599,
"text": "This article summarized the milestones in the development of baloxavir leading to this first global approval for influenza A or B virus infections.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29623652",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 357,
"text": "In February 2018, baloxavir received its first global approval in Japan for the treatment of influenza A or B virus infections."
}
]
| 11 | BioASQ-training11b | null | null | 5c58a74e86df2b917400000d | 2 |
yesno | Are there any digital biomarkers for Duchenne Muscular Dystrophy? | ['yes'] | [
"yes"
]
| ['Yes, the KineDMD ethomic biomarker is a digital biomarker for Duchenne Muscular Dystrophy.', 'Yes, wearable full-body motion tracking of activities of daily living is a digital biomarker for Duchenne Muscular Dystrophy that can predict disease trajectory', "Yes, there is a digital biomarker for Duchenne Muscular Dystrophy. It's called the KineDMD ethomic biomarker, which is derived from daily-life behavioral data.", 'Yes, a digital biomarker called the KineDMD ethomic biomarker has been developed for Duchenne Muscular Dystrophy. It is derived from daily-life behavioral data and can predict disease progression.', 'Yes, the KineDMD ethomic biomarker is a digital biomarker for Duchenne Muscular Dystrophy. It is derived from daily-life movement behavior and can predict disease progression in patients with muscular dystrophy and can potentially track the response to therapy', 'Yes, digital biomarkers have been developed for Duchenne Muscular Dystrophy.', 'Yes. Bayesian optimization, machine learning algorithms and movement behavioral fingerprints are used as digital biomarkers for Duchenne Muscular Dystrophy.', 'Yes, there are digital biomarkers for Duchenne Muscular Dystrophy.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36658421"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36658421",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Wearable full-body motion tracking of activities of daily living predicts disease trajectory in Duchenne muscular dystrophy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36658421",
"endSection": "abstract",
"offsetInBeginSection": 950,
"offsetInEndSection": 1145,
"text": "we constructed a behavioral biomarker, termed the KineDMD ethomic biomarker, which is derived from daily-life behavioral data and whose value progresses with age in an S-shaped sigmoid curve form"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36658421",
"endSection": "abstract",
"offsetInBeginSection": 1147,
"offsetInEndSection": 1367,
"text": "The biomarker developed in this study, derived from digital readouts of daily-life movement behavior, can predict disease progression in patients with muscular dystrophy and can potentially track the response to therapy."
}
]
| 13 | BioASQ-training13b | null | null | 66302174187cba990d00002e | 3 |
yesno | Are sleep apnea and snoring associated with cardiac arrhythmias? | ['yes'] | [
"yes"
]
| ['Evidence supports a causal association of sleep apnea with the incidence and morbidity of hypertension, coronary heart disease, arrhythmia, heart failure, and stroke.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28209226",
"http://www.ncbi.nlm.nih.gov/pubmed/16293956",
"http://www.ncbi.nlm.nih.gov/pubmed/28992834",
"http://www.ncbi.nlm.nih.gov/pubmed/3542725",
"http://www.ncbi.nlm.nih.gov/pubmed/20351955",
"http://www.ncbi.nlm.nih.gov/pubmed/331948",
"http://www.ncbi.nlm.nih.gov/pubmed/7774322",
"http://www.ncbi.nlm.nih.gov/pubmed/28040290",
"http://www.ncbi.nlm.nih.gov/pubmed/22160956",
"http://www.ncbi.nlm.nih.gov/pubmed/10613491",
"http://www.ncbi.nlm.nih.gov/pubmed/22520295",
"http://www.ncbi.nlm.nih.gov/pubmed/25252161",
"http://www.ncbi.nlm.nih.gov/pubmed/17655678",
"http://www.ncbi.nlm.nih.gov/pubmed/27914359",
"http://www.ncbi.nlm.nih.gov/pubmed/28181212",
"http://www.ncbi.nlm.nih.gov/pubmed/22826063",
"http://www.ncbi.nlm.nih.gov/pubmed/18024169",
"http://www.ncbi.nlm.nih.gov/pubmed/8178007",
"http://www.ncbi.nlm.nih.gov/pubmed/16149210",
"http://www.ncbi.nlm.nih.gov/pubmed/3106890",
"http://www.ncbi.nlm.nih.gov/pubmed/2654251"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28040290",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 244,
"text": "Atrial fibrillation (AF) is the commonest arrhythmia in clinical practice and is associated with increased cardiovascular morbidity and mortality. Obstructive sleep apnea (OSA), a common breathing disorder, is an independent risk factor for AF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27914359",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 280,
"text": "There is a growing consensus in the scientific community that suggests a strong association between obstructive sleep apnea (OSA) and cardiovascular (CVD) conditions and events, including coronary artery disease, hypertension, arrhythmia, heart failure, and sudden cardiac death. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28181212",
"endSection": "abstract",
"offsetInBeginSection": 127,
"offsetInEndSection": 386,
"text": "part from well-established risk factors that increase the odds for the development of AF, e.g. age or arterial hypertension, recent analyses indicate that obstructive sleep apnoea (OSA) may independently, negatively modify the arrhythmia occur-rence profile. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28209226",
"endSection": "abstract",
"offsetInBeginSection": 323,
"offsetInEndSection": 489,
"text": "Evidence supports a causal association of sleep apnea with the incidence and morbidity of hypertension, coronary heart disease, arrhythmia, heart failure, and stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3106890",
"endSection": "abstract",
"offsetInBeginSection": 263,
"offsetInEndSection": 390,
"text": "Severe snoring may be associated with pulmonary and systemic hypertension, secondary polycythemia, and cardiac arrhythmias.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3106890",
"endSection": "abstract",
"offsetInBeginSection": 263,
"offsetInEndSection": 386,
"text": "Severe snoring may be associated with pulmonary and systemic hypertension, secondary polycythemia, and cardiac arrhythmias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18024169",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "BACKGROUND AND PURPOSE Nocturnal cardiac arrhythmias occur in patients with obstructive sleep apnea (OSA), reportedly as a consequence of the autonomic effects of recurrent apnea with subsequent oxygen desaturation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16149210",
"endSection": "abstract",
"offsetInBeginSection": 2295,
"offsetInEndSection": 2500,
"text": "Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16293956",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 725,
"text": "Obstructive sleep apnea (OSA) is the most common form of sleep-disordered breathing, affecting 5-15% of the population. It is characterized by intermittent episodes of partial or complete obstruction of the upper airway during sleep that disrupts normal ventilation and sleep architecture, and is typically associated with excessive daytime sleepiness, snoring, and witnessed apneas. Patients with obstructive sleep apnea present risk to the general public safety by causing 8-fold increase in vehicle accidents, and they may themselves also suffer from the physiologic consequences of OSA; these include hypertension, coronary artery disease, stroke, congestive heart failure, pulmonary hypertension, and cardiac arrhythmias"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22160956",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Obstructive sleep apnea and central sleep apnea with Cheyne-Stokes respiration are associated with an increased risk of cardiac arrhythmia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17655678",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "Obstructive sleep apnea (OSA) affects approximately 4% of middle-aged men and 2% of middle-aged women. Cardiac arrhythmias are common problems in patients with OSA, even though the true prevalence and clinical relevance of cardiac arrhythmias remains to be determined. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/331948",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 284,
"text": "Cardiac arrhythmias during wakefulness and sleep in 15 patients with sleep-induced obstructive apnea, and the effect of atropine and tracheostomy on these arrhythmias were studied by continuous overnight Holter electrocardiographic, respiratory and electroencephalographic recordings."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20351955",
"endSection": "abstract",
"offsetInBeginSection": 49,
"offsetInEndSection": 410,
"text": "obstructive sleep apnea (OSA) as its most extreme variant, is characterized by intermittent episodes of partial or complete obstruction of the upper airway, leading to cessation of breathing while asleep. Cardiac arrhythmias are common problems in OSA patients, although the true prevalence and clinical relevance of cardiac arrhythmias remains to be determined"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25252161",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 183,
"text": "The mechanisms associated with the cardiovascular consequences of obstructive sleep apnea include abrupt changes in autonomic tone, which can trigger cardiac arrhythmias. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22520295",
"endSection": "abstract",
"offsetInBeginSection": 161,
"offsetInEndSection": 281,
"text": " Recent studies have shown that cardiac arrhythmias and conduction disorders are common in patients with SA. Sleep apnea"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22826063",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Severity of nocturnal cardiac arrhythmias correlates with intensity of sleep apnea in men"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2654251",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 380,
"text": "Patients affected with OSA are frequently hypertensive and can have dangerous cardiac arrhythmias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8178007",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Patients with stable cardiac failure who snore may present sleep hypopnea and cardiac arrhythmias. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28992834",
"endSection": "abstract",
"offsetInBeginSection": 17,
"offsetInEndSection": 170,
"text": " Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality. Cardiac arrhythmias are common in patients with OSA. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3542725",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 386,
"text": "Nocturnal hypoxia has been associated with serious ventricular tachyarrhythmias as well as life-threatening bradyarrhythmias. Obesity and snoring, both of which increase with age, have been identified as risk factors for sleep-related breathing disorders, as have hypertension and heart disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10613491",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 381,
"text": "Obstructive sleep apnea syndrome is associated with excess daytime sleepiness, depression, and an increased incidence of ischemic cardiopathy, cardiac arrhythmias, systemic hypertension and brain infarction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7774322",
"endSection": "abstract",
"offsetInBeginSection": 486,
"offsetInEndSection": 654,
"text": "We found 58 percent prevalence of arrhythmias in patients with sleep apnea (apnea/hypopnea index = AHI>10), vs 42 percent in nonapneic controls (chi 2 = 16.7, p<0.0001)"
}
]
| 11 | BioASQ-training11b | [
"http://www.disease-ontology.org/api/metadata/DOID:0050847",
"https://meshb.nlm.nih.gov/record/ui?ui=D012891",
"http://www.disease-ontology.org/api/metadata/DOID:9220",
"https://meshb.nlm.nih.gov/record/ui?ui=D012913",
"http://www.disease-ontology.org/api/metadata/DOID:0050848",
"https://meshb.nlm.nih.gov/record/ui?ui=D020181",
"https://meshb.nlm.nih.gov/record/ui?ui=D020182",
"https://meshb.nlm.nih.gov/record/ui?ui=D001049"
]
| null | 5a981dd0fcd1d6a10c00002e | 5 |
yesno | Is Vitamin D deficiency associated with sepsis mortality? | ['yes'] | [
"yes"
]
| ['Yes, Vitamin D deficiency is associated with increased mortality in patients with septic shock.', 'Yes, vitamin D deficiency is associated with mortality in sepsis patients.', 'Yes, vitamin D deficiency is associated with sepsis mortality in patients with severe vitamin D deficiency.', 'Yes, Vitamin D deficiency is prevalent in patients with septic shock and is associated with mortality.', 'Yes, there are studies that show that Vitamin D deficiency is associated with higher mortality in sepsis.', 'Yes, vitamin D deficiency was prevalent in patients with septic shock visiting the emergency department and was associated with mortality.', 'Yes, Vitamin D deficiency has been associated with higher mortality in sepsis patients', 'Yes, Vitamin D deficiency was associated with mortality in patients with septic shock visiting the ED', 'Yes, Vitamin D deficiency is prevalent in patients with septic shock and it has been associated with increased mortality', 'Yes, Vitamin D deficiency is associated with sepsis mortality', 'Yes, Vitamin D deficiency is associated with mortality in patients with septic shock visiting the ED.', 'Yes, Vitamin D deficiency was prevalent in patients with septic shock visiting the ED and was associated with mortality.', 'Yes, vitamin D deficiency is associated with increased mortality in patients with septic shock who visit the emergency department (ED).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36265656"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36265656",
"endSection": "abstract",
"offsetInBeginSection": 1504,
"offsetInEndSection": 1619,
"text": "Vitamin D deficiency was prevalent in patients with septic shock visiting the ED and was associated with mortality."
}
]
| 13 | BioASQ-training13b | null | null | 662f401b187cba990d00000e | 6 |
yesno | Is vemurafenib used for thyroid cancer? | ['yes'] | [
"yes"
]
| ['Yes. Vemurafenib, a selective BRAF inhibitor, appears to have promising clinical activity in patients with papillary thyroid cancer (PTC) harboring the BRAF(V600E) mutation.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27460442",
"http://www.ncbi.nlm.nih.gov/pubmed/27554612",
"http://www.ncbi.nlm.nih.gov/pubmed/27754804",
"http://www.ncbi.nlm.nih.gov/pubmed/24987354",
"http://www.ncbi.nlm.nih.gov/pubmed/23489023",
"http://www.ncbi.nlm.nih.gov/pubmed/26751190",
"http://www.ncbi.nlm.nih.gov/pubmed/27127178",
"http://www.ncbi.nlm.nih.gov/pubmed/26735176",
"http://www.ncbi.nlm.nih.gov/pubmed/25353071",
"http://www.ncbi.nlm.nih.gov/pubmed/25467940",
"http://www.ncbi.nlm.nih.gov/pubmed/26284586",
"http://www.ncbi.nlm.nih.gov/pubmed/22649416",
"http://www.ncbi.nlm.nih.gov/pubmed/26176686",
"http://www.ncbi.nlm.nih.gov/pubmed/26636651",
"http://www.ncbi.nlm.nih.gov/pubmed/24262022",
"http://www.ncbi.nlm.nih.gov/pubmed/27432558",
"http://www.ncbi.nlm.nih.gov/pubmed/24756795"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27460442",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Vemurafenib in patients with BRAF(V600E)-positive metastatic or unresectable papillary thyroid cancer refractory to radioactive iodine: a non-randomised, multicentre, open-label, phase 2 trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27460442",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 314,
"text": "Vemurafenib, an oncogenic BRAF kinase inhibitor approved for BRAF-positive melanoma, showed clinical benefit in three patients with BRAF(V600E)-positive papillary thyroid cancer in a phase 1 trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27460442",
"endSection": "abstract",
"offsetInBeginSection": 2338,
"offsetInEndSection": 2559,
"text": "INTERPRETATION: Vemurafenib showed antitumour activity in patients with progressive, BRAF(V600E)-positive papillary thyroid cancer refractory to radioactive iodine who had never been treated with a multikinase inhibitor. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25353071",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "CONTEXT: Vemurafenib, a selective BRAF inhibitor, appears to have promising clinical activity in patients with papillary thyroid cancer (PTC) harboring the BRAF(V600E) mutation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25353071",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Efficacy and tolerability of vemurafenib in patients with BRAF(V600E) -positive papillary thyroid cancer: M.D. Anderson Cancer Center off label experience."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25353071",
"endSection": "abstract",
"offsetInBeginSection": 1685,
"offsetInEndSection": 1840,
"text": "CONCLUSIONS: Vemurafenib is a potentially effective and well-tolerated treatment strategy in patients with advanced PTC harboring the BRAF(V600E) mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25467940",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 459,
"text": "The US Food and Drug Administration-approved BRAF inhibitors, vemurafenib and dabrafenib, have demonstrated superior efficacy in patients with BRAF-mutant melanomas but have limited efficacy in BRAF-mutant colorectal cancer. Little is known at this time regarding BRAF inhibitors in thyroid cancer. Initial reports in patients with progressive, radioactive iodine-refractory BRAF-mutant papillary thyroid cancer suggest response rates of approximately 30-40%."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26176686",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "Use of vemurafenib in anaplastic thyroid carcinoma: a case report."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27432558",
"endSection": "abstract",
"offsetInBeginSection": 1212,
"offsetInEndSection": 1361,
"text": "Finally, we found that propranolol can amplify the cytotoxicity of vemurafenib and sensitize thyroid cancer cells to cytotoxic effect of vemurafenib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25353071",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 399,
"text": "CONTEXT: Vemurafenib, a selective BRAF inhibitor, appears to have promising clinical activity in patients with papillary thyroid cancer (PTC) harboring the BRAF(V600E) mutation.OBJECTIVE: To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.DESIGN: A retrospective review at MD Anderson Cancer Center.METHODS: The best responses were evaluated using RECIST v1.1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25353071",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 361,
"text": "Vemurafenib, a selective BRAF inhibitor, appears to have promising clinical activity in patients with papillary thyroid cancer (PTC) harboring the BRAF(V600E) mutation.To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.A retrospective review at MD Anderson Cancer Center.The best responses were evaluated using RECIST v1.1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25353071",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 400,
"text": "CONTEXT: Vemurafenib, a selective BRAF inhibitor, appears to have promising clinical activity in patients with papillary thyroid cancer (PTC) harboring the BRAF(V600E) mutation.OBJECTIVE: To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.DESIGN: A retrospective review at MD Anderson Cancer Center.METHODS: The best responses were evaluated using RECIST v1.1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27432558",
"endSection": "abstract",
"offsetInBeginSection": 1220,
"offsetInEndSection": 1369,
"text": "Finally, we found that propranolol can amplify the cytotoxicity of vemurafenib and sensitize thyroid cancer cells to cytotoxic effect of vemurafenib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26284586",
"endSection": "abstract",
"offsetInBeginSection": 1237,
"offsetInEndSection": 1415,
"text": "Metformin or rapamycin adjuvant treatment may provide clinical benefits with minimal side effects to BRAFV600E-positive advanced thyroid cancer patients treated with vemurafenib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25353071",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 362,
"text": "Vemurafenib, a selective BRAF inhibitor, appears to have promising clinical activity in patients with papillary thyroid cancer (PTC) harboring the BRAF(V600E) mutation.To determine the efficacy and safety of vemurafenib when used outside of a clinical trial.A retrospective review at MD Anderson Cancer Center.The best responses were evaluated using RECIST v1.1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27754804",
"endSection": "abstract",
"offsetInBeginSection": 1515,
"offsetInEndSection": 1727,
"text": "Our data demonstrate that vemurafenib induces ER stress response-mediated autophagy in thyroid cancer and autophagy inhibition may be a beneficial strategy to sensitize BRAF-mutant thyroid cancer to vemurafenib.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26284586",
"endSection": "abstract",
"offsetInBeginSection": 552,
"offsetInEndSection": 729,
"text": "Combination of vemurafenib and metformin decreased cell viability and increased apoptosis in both BCPAP papillary thyroid cancer cells and 8505c anaplastic thyroid cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27754804",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Targeting autophagy sensitizes BRAF-mutant thyroid cancer to vemurafenib."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27432558",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Propranolol sensitizes thyroid cancer cells to cytotoxic effect of vemurafenib."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26284586",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "mTOR inhibitors sensitize thyroid cancer cells to cytotoxic effect of vemurafenib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27754804",
"endSection": "abstract",
"offsetInBeginSection": 1010,
"offsetInEndSection": 1092,
"text": "Vemurafenib induced a high level of autophagy in BRAF-mutant thyroid cancer cells."
}
]
| 6 | BioASQ-training6b | [
"http://www.disease-ontology.org/api/metadata/DOID:3963",
"http://www.disease-ontology.org/api/metadata/DOID:1781",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013964"
]
| [
{
"o": "VEMURAFENIB",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/rxnorm/id/1147220"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A20020623",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C3192263"
},
{
"o": "VEMURAFENIB",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A20020623"
},
{
"o": "http://linkedlifedata.com/resource/rxnorm/label/4224011",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/rxnorm/id/1147220"
},
{
"o": "VEMURAFENIB",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/rxnorm/label/4224011"
},
{
"o": "Vemurafenib",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/chembl/synonym/691867_Vemurafenib_USAN"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A19613644",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C3192263"
},
{
"o": "Vemurafenib",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A19613644"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A19649207",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C3192263"
},
{
"o": "Vemurafenib",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A19649207"
}
]
| 58848ea5e56acf517600000e | 7 |
yesno | Has the proteome of mice hippocampus been analysed? | ['yes'] | [
"yes"
]
| ['Yes, numerous proteomic studies of mice hippcampi has been performed.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26549202",
"http://www.ncbi.nlm.nih.gov/pubmed/28775826",
"http://www.ncbi.nlm.nih.gov/pubmed/26977433",
"http://www.ncbi.nlm.nih.gov/pubmed/27378549",
"http://www.ncbi.nlm.nih.gov/pubmed/27001617"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26549202",
"endSection": "abstract",
"offsetInBeginSection": 738,
"offsetInEndSection": 972,
"text": "We employed a discovery-based proteomic approach in subcellular fractions of hippocampal tissue from chronic intermittent alcohol (CIE)-exposed C57Bl/6J mice to gain insight into alcohol-induced changes in GluN2B signaling complexes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27001617",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 359,
"text": " We employed shotgun liquid chromatography-mass spectrometry (LC-MS) proteomic and metabonomic profiling approaches on prefrontal cortex (PFC) and hippocampal (HPC) tissue from Df(16)A+/-mice, a model of the 22q11.2 deletion syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28775826",
"endSection": "abstract",
"offsetInBeginSection": 743,
"offsetInEndSection": 1033,
"text": " Molecular alterations in the frontal cortex and hippocampus ofTsc1+/-and control mice, with or without rapamycin treatment, were investigated. A quantitative mass spectrometry-based shotgun proteomic approach (LC-MSE) was employed as an unbiased method to detect changes in protein levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26977433",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "This dataset reports on the analysis of mouse hippocampus by LC-MS/MS, from mice fed a diet that was either deficient in n-3 FA (n-3 Def) or sufficient in n-3 FA (n-3 Adq). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27378549",
"endSection": "abstract",
"offsetInBeginSection": 325,
"offsetInEndSection": 567,
"text": "Using isobaric tags for relative and absolute quantitation (iTRAQ) and proteomic methods, here we identified learning-induced changes in the hippocampal proteome of non-transgenic (NonTg) and 3 × Tg-AD mice, a widely used animal model of AD. "
}
]
| 11 | BioASQ-training11b | null | null | 5a8881118cb19eca6b000006 | 8 |
yesno | Is cytisine superior to nicotine replacement therapy for smoking cessation? | ['yes'] | [
"yes"
]
| ['Yes, one clinical trial that directly compared smoking cessation rates with cytisine versus nicotine replacement therapy reported that cytisine was superior to nicotine-replacement therapy in helping smokers quit smoking, but it was associated with a higher frequency of self-reported adverse events.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21328282",
"http://www.ncbi.nlm.nih.gov/pubmed/21385905",
"http://www.ncbi.nlm.nih.gov/pubmed/22104038",
"http://www.ncbi.nlm.nih.gov/pubmed/22513936",
"http://www.ncbi.nlm.nih.gov/pubmed/25517706",
"http://www.ncbi.nlm.nih.gov/pubmed/24831822",
"http://www.ncbi.nlm.nih.gov/pubmed/24574554",
"http://www.ncbi.nlm.nih.gov/pubmed/23978314",
"http://www.ncbi.nlm.nih.gov/pubmed/23834141",
"http://www.ncbi.nlm.nih.gov/pubmed/23728690",
"http://www.ncbi.nlm.nih.gov/pubmed/23404838",
"http://www.ncbi.nlm.nih.gov/pubmed/21154363",
"http://www.ncbi.nlm.nih.gov/pubmed/20040957",
"http://www.ncbi.nlm.nih.gov/pubmed/18646137",
"http://www.ncbi.nlm.nih.gov/pubmed/18076335",
"http://www.ncbi.nlm.nih.gov/pubmed/17825502",
"http://www.ncbi.nlm.nih.gov/pubmed/17253581",
"http://www.ncbi.nlm.nih.gov/pubmed/17220536",
"http://www.ncbi.nlm.nih.gov/pubmed/17130378"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25517706",
"endSection": "abstract",
"offsetInBeginSection": 1245,
"offsetInEndSection": 1541,
"text": "The effectiveness of cytisine for continuous abstinence was superior to that of nicotine-replacement therapy at 1 week, 2 months, and 6 months. In a prespecified subgroup analysis of the primary outcome, cytisine was superior to nicotine-replacement therapy among women and noninferior among men."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25517706",
"endSection": "abstract",
"offsetInBeginSection": 1833,
"offsetInEndSection": 2068,
"text": "CONCLUSIONS: When combined with brief behavioral support, cytisine was found to be superior to nicotine-replacement therapy in helping smokers quit smoking, but it was associated with a higher frequency of self-reported adverse events."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25517706",
"endSection": "abstract",
"offsetInBeginSection": 1245,
"offsetInEndSection": 1541,
"text": "The effectiveness of cytisine for continuous abstinence was superior to that of nicotine-replacement therapy at 1 week, 2 months, and 6 months. In a prespecified subgroup analysis of the primary outcome, cytisine was superior to nicotine-replacement therapy among women and noninferior among men."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25517706",
"endSection": "abstract",
"offsetInBeginSection": 1833,
"offsetInEndSection": 2068,
"text": "CONCLUSIONS: When combined with brief behavioral support, cytisine was found to be superior to nicotine-replacement therapy in helping smokers quit smoking, but it was associated with a higher frequency of self-reported adverse events."
}
]
| 5 | BioASQ-training5b | [
"http://www.biosemantics.org/jochem#4251343",
"http://www.biosemantics.org/jochem#4273701"
]
| []
| 54d77f0e3706e8952800001b | 10 |
yesno | Is Stat4 a transcription factor? | ['yes'] | [
"yes"
]
| ['Yes, Stat4 is a transcription factor.\nStat4 is a member of the signal transducer and activator of transcription (STAT) family of molecules that localizes to the cytoplasm. STAT4 regulates various genes expression as a transcription factor after it is phosphorylated, dimerizes and translocates to the nucleus.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25178516",
"http://www.ncbi.nlm.nih.gov/pubmed/25829541",
"http://www.ncbi.nlm.nih.gov/pubmed/25798064",
"http://www.ncbi.nlm.nih.gov/pubmed/25852285"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25829541",
"endSection": "abstract",
"offsetInBeginSection": 713,
"offsetInEndSection": 750,
"text": "transcription factors T-bet and STAT4"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25798064",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 272,
"text": "STAT4 is a member of the signal transducer and activator of transcription (STAT) family of molecules that localizes to the cytoplasm. STAT4 regulates various genes expression as a transcription factor after it is phosphorylated, dimerizes and translocates to the nucleus. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25178516",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "STAT4 is a latent cytosolic factor that encodes a transcription factor transmitting signals stimulated by cytokines. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25852285",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 168,
"text": " To investigate the role of signal transduction and activation of transcription 4 (STAT4) in the development and progression of human hepatocellular carcinoma (HCC)"
}
]
| 6 | BioASQ-training6b | null | null | 58bc58c302b8c60953000001 | 11 |
yesno | Can chronological age be predicted by measuring telomere length? | ['no'] | [
"no"
]
| ['No, telomere length measurement by real-time quantitative PCR cannot be used to predict age of a person, due to the presence of large inter-individual variations in telomere lengths.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23167566",
"http://www.ncbi.nlm.nih.gov/pubmed/18378481"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18378481",
"endSection": "abstract",
"offsetInBeginSection": 356,
"offsetInEndSection": 558,
"text": "Human somatic cells gradually lose telomeric repeats with age. This study investigated if one could use a correlation between telomere length and age, to predict the age of an individual from their DNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18378481",
"endSection": "abstract",
"offsetInBeginSection": 1519,
"offsetInEndSection": 1708,
"text": "Therefore, telomere length measurement by real-time quantitative PCR cannot be used to predict age of a person, due to the presence of large inter-individual variations in telomere lengths."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23167566",
"endSection": "abstract",
"offsetInBeginSection": 861,
"offsetInEndSection": 1194,
"text": "ur results provide the first clear and unambiguous evidence of a relationship between telomere length and mortality in the wild, and substantiate the prediction that telomere length and shortening rate can act as an indicator of biological age further to chronological age when exploring life history questions in natural conditions."
}
]
| 5 | BioASQ-training5b | []
| []
| 56d34fbcf22319765a000009 | 12 |
yesno | Was ALVAC-HIV effective for HIV prevention in the HVTN 702 trial? | ['no'] | [
"no"
]
| ['No. The ALVAC-gp120 regimen did not prevent HIV-1 infection among participants in South Africa despite previous evidence of immunogenicity'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33761206",
"http://www.ncbi.nlm.nih.gov/pubmed/34029515",
"http://www.ncbi.nlm.nih.gov/pubmed/32554928"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33761206",
"endSection": "abstract",
"offsetInBeginSection": 1258,
"offsetInEndSection": 1662,
"text": "During the 24-month follow-up, HIV-1 infection was diagnosed in 138 participants in the vaccine group and in 133 in the placebo group (hazard ratio, 1.02; 95% confidence interval, 0.81 to 1.30; P = 0.84).CONCLUSIONS: The ALVAC-gp120 regimen did not prevent HIV-1 infection among participants in South Africa despite previous evidence of immunogenicity. (HVTN 702 ClinicalTrials.gov number, NCT02968849.)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34029515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 433,
"text": "The advanced-phase HIV prevention vaccine trials done in South Africa (HVTN 702) and in Thailand (RV144), which both investigated canarypox vectors and adjuvanted gp120 proteins, gave rise to different results. The South African trial did not find vaccine efficacy, whereas the Thai trial had modest, but statistically significant, success with the modified intention-to-treat analysis prespecified in the protocols of both studies. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32554928",
"endSection": "abstract",
"offsetInBeginSection": 280,
"offsetInEndSection": 450,
"text": "However, with the recent failure of the HVTN 702 clinical trial, comprehensive profiling of humoral immune responses may provide insight for these disappointing results. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33761206",
"endSection": "abstract",
"offsetInBeginSection": 112,
"offsetInEndSection": 238,
"text": "A canarypox-protein HIV vaccine regimen (ALVAC-HIV plus AIDSVAX B/E) showed modest efficacy in reducing infection in Thailand."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33761206",
"endSection": "abstract",
"offsetInBeginSection": 1228,
"offsetInEndSection": 1567,
"text": "e vaccine and placebo groups. During the 24-month follow-up, HIV-1 infection was diagnosed in 138 participants in the vaccine group and in 133 in the placebo group (hazard ratio, 1.02; 95% confidence interval, 0.81 to 1.30; P = 0.84).CONCLUSIONS: The ALVAC-gp120 regimen did not prevent HIV-1 infection among participants in South Africa d"
}
]
| 11 | BioASQ-training11b | null | null | 61faa3bac9dfcb9c0900000b | 13 |
yesno | Can Enlimomab improve stroke outcomes? | ['no'] | [
"no"
]
| ['No. Anti-ICAM therapy with enlimomab is not an effective treatment for ischemic stroke and, indeed, may significantly worsen stroke outcome.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/19849665",
"http://www.ncbi.nlm.nih.gov/pubmed/12365824",
"http://www.ncbi.nlm.nih.gov/pubmed/9693236",
"http://www.ncbi.nlm.nih.gov/pubmed/12038658",
"http://www.ncbi.nlm.nih.gov/pubmed/9744839",
"http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"http://www.ncbi.nlm.nih.gov/pubmed/11692032"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19849665",
"endSection": "abstract",
"offsetInBeginSection": 1772,
"offsetInEndSection": 2068,
"text": "Treatment with a murine anti-ICAM-1 antibody (enlimomab) has been investigated in patients with acute ischemic stroke in the Enlimomab Acute Stroke Trial (EAST). Unfortunately, the case fatality rate in this trial was significantly higher in the enlimomab patient group than in the placebo group."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12365824",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 351,
"text": "The two clinical trials of therapy aimed at limiting the inflammatory response in acute stroke that have been carried out to date, however, have not shown a benefit to such therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12038658",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 696,
"text": "en classes of neuroprotective agents have reached phase III efficacy trials but have shown mixed results. They included calcium channel antagonists, NMDA receptor antagonists, lubeluzole, CDP-choline, the free radical scavenger tirilazad and ebselen, enlimomab, GABA agonist clomethiazole, the sodium channel antagonist fosphenytoin, magnesium, glycine site antagonist GV150526 and piracetam. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11692032",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "BACKGROUND AND PURPOSE: Enlimomab, a murine monoclonal anti-human intercellular adhesion molecule (ICAM)-1 antibody, had a negative outcome in a multicenter acute-stroke trial. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11692032",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Examination of several potential mechanisms for the negative outcome in a clinical stroke trial of enlimomab, a murine anti-human intercellular adhesion molecule-1 antibody: a bedside-to-bench study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 907,
"offsetInEndSection": 1358,
"text": "ESULTS: At day 90, the Modified Rankin Scale score was worse in patients treated with enlimomab than with placebo (p = 0.004). Fewer patients had symptom-free recovery on enlimomab than placebo (p = 0.004), and more died (22.2 versus 16.2%). The negative effect of enlimomab was apparent on days 5, 30, and 90 of treatment (p = 0.005). There were significantly more adverse events with enlimomab treatment than placebo, primarily infections and fever."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1434,
"offsetInEndSection": 1630,
"text": "CONCLUSIONS: The authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for ischemic stroke in the model studied and, indeed, may significantly worsen stroke outcome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1440,
"offsetInEndSection": 1636,
"text": "CONCLUSIONS\n\nThe authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for ischemic stroke in the model studied and, indeed, may significantly worsen stroke outcome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1247,
"offsetInEndSection": 1362,
"text": "There were significantly more adverse events with enlimomab treatment than placebo, primarily infections and fever."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 910,
"offsetInEndSection": 1037,
"text": "RESULTS\n\nAt day 90, the Modified Rankin Scale score was worse in patients treated with enlimomab than with placebo (p = 0.004)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1153,
"offsetInEndSection": 1246,
"text": "The negative effect of enlimomab was apparent on days 5, 30, and 90 of treatment (p = 0.005)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9744839",
"endSection": "abstract",
"offsetInBeginSection": 1441,
"offsetInEndSection": 1524,
"text": "However, this treatment failed to show benefit in the Enlimomab Acute Stroke Trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1242,
"offsetInEndSection": 1357,
"text": "There were significantly more adverse events with enlimomab treatment than placebo, primarily infections and fever."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11692032",
"endSection": "abstract",
"offsetInBeginSection": 1797,
"offsetInEndSection": 1974,
"text": "These observations provide several possible mechanisms for central nervous system-related clinical deterioration that occurred when Enlimomab was given in acute ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 910,
"offsetInEndSection": 1037,
"text": "RESULTS\nAt day 90, the Modified Rankin Scale score was worse in patients treated with enlimomab than with placebo (p = 0.004)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19849665",
"endSection": "abstract",
"offsetInBeginSection": 1934,
"offsetInEndSection": 2069,
"text": "Unfortunately, the case fatality rate in this trial was significantly higher in the enlimomab patient group than in the placebo group."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9693236",
"endSection": "abstract",
"offsetInBeginSection": 1284,
"offsetInEndSection": 1505,
"text": "CONCLUSIONS\nDoses of enlimomab between 140 and 480 mg administered over 5 days did not increase the risk of adverse events in patients with ischaemic or haemorrhagic stroke during an observation period of 30 +/- 10 days."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11692032",
"endSection": "abstract",
"offsetInBeginSection": 15,
"offsetInEndSection": 176,
"text": "PURPOSE: Enlimomab, a murine monoclonal anti-human intercellular adhesion molecule (ICAM)-1 antibody, had a negative outcome in a multicenter acute-stroke trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11692032",
"endSection": "abstract",
"offsetInBeginSection": 1791,
"offsetInEndSection": 1968,
"text": "These observations provide several possible mechanisms for central nervous system-related clinical deterioration that occurred when Enlimomab was given in acute ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11692032",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Enlimomab, a murine monoclonal anti-human intercellular adhesion molecule (ICAM)-1 antibody, had a negative outcome in a multicenter acute-stroke trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11692032",
"endSection": "abstract",
"offsetInBeginSection": 1739,
"offsetInEndSection": 1916,
"text": "These observations provide several possible mechanisms for central nervous system-related clinical deterioration that occurred when Enlimomab was given in acute ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1407,
"offsetInEndSection": 1590,
"text": "The authors conclude that anti-ICAM therapy with enlimomab is not an effective treatment for ischemic stroke in the model studied and, indeed, may significantly worsen stroke outcome."
}
]
| 11 | BioASQ-training11b | null | null | 5e44c33a48dab47f26000020 | 14 |
yesno | Have microRNAs been implicated in pharmacogenomics? | ['yes'] | [
"yes"
]
| ['Yes. MicroRNAs have been implicated in pharmacogenomics.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23376192",
"http://www.ncbi.nlm.nih.gov/pubmed/23189953",
"http://www.ncbi.nlm.nih.gov/pubmed/22630332",
"http://www.ncbi.nlm.nih.gov/pubmed/22445829",
"http://www.ncbi.nlm.nih.gov/pubmed/21499217",
"http://www.ncbi.nlm.nih.gov/pubmed/21412770",
"http://www.ncbi.nlm.nih.gov/pubmed/21047203",
"http://www.ncbi.nlm.nih.gov/pubmed/20585341",
"http://www.ncbi.nlm.nih.gov/pubmed/18187804",
"http://www.ncbi.nlm.nih.gov/pubmed/17483436",
"http://www.ncbi.nlm.nih.gov/pubmed/16854228",
"http://www.ncbi.nlm.nih.gov/pubmed/22909203"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23376192",
"endSection": "sections.0",
"offsetInBeginSection": 156,
"offsetInEndSection": 435,
"text": "A major discovery is the ability of miRNAs to determine the efficacy of drugs, which has given rise to the field of 'miRNA pharmacogenomics' through 'Pharmaco-miRs'. miRNAs play a significant role in pharmacogenomics by down-regulating genes that are important for drug function."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23189953",
"endSection": "sections.0",
"offsetInBeginSection": 878,
"offsetInEndSection": 1199,
"text": "The potential modulation of toxicology-related changes in miRNA expression, the role of miRNA in immune-mediated drug-induced liver injuries, the use of circulating miRNAs in body fluids as potential toxicological biomarkers, and the link between miRNA-related pharmacogenomics and adverse drug reactions are highlighted."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22445829",
"endSection": "sections.0",
"offsetInBeginSection": 232,
"offsetInEndSection": 531,
"text": "Single nucleotide polymorphisms (SNPs) in the miRNA target sequences may affect or impair the binding of miRNAs. Studies have shown that SNPs in miRNA target sites (miR-TS-SNPs) have a great influence on diverse biological functions, including pharmacogenomics and disease susceptibilities in human."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21499217",
"endSection": "sections.0",
"offsetInBeginSection": 454,
"offsetInEndSection": 782,
"text": "Pharmacogenomics genes can be divided into drug target genes termed as pharmacodynamics genes (PD) and genes involved in drug transport and metabolism termed as pharmacokinetics genes (PK). To clarify the regulatory potential of miRNAs in pharmacogenomics, we have examined the potential regulation by miRNAs of PK and PD genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21499217",
"endSection": "sections.0",
"offsetInBeginSection": 1284,
"offsetInEndSection": 1786,
"text": "Our analysis identify a striking difference in the level of miRNA regulation between PK and PD genes, with the former having less than half predicted conserved miRNA binding sites compared with the latter. Importantly, this finding is reflected in a highly significant difference in the shift in expression levels of PD versus PK genes after depletion of miRNAs. CONCLUSIONS: Our study emphasizes an intrinsic difference between PK and PD genes and helps clarify the role of miRNAs in pharmacogenomics."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21412770",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 419,
"text": "Pharmacogenomics, toxicogenomics, and small RNA expression analysis are three of the most active research topics in the biological, biomedical, pharmaceutical, and toxicological fields. All of these studies are based on gene expression analysis, which requires reference genes to reduce the variations derived from different amounts of starting materials and different efficiencies of RNA extraction and cDNA synthesis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21412770",
"endSection": "sections.0",
"offsetInBeginSection": 2269,
"offsetInEndSection": 2426,
"text": "In contrast, hTBCA and small RNAs are more stable during drug treatment, and they are better reference genes for pharmacogenomics and toxicogenomics studies."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21047203",
"endSection": "sections.0",
"offsetInBeginSection": 11,
"offsetInEndSection": 152,
"text": "Polymorphisms of genes involved in the pharmacokinetic and pharmacodynamic processes underlie the divergent drug responses among individuals."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21047203",
"endSection": "sections.0",
"offsetInBeginSection": 1036,
"offsetInEndSection": 1167,
"text": "A panel of drug-response genes was constructed, which contains 923 pharmacokinetic genes, 703 pharmacodynamic genes and 720 miRNAs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20585341",
"endSection": "sections.0",
"offsetInBeginSection": 123,
"offsetInEndSection": 243,
"text": "miRNA variations can affect drug resistance, efficacy, and metabolism, opening new avenues of pharmacogenomics research."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18187804",
"endSection": "sections.0",
"offsetInBeginSection": 260,
"offsetInEndSection": 467,
"text": "we studied the pharmacologic roles of three microRNAs previously implicated in cancer biology (let-7i, mir-16, and mir-21) and also used in silico methods to test pharmacologic microRNA effects more broadly."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18187804",
"endSection": "sections.0",
"offsetInBeginSection": 1322,
"offsetInEndSection": 1781,
"text": "n silico comparison of drug potencies with microRNA expression profiles across the entire NCI-60 panel revealed that approximately 30 microRNAs, including mir-21, show highly significant correlations with numerous anticancer agents. Ten of those microRNAs have already been implicated in cancer biology. Our results support a substantial role for microRNAs in anticancer drug response, suggesting novel potential approaches to the improvement of chemotherapy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17483436",
"endSection": "sections.0",
"offsetInBeginSection": 392,
"offsetInEndSection": 603,
"text": "The NCI-60 has also been profiled for mRNA and protein expression, mutational status, chromosomal aberrations, and DNA copy number, generating an unparalleled public resource for integrated chemogenomic studies."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17483436",
"endSection": "sections.0",
"offsetInBeginSection": 738,
"offsetInEndSection": 941,
"text": "To complement the existing NCI-60 data sets, we have measured expression levels of microRNAs in the NCI-60 and incorporated the resulting data into the CellMiner program package for integrative analysis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17483436",
"endSection": "sections.0",
"offsetInBeginSection": 1375,
"offsetInEndSection": 1765,
"text": ". Comparison of microRNA expression patterns and compound potency patterns showed significant correlations, suggesting that microRNAs may play a role in chemoresistance. Combined with gene expression and other biological data using multivariate analysis, microRNA expression profiles may provide a critical link for understanding mechanisms involved in chemosensitivity and chemoresistance."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22909203",
"endSection": "sections.0",
"offsetInBeginSection": 296,
"offsetInEndSection": 364,
"text": "This study reports on miRNAs implicated in SSRI sensitivity of LCLs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22909203",
"endSection": "sections.0",
"offsetInBeginSection": 949,
"offsetInEndSection": 1071,
"text": "these miRNAs as tentative SSRI response biomarkers awaits validation with lymphocyte samples of major depression patients."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D010597",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D035683"
]
| [
{
"o": "http://purl.uniprot.org/pubmed/12052143",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://purl.uniprot.org/pubmed/12052143"
},
{
"o": "Pharmacogenomics",
"p": "http://purl.uniprot.org/core/name",
"s": "http://purl.uniprot.org/pubmed/15584875"
},
{
"o": "http://purl.uniprot.org/pubmed/16886893",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://purl.uniprot.org/pubmed/16886893"
},
{
"o": "Pharmacogenomics",
"p": "http://purl.uniprot.org/core/name",
"s": "http://purl.uniprot.org/pubmed/16981842"
},
{
"o": "Pharmacogenomics",
"p": "http://purl.uniprot.org/core/name",
"s": "http://purl.uniprot.org/pubmed/17638511"
},
{
"o": "http://purl.uniprot.org/pubmed/17391071",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://purl.uniprot.org/pubmed/17391071"
},
{
"o": "http://purl.uniprot.org/pubmed/17716225",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://purl.uniprot.org/pubmed/17716225"
},
{
"o": "Pharmacogenomics",
"p": "http://purl.uniprot.org/core/name",
"s": "http://purl.uniprot.org/pubmed/17979512"
}
]
| 5162a089298dcd4e51000043 | 15 |
yesno | Is there an association between Muenke Syndrome and FGFR3 gene mutation? | ['yes'] | [
"yes"
]
| ['Yes, Muenke syndrome is caused by point mutation (C749G) in the Fibroblast Growth Factor Receptor3 (FGFR3) gene. It affects 1 in 30,000 newborns and accounts for 25% to 30% of genetic causes of craniosynostosis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/17103449",
"http://www.ncbi.nlm.nih.gov/pubmed/11571861",
"http://www.ncbi.nlm.nih.gov/pubmed/21403557",
"http://www.ncbi.nlm.nih.gov/pubmed/22872265",
"http://www.ncbi.nlm.nih.gov/pubmed/21233754",
"http://www.ncbi.nlm.nih.gov/pubmed/10696568",
"http://www.ncbi.nlm.nih.gov/pubmed/14613973",
"http://www.ncbi.nlm.nih.gov/pubmed/18818193",
"http://www.ncbi.nlm.nih.gov/pubmed/19086028",
"http://www.ncbi.nlm.nih.gov/pubmed/24686979",
"http://www.ncbi.nlm.nih.gov/pubmed/26740388",
"http://www.ncbi.nlm.nih.gov/pubmed/15241680",
"http://www.ncbi.nlm.nih.gov/pubmed/26028288",
"http://www.ncbi.nlm.nih.gov/pubmed/19215249",
"http://www.ncbi.nlm.nih.gov/pubmed/19755431",
"http://www.ncbi.nlm.nih.gov/pubmed/24168007",
"http://www.ncbi.nlm.nih.gov/pubmed/20592905",
"http://www.ncbi.nlm.nih.gov/pubmed/18000976",
"http://www.ncbi.nlm.nih.gov/pubmed/23044018",
"http://www.ncbi.nlm.nih.gov/pubmed/24448525",
"http://www.ncbi.nlm.nih.gov/pubmed/16251895",
"http://www.ncbi.nlm.nih.gov/pubmed/24705944",
"http://www.ncbi.nlm.nih.gov/pubmed/19449410",
"http://www.ncbi.nlm.nih.gov/pubmed/14963686",
"http://www.ncbi.nlm.nih.gov/pubmed/17070479",
"http://www.ncbi.nlm.nih.gov/pubmed/22446440",
"http://www.ncbi.nlm.nih.gov/pubmed/23378035",
"http://www.ncbi.nlm.nih.gov/pubmed/22016144",
"http://www.ncbi.nlm.nih.gov/pubmed/22544111"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028288",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 810,
"text": "RESULTS: Forty-four with a positive FGFR3 mutation, median age 9 years, range 7 months to 52 years were enrolled. In addition, 10 unaffected siblings served as controls (5 males, 5 females; median age, 13 years; range, 3-18 years)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24168007",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Muenke is a fibroblast growth factor receptor 3 (FGFR-3)-associated syndrome, which was first described in late 1990 s. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24168007",
"endSection": "abstract",
"offsetInBeginSection": 275,
"offsetInEndSection": 455,
"text": "The syndrome is defined molecularly by a unique point mutation c.749C>G in exon 7 of the FGFR3 gene which results to an amino acid substitution p.Pro250Arg of the protein product. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24448525",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Muenke syndrome caused by point mutation (C749G) in the FGFR3 gene affects 1 in 30,000 newborns and accounts for 25% to 30% of genetic causes of craniosynostosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24705944",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Phenotypic variability in two families of Muenke syndrome with FGFR3 mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24686979",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 282,
"text": "PURPOSE: There are a number of craniosynostosis syndromes with hearing loss-including Muenke, Apert, Pfeiffer, Crouzon, Beare-Stevenson, Crouzon with acanthosis nigricans, and Jackson-Weiss syndromes-that result from mutations in the fibroblast growth factor receptor (FGFR) genes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23378035",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Muenke syndrome is an autosomal dominant craniosynostosis syndrome resulting from a defining point mutation in the Fibroblast Growth Factor Receptor3 (FGFR3) gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23378035",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Talocalcaneal coalition in Muenke syndrome: report of a patient, review of the literature in FGFR-related craniosynostoses, and consideration of mechanism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22872265",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 591,
"text": "To better understand the pathophysiology of the Muenke syndrome, we present collective findings from several recent studies that have characterized a genetically equivalent mouse model for Muenke syndrome (FgfR3 (P244R)) and compare them with human phenotypes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22016144",
"endSection": "abstract",
"offsetInBeginSection": 407,
"offsetInEndSection": 733,
"text": "We show in this study that knock-in mice harboring the mutation responsible for the Muenke syndrome (FgfR3(P244R)) display postnatal shortening of the cranial base along with synchondrosis growth plate dysfunction characterized by loss of resting, proliferating and hypertrophic chondrocyte zones and decreased Ihh expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23044018",
"endSection": "abstract",
"offsetInBeginSection": 408,
"offsetInEndSection": 526,
"text": "Muenke syndrome is caused by a single defining point mutation in the fibroblast growth factor receptor 3 (FGFR3) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21403557",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 434,
"text": "The Pro250Arg mutation in the FGFR3 gene is found in patients with Muenke syndrome and is one of the most frequently encountered mutations in craniosynostosis syndromes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23044018",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 60,
"text": "Epilepsy in Muenke syndrome: FGFR3-related craniosynostosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18000976",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Muenke syndrome (FGFR3-related craniosynostosis): expansion of the phenotype and review of the literature."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21403557",
"endSection": "abstract",
"offsetInBeginSection": 267,
"offsetInEndSection": 436,
"text": "The Pro250Arg mutation in the FGFR3 gene is found in patients with Muenke syndrome and is one of the most frequently encountered mutations in craniosynostosis syndromes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22872265",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "PURPOSE: The Muenke syndrome mutation (FGFR3 (P250R)), which was discovered 15 years ago, represents the single most common craniosynostosis mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18818193",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 233,
"text": "The heterozygous Pro250Arg substitution mutation in fibroblast growth factor receptor 3 (FGFR3), which increases ligand-dependent signalling, is the most common genetic cause of craniosynostosis in humans and defines Muenke syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17103449",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "P250R mutation in the FGFR3 gene also known as Muenke syndrome is associated with coronal craniosynostosis, sensorineural deafness, craniofacial, and digital abnormalities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22446440",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Muenke syndrome caused by the FGFR3 Pro250Arg mutation is associated with craniosynostosis, hearing loss, and various bony anomalies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18000976",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "Muenke syndrome is an autosomal dominant disorder characterized by coronal suture craniosynostosis, hearing loss, developmental delay, carpal and tarsal fusions, and the presence of the Pro250Arg mutation in the FGFR3 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19086028",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Muenke syndrome, defined by heterozygosity for a Pro250Arg substitution in fibroblast growth factor receptor 3 (FGFR3), is the most common genetic cause of craniosynostosis in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22872265",
"endSection": "abstract",
"offsetInBeginSection": 1041,
"offsetInEndSection": 1173,
"text": "In addition, sensorineural hearing loss is detected in all FgfR3 (P244R) mutant mice as in the majority of Muenke syndrome patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19755431",
"endSection": "abstract",
"offsetInBeginSection": 133,
"offsetInEndSection": 772,
"text": "Genetic testing identifies a pathogenic mutation or chromosomal abnormality in ∼ 21% of cases, but it is likely that further causative mutations remain to be discovered.To identify a shared signature of genetically determined craniosynostosis by comparing the expression patterns in three monogenic syndromes with a control group of patients with non-syndromic sagittal synostosis.Fibroblasts from 10 individuals each with Apert syndrome (FGFR2 substitution S252W), Muenke syndrome (FGFR3 substitution P250R), Saethre-Chotzen syndrome (various mutations in TWIST1) and non-syndromic sagittal synostosis (no mutation detected) were cultured"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11571861",
"endSection": "abstract",
"offsetInBeginSection": 581,
"offsetInEndSection": 819,
"text": "The craniosynostosis syndromes: Apert syndrome, Beare-Stevenson syndrome, Crouzon syndrome, Jackson-Weiss syndrome, Muenke syndrome, Pfeiffer syndrome and Saethre-Chotzen syndrome can be caused by mutation in either FGFR1, FGFR2, or FGFR3"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14613973",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Identical proline-->arginine gain-of-function mutations in fibroblast growth factor receptor (FGFR) 1 (Pro252Arg), FGFR2 (Pro253Arg) and FGFR3 (Pro250Arg), result in type I Pfeiffer, Apert and Muenke craniosynostosis syndromes, respectively"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21403557",
"endSection": "abstract",
"offsetInBeginSection": 267,
"offsetInEndSection": 435,
"text": "The Pro250Arg mutation in the FGFR3 gene is found in patients with Muenke syndrome and is one of the most frequently encountered mutations in craniosynostosis syndromes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21233754",
"endSection": "abstract",
"offsetInBeginSection": 818,
"offsetInEndSection": 1043,
"text": "Mutation analysis of FGFR-3 revealed a missense mutation in exon 6, c.749 C>G, with a resultant amino acid change from proline to arginine at codon 250 (P250R), in keeping with Muenke syndrome (Am J Hum Genet 1997;60:555-564)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16251895",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 441,
"text": "In an attempt to delineate functional features separating SCS from Muenkes syndrome, we screened patients presenting with coronal suture synostosis for mutations in the TWIST 1 gene, and for the Pro250Arg mutation in FGFR3"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10696568",
"endSection": "abstract",
"offsetInBeginSection": 942,
"offsetInEndSection": 1237,
"text": "Since the Gly380Arg achondroplasia mutation was recognized, similar observations regarding the conserved nature of FGFR mutations and resulting phenotype have been made regarding other skeletal phenotypes, including hypochondroplasia, thanatophoric dysplasia, and Muenke coronal craniosynostosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19215249",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 418,
"text": "Mutations in the gene that encodes Fibroblast Growth Factor Receptor 3 (FGFR3) are associated with Achondroplasia (MIM 100800), Hypochondroplasia (MIM 146000), Muenke Syndrome (MIM 602849), Thanatophoric Dysplasia (MIM 187600, MIM 187601) and Lacrimo-Auriculo-Dento-Digital Syndrome (MIM 149730).Here we report a clinical and molecular study in a large cohort of 125 Portuguese patients with these skeletal disorders. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20592905",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 252,
"text": "The Muenke syndrome (MS) is characterized by unicoronal or bicoronal craniosynostosis, midfacial hypoplasia, ocular hypertelorism, and a variety of minor abnormalities associated with a mutation in the fibroblast growth factor receptor 3 (FGFR3) gene. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17103449",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "P250R mutation in the FGFR3 gene also known as Muenke syndrome is associated with coronal craniosynostosis, sensorineural deafness, craniofacial, and digital abnormalities. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19755431",
"endSection": "abstract",
"offsetInBeginSection": 539,
"offsetInEndSection": 808,
"text": "METHODS: Fibroblasts from 10 individuals each with Apert syndrome (FGFR2 substitution S252W), Muenke syndrome (FGFR3 substitution P250R), Saethre-Chotzen syndrome (various mutations in TWIST1) and non-syndromic sagittal synostosis (no mutation detected) were cultured. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18000976",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "Muenke syndrome is an autosomal dominant disorder characterized by coronal suture craniosynostosis, hearing loss, developmental delay, carpal and tarsal fusions, and the presence of the Pro250Arg mutation in the FGFR3 gene. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15241680",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 270,
"text": "Muenke syndrome, also known as FGFR3-associated coronal synostosis, is defined molecularly by the presence of a heterozygous nucleotide transversion, c.749C>G, encoding the amino acid substitution Pro250Arg, in the fibroblast growth factor receptor type 3 gene (FGFR3). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14963686",
"endSection": "abstract",
"offsetInBeginSection": 323,
"offsetInEndSection": 487,
"text": "In spite of a variable phenotype, Muenke syndrome has been related to a unique mutation on the FGFR3 gene, Pro 250 to Arg, which is characteristic of this disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19086028",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Skeletal analysis of the Fgfr3(P244R) mouse, a genetic model for the Muenke craniosynostosis syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23044018",
"endSection": "abstract",
"offsetInBeginSection": 410,
"offsetInEndSection": 528,
"text": "Muenke syndrome is caused by a single defining point mutation in the fibroblast growth factor receptor 3 (FGFR3) gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23044018",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "Epilepsy in Muenke syndrome: FGFR3-related craniosynostosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15241680",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "Muenke syndrome, also known as FGFR3-associated coronal synostosis, is defined molecularly by the presence of a heterozygous nucleotide transversion, c.749C>G, encoding the amino acid substitution Pro250Arg, in the fibroblast growth factor receptor type 3 gene (FGFR3)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22872265",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "The Muenke syndrome mutation (FGFR3 (P250R)), which was discovered 15 years ago, represents the single most common craniosynostosis mutation."
}
]
| 6 | BioASQ-training6b | [
"http://www.uniprot.org/uniprot/FGFR3_CHICK",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001244",
"http://www.disease-ontology.org/api/metadata/DOID:0060703",
"http://www.uniprot.org/uniprot/FGFR3_PLEWA",
"http://www.uniprot.org/uniprot/FGFR3_HUMAN",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051498"
]
| null | 5895ec5e7d9090f353000015 | 16 |
yesno | Is the apilimod inhibitor effective against SARS-CoV-2? | ['yes'] | [
"yes"
]
| ['To identify therapeutics that can be repurposed as SARS-CoV-2 antivirals, a library of known drugs encompassing approximately 12,000 clinical-stage or FDA-approved small molecules were profiled. In a study the identification of 30 known drugs that inhibit viral replication was reportedd. Of these, six were characterized for cellular dose-activity relationships, and showed effective concentrations likely to be commensurate with therapeutic doses in patients. These include the PIKfyve kinase inhibitor Apilimod, cysteine protease inhibitors MDL-28170, Z LVG CHN2, VBY-825, and ONO 5334, and the CCR1 antagonist MLN-3897. Since many of these molecules have advanced into the clinic, the known pharmacological and human safety profiles of these compounds will accelerate their preclinical and clinical evaluation for COVID-19 treatment.', 'Yes, apilimod inhibition is effective for treatment of SARS-CoV-2.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/32511357"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32511357",
"endSection": "abstract",
"offsetInBeginSection": 656,
"offsetInEndSection": 1482,
"text": "To identify therapeutics that can be repurposed as SARS-CoV-2 antivirals, we profiled a library of known drugs encompassing approximately 12,000 clinical-stage or FDA-approved small molecules. Here, we report the identification of 30 known drugs that inhibit viral replication. Of these, six were characterized for cellular dose-activity relationships, and showed effective concentrations likely to be commensurate with therapeutic doses in patients. These include the PIKfyve kinase inhibitor Apilimod, cysteine protease inhibitors MDL-28170, Z LVG CHN2, VBY-825, and ONO 5334, and the CCR1 antagonist MLN-3897. Since many of these molecules have advanced into the clinic, the known pharmacological and human safety profiles of these compounds will accelerate their preclinical and clinical evaluation for COVID-19 treatment."
}
]
| 11 | BioASQ-training11b | null | null | 60324b771cb411341a000139 | 17 |
yesno | Is Growth factor independence 1b (GFI1B) important for hematopoiesis? | ['yes'] | [
"yes"
]
| ['Yes. Gfi-1B is a transcriptional repressor essential for the regulation of erythropoiesis and megakaryopoiesis. Gfi-1b(-/-) embryonic stem cells fail to contribute to red cells of adult chimeras. Gfi-1b(-/-) embryos exhibit delayed maturation of primitive erythrocytes and subsequently die with failure to produce definitive enucleated erythrocytes.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"http://www.ncbi.nlm.nih.gov/pubmed/22699452",
"http://www.ncbi.nlm.nih.gov/pubmed/22668850",
"http://www.ncbi.nlm.nih.gov/pubmed/22399799",
"http://www.ncbi.nlm.nih.gov/pubmed/21606163",
"http://www.ncbi.nlm.nih.gov/pubmed/21170035",
"http://www.ncbi.nlm.nih.gov/pubmed/20861919",
"http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"http://www.ncbi.nlm.nih.gov/pubmed/19958752",
"http://www.ncbi.nlm.nih.gov/pubmed/19773260",
"http://www.ncbi.nlm.nih.gov/pubmed/18224412",
"http://www.ncbi.nlm.nih.gov/pubmed/17707228",
"http://www.ncbi.nlm.nih.gov/pubmed/17095621",
"http://www.ncbi.nlm.nih.gov/pubmed/16397623",
"http://www.ncbi.nlm.nih.gov/pubmed/14530176",
"http://www.ncbi.nlm.nih.gov/pubmed/12351384",
"http://www.ncbi.nlm.nih.gov/pubmed/11825872",
"http://www.ncbi.nlm.nih.gov/pubmed/24800817",
"http://www.ncbi.nlm.nih.gov/pubmed/23308270",
"http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"http://www.ncbi.nlm.nih.gov/pubmed/20826720",
"http://www.ncbi.nlm.nih.gov/pubmed/21732494",
"http://www.ncbi.nlm.nih.gov/pubmed/22885124",
"http://www.ncbi.nlm.nih.gov/pubmed/16177182",
"http://www.ncbi.nlm.nih.gov/pubmed/15507521"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 252,
"text": "Growth Factor Independence (Gfi) transcription factors play essential roles in hematopoiesis, differentially activating and repressing transcriptional programs required for hematopoietic stem/progenitor cell (HSPC) development and lineage specification"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 872,
"offsetInEndSection": 974,
"text": "gfi1aa and gfi1b have distinct roles in regulating primitive and definitive hematopoietic progenitors,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 1151,
"offsetInEndSection": 1197,
"text": "gfi1b is required for definitive hematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699452",
"endSection": "abstract",
"offsetInBeginSection": 1052,
"offsetInEndSection": 1140,
"text": "LSD1-kd was associated with the upregulation of key hematopoietic genes, including Gfi1b"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22668850",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "GFI1 and GFI1B control the loss of endothelial identity of hemogenic endothelium during hematopoietic commitment"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22668850",
"endSection": "abstract",
"offsetInBeginSection": 856,
"offsetInEndSection": 1076,
"text": " Taken together, our findings demonstrate a critical and specific role of the GFI1 transcription factors in the first steps of the process leading to the generation of hematopoietic progenitors from hemogenic endothelium"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22399799",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 57,
"text": "A short Gfi-1B isoform controls erythroid differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22399799",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Gfi-1B is a transcriptional repressor essential for the regulation of erythropoiesis and megakaryopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21606163",
"endSection": "abstract",
"offsetInBeginSection": 1070,
"offsetInEndSection": 1162,
"text": "Among the few down-regulated genes was Gfi1b, a known repressor of erythroid differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21170035",
"endSection": "abstract",
"offsetInBeginSection": 722,
"offsetInEndSection": 922,
"text": "This reversible modulation of endothelial-haematopoietic state is accomplished by targeting key haematopoietic transcription factors for downregulation, including Runx1, Gata1, Gfi1B, Ikaros, and PU.1"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20861919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "Gfi1 and Gfi1b: key regulators of hematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20861919",
"endSection": "abstract",
"offsetInBeginSection": 630,
"offsetInEndSection": 851,
"text": "we review how Gfi1 and its paralogue Gfi1b control the development of blood cells, discuss how changes in Gfi1 and Gfi1b function contribute to hematological disease and report on the molecular function of these proteins."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Gfi-1B controls human erythroid and megakaryocytic differentiation by regulating TGF-beta signaling at the bipotent erythro-megakaryocytic progenitor stage"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Growth factor independence-1B (Gfi-1B) is a transcriptional repressor essential for erythropoiesis and megakaryopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 312,
"text": "Targeted gene disruption of GFI1B in mice leads to embryonic lethality resulting from failure to produce definitive erythrocytes, hindering the study of Gfi-1B function in adult hematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 314,
"offsetInEndSection": 509,
"text": "We here show that, in humans, Gfi-1B controls the development of erythrocytes and megakaryocytes by regulating the proliferation and differentiation of bipotent erythro-megakaryocytic progenitors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19958752",
"endSection": "abstract",
"offsetInBeginSection": 1509,
"offsetInEndSection": 1677,
"text": "To date, we have identified two common integration sites involving genes encoding transcription factors that play a critical role in hematopoiesis (Evi1 and Gfi1b loci)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19773260",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 304,
"text": "Transcription factors play essential roles in both normal and malignant hematopoiesis. This is the case for the growth factor independent 1b (GFI1B) transcription factor, which is required for erythroid and megakaryocytic differentiation and over-expressed in leukemic patients and cell lines"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19773260",
"endSection": "abstract",
"offsetInBeginSection": 1022,
"offsetInEndSection": 1450,
"text": "We localized several conserved non-coding elements containing multiple erythroid specific transcription factor binding sites at the GFI1B locus. In GFI1B-expressing cells a subset of these conserved non-coding elements and the promoter adopt a close spatial conformation, localize with open chromatin sites, harbor chromatin modifications associated with gene activation and bind multiple transcription factors and co-repressors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19773260",
"endSection": "abstract",
"offsetInBeginSection": 1464,
"offsetInEndSection": 1552,
"text": "Our findings indicate that GFI1B regulatory elements behave as activators and repressors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18224412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "To investigate the molecular effects of growth factor independence 1B (Gfi-1B), a transcription factor essential for the development of hematopoietic cells and differentiation of erythroid and megakaryocytic lineages"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18224412",
"endSection": "abstract",
"offsetInBeginSection": 1760,
"offsetInEndSection": 1877,
"text": "Our data indicate that Gfi-1B signalling is important for commitment and maturation of hematopoietic cell populations"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17707228",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Gfi-1 and Gfi-1b are homologous transcriptional repressors involved in diverse developmental contexts, including hematopoiesis and oncogenesis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17095621",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Gfi1b:green fluorescent protein knock-in mice reveal a dynamic expression pattern of Gfi1b during hematopoiesis that is largely complementary to Gfi1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17095621",
"endSection": "abstract",
"offsetInBeginSection": 546,
"offsetInEndSection": 958,
"text": "We found highly dynamic expression patterns of Gfi1b in erythroid cells, megakaryocytes, and their progenitor cells (MEPS) where Gfi1 is not detected. Vice versa, Gfi1b could not be found in granulocytes, activated macrophages, or their granulomonocytic precursors (GMPs) or in mature naive or activated lymphocytes where Gfi1 is expressed, suggesting a complementary regulation of both loci during hematopoiesis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16397623",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 49,
"text": "Gfi1 and Gfi1b act equivalently in haematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16397623",
"endSection": "abstract",
"offsetInBeginSection": 668,
"offsetInEndSection": 814,
"text": "our findings show that an intact SNAG domain is essential for all functions of Gfi1 and that Gfi1b can replace Gfi1 functionally in haematopoiesis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14530176",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 35,
"text": "Gfi-1 oncoproteins in hematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14530176",
"endSection": "abstract",
"offsetInBeginSection": 101,
"offsetInEndSection": 239,
"text": "Recent gene targeting experiments and mutational screening in humans have revealed an essential role for Gfi-1 and Gfi-1B in hematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14530176",
"endSection": "abstract",
"offsetInBeginSection": 608,
"offsetInEndSection": 747,
"text": "Gfi-1B disruption is embryonic lethal due to a block of erythropoiesis. Gfi-1B is required for both erythroid and megakaryocyte development"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12351384",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Erythroid expansion mediated by the Gfi-1B zinc finger protein: role in normal hematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12351384",
"endSection": "abstract",
"offsetInBeginSection": 62,
"offsetInEndSection": 222,
"text": " we identified that the expression of Gfi-1B (growth factor independence-1B) is highly restricted to hematopoietic stem cells, erythroblasts, and megakaryocytes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12351384",
"endSection": "abstract",
"offsetInBeginSection": 1470,
"offsetInEndSection": 1665,
"text": "These findings establish Gfi-1B as a novel erythroid regulator and reveal its specific involvement in the regulation of erythroid cell growth through modulating erythroid-specific gene expression"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11825872",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "The zinc-finger proto-oncogene Gfi-1b is essential for development of the erythroid and megakaryocytic lineages"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11825872",
"endSection": "abstract",
"offsetInBeginSection": 112,
"offsetInEndSection": 237,
"text": "we establish that Gfi-1b is required for the development of two related blood lineages, erythroid and megakaryocytic, in mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11825872",
"endSection": "abstract",
"offsetInBeginSection": 239,
"offsetInEndSection": 475,
"text": "Gfi-1b(-/-) embryonic stem cells fail to contribute to red cells of adult chimeras. Gfi-1b(-/-) embryos exhibit delayed maturation of primitive erythrocytes and subsequently die with failure to produce definitive enucleated erythrocytes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11825872",
"endSection": "abstract",
"offsetInBeginSection": 623,
"offsetInEndSection": 714,
"text": "Gfi-1b is an essential transcriptional regulator of erythroid and megakaryocyte development"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24800817",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Growth factor independence 1b (GFI1B) is a DNA binding repressor of transcription with vital functions in hematopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 1060,
"offsetInEndSection": 1191,
"text": "Conversely, loss of gfi1b silences runx-1, c-myb, ikaros and cd41, indicating that gfi1b is required for definitive hematopoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17095621",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Gfi1b:green fluorescent protein knock-in mice reveal a dynamic expression pattern of Gfi1b during hematopoiesis that is largely complementary to Gfi1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20861919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Gfi1 and Gfi1b: key regulators of hematopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 713,
"offsetInEndSection": 826,
"text": "We show that gfi1aa and gfi1b are expressed in the primitive and definitive sites of hematopoiesis in zebrafish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 312,
"text": "Targeted gene disruption of GFI1B in mice leads to embryonic lethality resulting from failure to produce definitive erythrocytes, hindering the study of Gfi-1B function in adult hematopoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24800817",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Growth factor independence 1b (gfi1b) is important for the maturation of erythroid cells and the regulation of embryonic globin expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Growth factor-independence 1b (Gfi1b) is a zinc finger transcription factor essential for erythroid and megakaryocytic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24800817",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Growth factor independence 1b (GFI1B) is a DNA binding repressor of transcription with vital functions in hematopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 1060,
"offsetInEndSection": 1191,
"text": "Conversely, loss of gfi1b silences runx-1, c-myb, ikaros and cd41, indicating that gfi1b is required for definitive hematopoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20861919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Gfi1 and Gfi1b: key regulators of hematopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 713,
"offsetInEndSection": 826,
"text": "We show that gfi1aa and gfi1b are expressed in the primitive and definitive sites of hematopoiesis in zebrafish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 312,
"text": "Targeted gene disruption of GFI1B in mice leads to embryonic lethality resulting from failure to produce definitive erythrocytes, hindering the study of Gfi-1B function in adult hematopoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24800817",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Growth factor independence 1b (gfi1b) is important for the maturation of erythroid cells and the regulation of embryonic globin expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Growth factor-independence 1b (Gfi1b) is a zinc finger transcription factor essential for erythroid and megakaryocytic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24800817",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Growth factor independence 1b (GFI1B) is a DNA binding repressor of transcription with vital functions in hematopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 1060,
"offsetInEndSection": 1191,
"text": "Conversely, loss of gfi1b silences runx-1, c-myb, ikaros and cd41, indicating that gfi1b is required for definitive hematopoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20861919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Gfi1 and Gfi1b: key regulators of hematopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 713,
"offsetInEndSection": 826,
"text": "We show that gfi1aa and gfi1b are expressed in the primitive and definitive sites of hematopoiesis in zebrafish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 312,
"text": "Targeted gene disruption of GFI1B in mice leads to embryonic lethality resulting from failure to produce definitive erythrocytes, hindering the study of Gfi-1B function in adult hematopoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24800817",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Growth factor independence 1b (gfi1b) is important for the maturation of erythroid cells and the regulation of embryonic globin expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Growth factor-independence 1b (Gfi1b) is a zinc finger transcription factor essential for erythroid and megakaryocytic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24800817",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Growth factor independence 1b (GFI1B) is a DNA binding repressor of transcription with vital functions in hematopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 1060,
"offsetInEndSection": 1191,
"text": "Conversely, loss of gfi1b silences runx-1, c-myb, ikaros and cd41, indicating that gfi1b is required for definitive hematopoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20861919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Gfi1 and Gfi1b: key regulators of hematopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 713,
"offsetInEndSection": 826,
"text": "We show that gfi1aa and gfi1b are expressed in the primitive and definitive sites of hematopoiesis in zebrafish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 312,
"text": "Targeted gene disruption of GFI1B in mice leads to embryonic lethality resulting from failure to produce definitive erythrocytes, hindering the study of Gfi-1B function in adult hematopoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24800817",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Growth factor independence 1b (gfi1b) is important for the maturation of erythroid cells and the regulation of embryonic globin expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23308270",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Gfi1b (growth factor independence 1b) is a zinc finger transcription factor essential for development of the erythroid and megakaryocytic lineages."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Growth factor-independence 1b (Gfi1b) is a zinc finger transcription factor essential for erythroid and megakaryocytic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22885124",
"endSection": "abstract",
"offsetInBeginSection": 683,
"offsetInEndSection": 1072,
"text": "In fact, we demonstrate that VPA treatment is able to induce the expression of growth factor-independent protein 1B (GFI1B) and of mixed-lineage leukemia translocated to chromosome 3 protein (MLLT3), which are crucial regulators of erythrocyte and megakaryocyte differentiation, and that the up-regulation of these genes is mediated by the histone hyperacetylation at their promoter sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Growth factor-independence 1b (Gfi1b) is a zinc finger transcription factor essential for erythroid and megakaryocytic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Growth factor independence-1B (Gfi-1B) is a transcriptional repressor essential for erythropoiesis and megakaryopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16177182",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Gfi-1B (growth factor independence-1B) gene is an erythroid-specific transcription factor, whose expression plays an essential role in erythropoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20826720",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Evidence that growth factor independence 1b regulates dormancy and peripheral blood mobilization of hematopoietic stem cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20826720",
"endSection": "abstract",
"offsetInBeginSection": 263,
"offsetInEndSection": 455,
"text": "We report here that adult mice conditionally deficient for the transcription Growth factor independence 1b (Gfi1b) show a significant expansion of functional HSCs in the bone marrow and blood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Growth factor-independence 1b (Gfi1b) is a zinc finger transcription factor essential for erythroid and megakaryocytic development"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Teleost growth factor independence (gfi) genes differentially regulate successive waves of hematopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 252,
"text": "Growth Factor Independence (Gfi) transcription factors play essential roles in hematopoiesis, differentially activating and repressing transcriptional programs required for hematopoietic stem/progenitor cell (HSPC) development and lineage specification"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16177182",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Gfi-1B (growth factor independence-1B) gene is an erythroid-specific transcription factor, whose expression plays an essential role in erythropoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Growth factor independence-1B (Gfi-1B) is a transcriptional repressor essential for erythropoiesis and megakaryopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18224412",
"endSection": "abstract",
"offsetInBeginSection": 1760,
"offsetInEndSection": 1878,
"text": "Our data indicate that Gfi-1B signalling is important for commitment and maturation of hematopoietic cell populations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Growth factor-independence 1b (Gfi1b) is a zinc finger transcription factor essential for erythroid and megakaryocytic development"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20826720",
"endSection": "abstract",
"offsetInBeginSection": 263,
"offsetInEndSection": 454,
"text": "We report here that adult mice conditionally deficient for the transcription Growth factor independence 1b (Gfi1b) show a significant expansion of functional HSCs in the bone marrow and blood"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16177182",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Gfi-1B (growth factor independence-1B) gene is an erythroid-specific transcription factor, whose expression plays an essential role in erythropoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 312,
"text": "Targeted gene disruption of GFI1B in mice leads to embryonic lethality resulting from failure to produce definitive erythrocytes, hindering the study of Gfi-1B function in adult hematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Growth factor independence-1B (Gfi-1B) is a transcriptional repressor essential for erythropoiesis and megakaryopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Growth factor-independence 1b (Gfi1b) is a zinc finger transcription factor essential for erythroid and megakaryocytic development"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16177182",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Gfi-1B (growth factor independence-1B) gene is an erythroid-specific transcription factor, whose expression plays an essential role in erythropoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 312,
"text": "Targeted gene disruption of GFI1B in mice leads to embryonic lethality resulting from failure to produce definitive erythrocytes, hindering the study of Gfi-1B function in adult hematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Growth factor independence-1B (Gfi-1B) is a transcriptional repressor essential for erythropoiesis and megakaryopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Growth factor-independence 1b (Gfi1b) is a zinc finger transcription factor essential for erythroid and megakaryocytic development"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22960038",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 252,
"text": "Growth Factor Independence (Gfi) transcription factors play essential roles in hematopoiesis, differentially activating and repressing transcriptional programs required for hematopoietic stem/progenitor cell (HSPC) development and lineage specification"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16177182",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Gfi-1B (growth factor independence-1B) gene is an erythroid-specific transcription factor, whose expression plays an essential role in erythropoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18224412",
"endSection": "abstract",
"offsetInBeginSection": 1760,
"offsetInEndSection": 1878,
"text": "Our data indicate that Gfi-1B signalling is important for commitment and maturation of hematopoietic cell populations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20124515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Growth factor independence-1B (Gfi-1B) is a transcriptional repressor essential for erythropoiesis and megakaryopoiesis"
}
]
| 5 | BioASQ-training5b | [
"http://www.uniprot.org/uniprot/GFI1B_HUMAN",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0030097",
"http://www.uniprot.org/uniprot/GFI1B_MOUSE"
]
| []
| 553bd2f0f321868558000008 | 18 |
yesno | Is rilonacept effective for pericarditis? | ['yes'] | [
"yes"
]
| ['Yes, rilonacept is effective for pericarditis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34459270",
"http://www.ncbi.nlm.nih.gov/pubmed/34556390",
"http://www.ncbi.nlm.nih.gov/pubmed/34599390",
"http://www.ncbi.nlm.nih.gov/pubmed/34528670",
"http://www.ncbi.nlm.nih.gov/pubmed/34569270"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34556390",
"endSection": "abstract",
"offsetInBeginSection": 783,
"offsetInEndSection": 1150,
"text": " Concerning acute recurrent pericarditis (RP), an innovative interaction between cardiologists, internists and pediatric rheumatologists led to the intuition of a pivotal role of IL-1 in recurrent pericarditis characterized by an evident inflammatory recurrent phenotype, and recent data have shown the striking efficacy of anakinra and rilonacept in these patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34599390",
"endSection": "abstract",
"offsetInBeginSection": 669,
"offsetInEndSection": 1258,
"text": "Pericarditis is regarded as a stereotypical response to an acute damage of the mesothelial cells of the pericardial layers. NLRP3 inflammasome, a macromolecular structure sensing damage and releasing pro-inflammatory cytokines, is centrally involved as it releases interleukin (IL)-1β, whose auto-induction feeds an autoinflammatory disease, mostly responsible for recurrences. Colchicine, an inhibitor of NLRP3 inflammasome formation, and IL-1-targeted therapies, such as anakinra and rilonacept, were found to effectively blunt the acute inflammation and reduce the risk for recurrences."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34569270",
"endSection": "abstract",
"offsetInBeginSection": 810,
"offsetInEndSection": 1069,
"text": "Currently, anakinra and rilonacept, have demonstrated beneficial impact in clinical outcomes with a reasonable safety profile in randomized clinical trials. There is still paucity of data regarding the use of canakinumab in the treatment of patients with RP. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34459270",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "Rilonacept: A Newly Approved Treatment for Recurrent Pericarditis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34459270",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "OBJECTIVE: To review the pharmacology, efficacy, and safety of rilonacept for the prevention and treatment of recurrent pericarditis (RP)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34459270",
"endSection": "abstract",
"offsetInBeginSection": 1552,
"offsetInEndSection": 1763,
"text": "CONCLUSION: Rilonacept is a safe, once weekly, subcutaneously administered IL-1 \"trap,\" indicated for the treatment of RP, and reduction in risk of recurrent pericarditis in adults and children ≥12 years of age."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34528670",
"endSection": "abstract",
"offsetInBeginSection": 394,
"offsetInEndSection": 835,
"text": "Overproduction of both IL-1α (released by inflamed/damaged pericardial cells) and IL-1β (released by inflammatory cells) is now a well-recognized therapeutic target in patients with recurrent idiopathic pericarditis. Currently, there are three available anti-IL-1 agents: anakinra (recombinant human IL-1Ra), rilonacept (a soluble decoy receptor 'trap', binding both IL-1α and IL-1β), and canakinumab (human monoclonal anti-IL-1β antibody). "
}
]
| 12 | BioASQ-training12b | null | null | 61f7cb37882a024a10000029 | 19 |
yesno | Are Conserved Nonexonic Elements (CNEEs) important in phylogenomics research? | ['yes'] | [
"yes"
]
| ['Yes. Conserved Nonexonic Elements (CNEEs) appear to be promising as phylogenomic markers, yielding phylogenetic resolution as high as for UCEs and introns but with fewer gaps, less ambiguity in alignments and with patterns of nucleotide substitution more consistent with the assumptions of commonly used methods of phylogenetic analysis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28417603",
"http://www.ncbi.nlm.nih.gov/pubmed/28637293"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28637293",
"endSection": "abstract",
"offsetInBeginSection": 1555,
"offsetInEndSection": 1865,
"text": "Overall, CNEEs appear to be promising as phylogenomic markers, yielding phylogenetic resolution as high as for UCEs and introns but with fewer gaps, less ambiguity in alignments and with patterns of nucleotide substitution more consistent with the assumptions of commonly used methods of phylogenetic analysis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28637293",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "Conserved Nonexonic Elements: A Novel Class of Marker for Phylogenomics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28417603",
"endSection": "abstract",
"offsetInBeginSection": 316,
"offsetInEndSection": 583,
"text": "Target capture for vertebrate animals is currently dominated by two approaches-anchored hybrid enrichment (AHE) and ultraconserved elements (UCE)-and both approaches have proven useful for addressing questions in phylogenomics, phylogeography and population genomics."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28637293",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "conserved nonexonic elements a novel class of marker for phylogenomics"
}
]
| 11 | BioASQ-training11b | null | null | 5a6e18d8b750ff4455000038 | 20 |
yesno | Does Rhamnose have any effect on aging? | ['yes'] | [
"yes"
]
| ['Yes, Rhamnose does have an effect on aging.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28855134",
"http://www.ncbi.nlm.nih.gov/pubmed/22099844"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28855134",
"endSection": "abstract",
"offsetInBeginSection": 740,
"offsetInEndSection": 892,
"text": "The monosaccharide analysis showed that rhamnose (Rha) and glucose (Glu) may play vital roles in maintaining the antioxidant and anti-aging activities. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22099844",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 830,
"text": "Some of these mechanisms will be reviewed as well as the capacity of fucose- and rhamnose-rich oligo- and polysaccharides (FROP and RROP) to counteract several of the mechanisms involved in skin aging."
}
]
| 11 | BioASQ-training11b | null | null | 5c840daf617e120c34000007 | 21 |
yesno | Is telomestatin, a novel statin drug used to treat high cholesterol? | ['no'] | [
"no"
]
| ['Telomestatin is a natural product isolated from Streptomyces anulatus 3533-SV4 and has been shown to be a very potent telomerase inhibitor and is used to treat cancer.', 'Telomestatin is a natural product isolated from Streptomyces anulatus 3533-SV4 and has been shown to be a very potent telomerase inhibitor.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/11878947",
"http://www.ncbi.nlm.nih.gov/pubmed/28611443",
"http://www.ncbi.nlm.nih.gov/pubmed/23909929",
"http://www.ncbi.nlm.nih.gov/pubmed/16652154",
"http://www.ncbi.nlm.nih.gov/pubmed/15283144",
"http://www.ncbi.nlm.nih.gov/pubmed/12917635"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11878947",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Telomestatin is a natural product isolated from Streptomyces anulatus 3533-SV4 and has been shown to be a very potent telomerase inhibitor."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11878947",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Telomestatin, a potent telomerase inhibitor that interacts quite specifically with the human telomeric intramolecular g-quadruplex."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12917635",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Activity of a novel G-quadruplex-interactive telomerase inhibitor, telomestatin (SOT-095), "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12917635",
"endSection": "abstract",
"offsetInBeginSection": 149,
"offsetInEndSection": 220,
"text": " G-quadruplex-interactive telomerase inhibitor, telomestatin (SOT-095),"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12917635",
"endSection": "abstract",
"offsetInBeginSection": 380,
"offsetInEndSection": 509,
"text": " We found that treatment with telomestatin reproducibly inhibited telomerase activity in the BCR-ABL-positive leukemic cell lines"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15283144",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "A novel telomerase inhibitor, telomestatin, isolated from Streptomyces anulatus is the most potent telomerase inhibitor so far."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15283144",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 93,
"text": "Telomerase inhibitor, telomestatin, a specific mechanism to interact with telomere structure"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15283144",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 232,
"text": "Telomestatin specifically inhibited telomerase without affecting reverse transcriptases and polymerases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15283144",
"endSection": "abstract",
"offsetInBeginSection": 233,
"offsetInEndSection": 379,
"text": "In addition, telomestatin induced telomere shortening, but its ratio was extremely faster than that observed in physiological telomere shortening."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15283144",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "A novel telomerase inhibitor, telomestatin, isolated from Streptomyces anulatus is the most potent telomerase inhibitor so far. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23909929",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 530,
"text": "ructure has been yet resolved for the complex with telomestatin, one of the most promising G-quadruplex-targeting anticancer drug candidates. Here"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28611443",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Telomestatin, a strong telomerase inhibitor with G-quadruplex stabilizing activity, is a potential therapeutic agent for treating cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15283144",
"endSection": "abstract",
"offsetInBeginSection": 871,
"offsetInEndSection": 961,
"text": "Thus, telomestatin provide the novel therapeutic molecular target for cancer chemotherapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16652154",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Telomerase inhibition with a novel G-quadruplex-interactive agent, telomestatin: in vitro and in vivo studies in acute leukemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12917635",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Activity of a novel G-quadruplex-interactive telomerase inhibitor, telomestatin (SOT-095), against human leukemia cells: involvement of ATM-dependent DNA damage response pathways."
}
]
| 11 | BioASQ-training11b | null | null | 623a24d6f0baec9a1b000002 | 22 |
yesno | Was modafinil tested for schizophrenia treatment? | ['yes'] | [
"yes"
]
| ['Yes. Modafinil has been shown to improve attention, memory, executive function and antipsychotic-induced parkinsonism in patients with schizophrenia. However, some authors have failed to demonstrate beneficial action of modafinil for schizophrenia.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23938173",
"http://www.ncbi.nlm.nih.gov/pubmed/22820555",
"http://www.ncbi.nlm.nih.gov/pubmed/22820554",
"http://www.ncbi.nlm.nih.gov/pubmed/23983964",
"http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"http://www.ncbi.nlm.nih.gov/pubmed/21909634",
"http://www.ncbi.nlm.nih.gov/pubmed/21565464",
"http://www.ncbi.nlm.nih.gov/pubmed/21412225",
"http://www.ncbi.nlm.nih.gov/pubmed/21109234",
"http://www.ncbi.nlm.nih.gov/pubmed/20810469",
"http://www.ncbi.nlm.nih.gov/pubmed/20653641",
"http://www.ncbi.nlm.nih.gov/pubmed/19914296",
"http://www.ncbi.nlm.nih.gov/pubmed/19689921",
"http://www.ncbi.nlm.nih.gov/pubmed/19572020",
"http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"http://www.ncbi.nlm.nih.gov/pubmed/18729534",
"http://www.ncbi.nlm.nih.gov/pubmed/18516718",
"http://www.ncbi.nlm.nih.gov/pubmed/18392753",
"http://www.ncbi.nlm.nih.gov/pubmed/17712350",
"http://www.ncbi.nlm.nih.gov/pubmed/17634412",
"http://www.ncbi.nlm.nih.gov/pubmed/17503979",
"http://www.ncbi.nlm.nih.gov/pubmed/17151173",
"http://www.ncbi.nlm.nih.gov/pubmed/17077439",
"http://www.ncbi.nlm.nih.gov/pubmed/16965205",
"http://www.ncbi.nlm.nih.gov/pubmed/16634707",
"http://www.ncbi.nlm.nih.gov/pubmed/16013898",
"http://www.ncbi.nlm.nih.gov/pubmed/15994572",
"http://www.ncbi.nlm.nih.gov/pubmed/15090936",
"http://www.ncbi.nlm.nih.gov/pubmed/15085092",
"http://www.ncbi.nlm.nih.gov/pubmed/24964814",
"http://www.ncbi.nlm.nih.gov/pubmed/25306261"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23938173",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "Modafinil improves antipsychotic-induced parkinsonism but not excessive daytime sleepiness, psychiatric symptoms or cognition in schizophrenia and schizoaffective disorder: a randomized, double-blind, placebo-controlled study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23938173",
"endSection": "abstract",
"offsetInBeginSection": 1382,
"offsetInEndSection": 1565,
"text": "CONCLUSION: The data suggest that modafinil was a safe adjunctive treatment which improved parkinsonian symptoms and signs in patients with schizophrenia or schizoaffective disorder. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820555",
"endSection": "abstract",
"offsetInBeginSection": 747,
"offsetInEndSection": 1027,
"text": "A review of its effects in schizophrenia suggests that modafinil facilitates cognitive functions, with pro-mnemonic effects and problem solving improvements. Emotional processing also appears to be enhanced by the drug, although to date there are only a limited number of studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820554",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "BACKGROUND: Modafinil, a putative cognitive enhancing drug, has previously been shown to improve performance of healthy volunteers as well as patients with attention deficit disorder and schizophrenia, mainly in tests of executive functions. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23983964",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "A review of modafinil and armodafinil as add-on therapy in antipsychotic-treated patients with schizophrenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23983964",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 487,
"text": "It has been suggested that modafinil and its isomer armodafinil as an add-on strategy to antipsychotic treatment in patients with schizophrenia may improve cognitive functioning, attenuate fatigue, inactiveness and other negative functions as well as weight gain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23983964",
"endSection": "abstract",
"offsetInBeginSection": 794,
"offsetInEndSection": 1235,
"text": "Evidence for the use of modafinil or armodafinil as add-on therapy to antipsychotic drugs to alleviate fatigue, sleepiness and inactivity is inconclusive. One cohort study and one out of two single-dose crossover RCTs in which modafinil addition was studied could demonstrate a positive effect. All five RCTs of modafinil (three RCTs) and armodafinil (two RCTs) addition with a longer study duration could not demonstrate a positive effect. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23983964",
"endSection": "abstract",
"offsetInBeginSection": 1351,
"offsetInEndSection": 2139,
"text": "In RCTs with a treatment duration of 4 weeks or more, however, no positive effect could be demonstrated on cognitive functioning with modafinil and armodafinil addition. Yet, four single-dose crossover RCTs of modafinil addition show significant positive effects on executive functioning, verbal memory span, visual memory, working memory, spatial planning, slowing in latency, impulse control and recognition of faces expressing sadness and sadness misattribution in the context of disgust recognition. The addition of modafinil or armodafinil to an antipsychotic regime, despite theoretical and preclinical considerations, has not been proved to enhance cognitive function, attenuate fatigue, enhance activity, improve negative symptoms and reduce weight in patients with schizophrenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "RATIONAL: In recent years, evidence suggests that modafinil may be useful for certain symptom domains of schizophrenia, especially for the negative and cognitive symptoms. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 1243,
"offsetInEndSection": 1405,
"text": "CONCLUSION: The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of schizophrenia particularly the negative symptoms. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21909634",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 324,
"text": "Modafinil is a wake-promoting drug that has been shown to improve attention, memory and executive function in the healthy population and in patients with schizophrenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21565464",
"endSection": "abstract",
"offsetInBeginSection": 1097,
"offsetInEndSection": 1261,
"text": "CONCLUSIONS: Results of this pilot trial do not support routine use of modafinil to counteract increased weight and metabolic diseases in patients taking clozapine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21412225",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Modafinil (2-((diphenylmethyl)sulfinyl)acetamide) is described as an atypical stimulant and is a putative cognition enhancer for schizophrenia, but the precise mechanisms of action remain unclear."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21109234",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 319,
"text": "Modafinil is a wake-promoting drug that has been shown to improve emotion discrimination in healthy individuals and attention and executive function in schizophrenia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810469",
"endSection": "abstract",
"offsetInBeginSection": 1613,
"offsetInEndSection": 1900,
"text": "CONCLUSIONS: These data support clinical evidence that modafinil may alleviate cognitive deficits in schizophrenia and also demonstrate the benefit of applying PLSR modeling to characterize functional brain networks in translational models relevant to central nervous system dysfunction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20653641",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 257,
"text": "Modafinil improves working memory in healthy subjects and individuals diagnosed with schizophrenia and Attention Deficit/Hyperactivity Disorder, though the effects of modafinil have not been evaluated on working memory in methamphetamine-dependent subjects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19914296",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "Modafinil is a psychostimulant approved for treating excessive sleepiness in adults; off-label uses (e.g., treatment of cognitive impairment in schizophrenia, ADHD and age-related dementias) are currently being explored. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19689921",
"endSection": "abstract",
"offsetInBeginSection": 1064,
"offsetInEndSection": 1241,
"text": "CONCLUSIONS: Results of this pilot trial do not support routine use of modafinil to treat negative symptoms, cognitive deficits, or wakefulness/fatigue in patients on clozapine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19572020",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 316,
"text": "We have previously shown that the amount of movement exhibited by patients with schizophrenia is positively correlated with the volume of left anterior cingulate cortex and that this quantity of movement can be increased by modafinil. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 456,
"text": "OBJECTIVE: Given recent reports about the off-label use of modafinil as an adjuvant for the treatment of antipsychotic-associated sedation in schizophrenia patients and the recent interest in its putative cognitive-enhancing effects in this population, we present a systematic review of available data on trials of modafinil as an adjuvant in the treatment of cognitive deficits, negative symptoms, and antipsychotic-induced fatigue, and its tolerability. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 1281,
"offsetInEndSection": 1648,
"text": "RESULTS: One of 4 reviewed studies found a significant effect of modafinil as an alerting agent for antipsychotic-induced fatigue and sedation. Neither of 2 reviewed studies found modafinil to improve negative symptoms of schizophrenia. Three of 6 reviewed studies showed that modafinil may improve short-term memory, attention, and the ability to shift mental sets. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 1972,
"offsetInEndSection": 2439,
"text": "CONCLUSIONS: While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of schizophrenia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 2743,
"offsetInEndSection": 2883,
"text": "Hence, before prescribing modafinil to a schizophrenia patient, the possible risks and benefits of each particular case should be evaluated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18729534",
"endSection": "abstract",
"offsetInBeginSection": 2211,
"offsetInEndSection": 2506,
"text": "Modafinil had a substantial placebo effect on outcomes such as fatigue, excessive sleepiness and depression in patients with traumatic brain injury, major depressive disorder, schizophrenia, post-polio fatigue and multiple sclerosis; however, it did not provide any benefit greater than placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18516718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "RATIONALE: The wake-promoting agent modafinil selectively improves neuropsychological task performance in healthy volunteers, in adults with attention deficit hyperactivity disorder (ADHD) and in schizophrenia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18392753",
"endSection": "abstract",
"offsetInBeginSection": 271,
"offsetInEndSection": 394,
"text": "Recently, however, modafinil has been shown to improve attentional set-shifting performance in patients with schizophrenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17712350",
"endSection": "abstract",
"offsetInBeginSection": 261,
"offsetInEndSection": 462,
"text": "In addition, modafinil shows initial promise for a variety of off-label indications in psychiatry, including treatment-resistant depression, attention-deficit/hyperactivity disorder, and schizophrenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17634412",
"endSection": "abstract",
"offsetInBeginSection": 226,
"offsetInEndSection": 396,
"text": "There is increasing interest in the use of modafinil to improve cognition in schizophrenia as well as in other disorders such as attention-deficit/hyperactivity disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17634412",
"endSection": "abstract",
"offsetInBeginSection": 560,
"offsetInEndSection": 702,
"text": "Initial findings indicate that modafinil may lead to better executive functioning and attentional performance in patients with schizophrenia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17503979",
"endSection": "abstract",
"offsetInBeginSection": 1501,
"offsetInEndSection": 1701,
"text": "CONCLUSIONS: Although no effect on negative symptoms was found, adjunctive therapy with modafinil may result in global improvements in patients with schizophrenia who have prominent negative symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17151173",
"endSection": "abstract",
"offsetInBeginSection": 972,
"offsetInEndSection": 1059,
"text": "CONCLUSIONS: Modafinil did not improve cognitive control in all schizophrenia patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17077439",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 492,
"text": ". These data suggest that modafinil increases quantifiable motor behaviour in schizophrenia and may have an impact on avolition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16965205",
"endSection": "abstract",
"offsetInBeginSection": 1537,
"offsetInEndSection": 1784,
"text": "One patient was on treatment with both modafinil and trazodone and reported no change after tapering each in separate discontinuation trials, while another 3 patients were taking sleeping medications and also noted no change after discontinuation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16634707",
"endSection": "abstract",
"offsetInBeginSection": 551,
"offsetInEndSection": 743,
"text": " Neuroprotective agents as add-on therapies (e.g., modafinil, erythropoietin, glycine, D-serine, memantine and celecoxib) are currently being evaluated in schizophrenia and related disorders. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16013898",
"endSection": "abstract",
"offsetInBeginSection": 666,
"offsetInEndSection": 887,
"text": "In the modafinil (N = 10) and placebo (N = 10) groups, fatigue improved significantly over time (p < .01), but there were no differences between groups on changes in fatigue, positive and negative symptoms, or cognition. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15994572",
"endSection": "abstract",
"offsetInBeginSection": 929,
"offsetInEndSection": 1136,
"text": "CONCLUSIONS: Modafinil modulates anterior cingulate cortex function in chronic schizophrenia but its beneficial cognitive effects may be restricted to a subset of patients requiring further characterisation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15090936",
"endSection": "abstract",
"offsetInBeginSection": 687,
"offsetInEndSection": 873,
"text": "Modafinil significantly improved overall clinical condition, with 64% and 82% of patients rated as clinically improved at week 4 by a blinded clinician and the investigator respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15090936",
"endSection": "abstract",
"offsetInBeginSection": 955,
"offsetInEndSection": 1068,
"text": "Modafinil significantly improved fatigue (P = 0.025, week 3) and tended to improve cognitive functioning scores. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15090936",
"endSection": "abstract",
"offsetInBeginSection": 1349,
"offsetInEndSection": 1597,
"text": "Although preliminary, these results suggest modafinil may be an effective and well-tolerated adjunct treatment that improves global functioning and clinical condition, and reduces fatigue in patients with schizophrenia or schizoaffective disorder. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15085092",
"endSection": "abstract",
"offsetInBeginSection": 666,
"offsetInEndSection": 807,
"text": "Modafinil had some cognitive enhancing properties in schizophrenia similar to those observed in healthy adults and adult patients with ADHD. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15085092",
"endSection": "abstract",
"offsetInBeginSection": 1222,
"offsetInEndSection": 1407,
"text": "Modafinil may have potential as an important therapy for cognitive impairment in patients with schizophrenia, particularly because of its beneficial effects on attentional set shifting."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 1887,
"offsetInEndSection": 2340,
"text": "While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of schizophrenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 444,
"text": "Given recent reports about the off-label use of modafinil as an adjuvant for the treatment of antipsychotic-associated sedation in schizophrenia patients and the recent interest in its putative cognitive-enhancing effects in this population, we present a systematic review of available data on trials of modafinil as an adjuvant in the treatment of cognitive deficits, negative symptoms, and antipsychotic-induced fatigue, and its tolerability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 1190,
"offsetInEndSection": 1339,
"text": "The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of schizophrenia particularly the negative symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23983964",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 485,
"text": " It has been suggested that modafinil and its isomer armodafinil as an add-on strategy to antipsychotic treatment in patients with schizophrenia may improve cognitive functioning, attenuate fatigue, inactiveness and other negative functions as well as weight gain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23983964",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 487,
"text": "It has been suggested that modafinil and its isomer armodafinil as an add-on strategy to antipsychotic treatment in patients with schizophrenia may improve cognitive functioning, attenuate fatigue, inactiveness and other negative functions as well as weight gain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 1243,
"offsetInEndSection": 1404,
"text": "CONCLUSION: The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of schizophrenia particularly the negative symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 455,
"text": "OBJECTIVE: Given recent reports about the off-label use of modafinil as an adjuvant for the treatment of antipsychotic-associated sedation in schizophrenia patients and the recent interest in its putative cognitive-enhancing effects in this population, we present a systematic review of available data on trials of modafinil as an adjuvant in the treatment of cognitive deficits, negative symptoms, and antipsychotic-induced fatigue, and its tolerability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 1971,
"offsetInEndSection": 2437,
"text": "CONCLUSIONS: While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of schizophrenia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23938173",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "Modafinil improves antipsychotic-induced parkinsonism but not excessive daytime sleepiness, psychiatric symptoms or cognition in schizophrenia and schizoaffective disorder: a randomized, double-blind, placebo-controlled study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23938173",
"endSection": "abstract",
"offsetInBeginSection": 1382,
"offsetInEndSection": 1565,
"text": "CONCLUSION: The data suggest that modafinil was a safe adjunctive treatment which improved parkinsonian symptoms and signs in patients with schizophrenia or schizoaffective disorder. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of schizophrenia particularly the negative symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15090936",
"endSection": "abstract",
"offsetInBeginSection": 1349,
"offsetInEndSection": 1596,
"text": "Although preliminary, these results suggest modafinil may be an effective and well-tolerated adjunct treatment that improves global functioning and clinical condition, and reduces fatigue in patients with schizophrenia or schizoaffective disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23983964",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 487,
"text": "It has been suggested that modafinil and its isomer armodafinil as an add-on strategy to antipsychotic treatment in patients with schizophrenia may improve cognitive functioning, attenuate fatigue, inactiveness and other negative functions as well as weight gain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 1909,
"offsetInEndSection": 2361,
"text": "While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of schizophrenia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 1208,
"offsetInEndSection": 1356,
"text": "The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of schizophrenia particularly the negative symptoms"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820554",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Modafinil, a putative cognitive enhancing drug, has previously been shown to improve performance of healthy volunteers as well as patients with attention deficit disorder and schizophrenia, mainly in tests of executive functions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 1909,
"offsetInEndSection": 2361,
"text": "While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of schizophrenia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 1208,
"offsetInEndSection": 1356,
"text": "The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of schizophrenia particularly the negative symptoms"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 1909,
"offsetInEndSection": 2361,
"text": "While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of schizophrenia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 1208,
"offsetInEndSection": 1356,
"text": "The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of schizophrenia particularly the negative symptoms"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 444,
"text": "Given recent reports about the off-label use of modafinil as an adjuvant for the treatment of antipsychotic-associated sedation in schizophrenia patients and the recent interest in its putative cognitive-enhancing effects in this population, we present a systematic review of available data on trials of modafinil as an adjuvant in the treatment of cognitive deficits, negative symptoms, and antipsychotic-induced fatigue, and its tolerability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 1909,
"offsetInEndSection": 2361,
"text": "While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of schizophrenia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 1208,
"offsetInEndSection": 1356,
"text": "The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of schizophrenia particularly the negative symptoms"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 444,
"text": "Given recent reports about the off-label use of modafinil as an adjuvant for the treatment of antipsychotic-associated sedation in schizophrenia patients and the recent interest in its putative cognitive-enhancing effects in this population, we present a systematic review of available data on trials of modafinil as an adjuvant in the treatment of cognitive deficits, negative symptoms, and antipsychotic-induced fatigue, and its tolerability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026265",
"endSection": "abstract",
"offsetInBeginSection": 1909,
"offsetInEndSection": 2361,
"text": "While the available data suggest that modafinil is generally well tolerated and may have some efficacy in the treatment of antipsychotic-induced sedation and cognitive domains, the small sample sizes, contradictory results, and methodological differences between trials, especially with respect to cognitive testing, make it difficult to draw firm conclusions about the overall effectiveness of modafinil as an adjunct in the treatment of schizophrenia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21947320",
"endSection": "abstract",
"offsetInBeginSection": 1208,
"offsetInEndSection": 1356,
"text": "The present study indicates modafinil as a potential adjunctive treatment strategy for treatment of schizophrenia particularly the negative symptoms"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820554",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Modafinil, a putative cognitive enhancing drug, has previously been shown to improve performance of healthy volunteers as well as patients with attention deficit disorder and schizophrenia, mainly in tests of executive functions"
}
]
| 5 | BioASQ-training5b | [
"http://www.biosemantics.org/jochem#4259639",
"http://www.disease-ontology.org/api/metadata/DOID:5419"
]
| []
| 54fc845e6ea36a810c000005 | 23 |
yesno | Is Alpers disease inherited in an autosomal recessive mode? | ['yes'] | [
"yes"
]
| ['Alpers disease is a fatal neurogenetic disorder first described more than 70 years ago. It is an autosomal recessive, developmental mitochondrial DNA depletion disorder characterized by deficiency in mitochondrial DNA polymerase gamma (POLG) catalytic activity, refractory seizures, neurodegeneration, and liver disease.', 'Alpers-Huttenlocher syndrome (AHS) is a very rare autosomal recessive disorder', 'Alpers-Huttenlocher syndrome (AHS) is a very rare autosomal recessive disorder', 'Alpers-Huttenlocher syndrome (AHS) is a very rare autosomal recessive disorder', 'Alpers-Huttenlocher syndrome (AHS) is a very rare autosomal recessive disorder', 'Alpers-Huttenlocher syndrome (AHS) is a very rare autosomal recessive disorder'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22006280",
"http://www.ncbi.nlm.nih.gov/pubmed/16181814",
"http://www.ncbi.nlm.nih.gov/pubmed/15122711",
"http://www.ncbi.nlm.nih.gov/pubmed/7897414",
"http://www.ncbi.nlm.nih.gov/pubmed/1861211",
"http://www.ncbi.nlm.nih.gov/pubmed/21451360",
"http://www.ncbi.nlm.nih.gov/pubmed/22000311"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22006280",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Alpers-Huttenlocher syndrome (AHS) is a very rare autosomal recessive disorder"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16181814",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Alpers syndrome is an autosomal recessive mitochondrial DNA depletion disorder that affects children and young adults"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15122711",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 321,
"text": "Alpers' syndrome is a fatal neurogenetic disorder first described more than 70 years ago. It is an autosomal recessive, developmental mitochondrial DNA depletion disorder characterized by deficiency in mitochondrial DNA polymerase gamma (POLG) catalytic activity, refractory seizures, neurodegeneration, and liver disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7897414",
"endSection": "abstract",
"offsetInBeginSection": 448,
"offsetInEndSection": 883,
"text": "Histopathological findings in both patients ((a) chronic hepatitis with prominent bile duct proliferation, fatty change, and fibrosis; (b) in the brain a patchy destruction of the cerebral cortex, predominantly involving striate cortex) were characteristic of progressive neuronal degeneration of childhood with liver disease--Alpers-Huttenlocher syndrome--a rare autosomal recessive disorder usually seen in infants and young children"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7897414",
"endSection": "abstract",
"offsetInBeginSection": 881,
"offsetInEndSection": 1317,
"text": "Histopathological findings in both patients ((a) chronic hepatitis with prominent bile duct proliferation, fatty change, and fibrosis; (b) in the brain a patchy destruction of the cerebral cortex, predominantly involving striate cortex) were characteristic of progressive neuronal degeneration of childhood with liver disease--Alpers-Huttenlocher syndrome--a rare autosomal recessive disorder usually seen in infants and young children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22000311",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Alpers syndrome is a rare autosomal recessive hepatocerebral degenerative disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21451360",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Alpers disease is a recessive mitochondrial disorder caused by mutations in POLG1 and characterized primarily by progressive neurological and hepatic degeneration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7897414",
"endSection": "abstract",
"offsetInBeginSection": 881,
"offsetInEndSection": 1317,
"text": "Histopathological findings in both patients ((a) chronic hepatitis with prominent bile duct proliferation, fatty change, and fibrosis; (b) in the brain a patchy destruction of the cerebral cortex, predominantly involving striate cortex) were characteristic of progressive neuronal degeneration of childhood with liver disease--Alpers-Huttenlocher syndrome--a rare autosomal recessive disorder usually seen in infants and young children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16181814",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "Alpers syndrome is an autosomal recessive mitochondrial DNA depletion disorder that affects children and young adults."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21451360",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Alpers disease is a recessive mitochondrial disorder caused by mutations in POLG1 and characterized primarily by progressive neurological and hepatic degeneration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1861211",
"endSection": "abstract",
"offsetInBeginSection": 1596,
"offsetInEndSection": 1829,
"text": "We conclude that Alpers disease can be a cause of rapidly progressive liver failure in early childhood. Although the cause of this autosomal recessive disease is not known, it does not appear to be related to peroxisomal dysfunction."
}
]
| 5 | BioASQ-training5b | []
| []
| 5718a69e7de986d80d00000a | 24 |
yesno | Are there interactomes available for POU5F1 and SOX2? | ['yes'] | [
"yes"
]
| ['Yes. Long-range chromosomal interactions on putative enhancers of POU5F1 and SOX2 genes in human embryonic stem cells (hESCs) have been assayed using 4C-Seq technique. Their frequent interacting regions mainly overlap with early DNA replication domains. The interactomes are associated with active histone marks and enriched with 5-hydroxymethylcytosine sites.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23549118"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 817,
"text": "We assayed long-range chromosomal interactions on putative enhancers of POU5F1 and SOX2 genes in human embryonic stem cells (hESCs) using 4C-Seq technique. We discovered that their frequent interacting regions mainly overlap with early DNA replication domains. The interactomes are associated with active histone marks and enriched with 5-hydroxymethylcytosine sites. In hESCs, genes within the interactomes have elevated expression. Additionally, some genes associated with the POU5F1 enhancer contribute to pluripotency. Binding sites for multiple DNA binding proteins, including ATF3, CTCF, GABPA, JUND, NANOG, RAD21 and YY1, are enriched in both interactomes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23549118",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The interactomes of POU5F1 and SOX2 enhancers in human embryonic stem cells."
}
]
| 5 | BioASQ-training5b | [
"http://www.uniprot.org/uniprot/PO5F1_HUMAN",
"http://www.uniprot.org/uniprot/PO5F1_MACMU",
"http://www.uniprot.org/uniprot/PO5F1_DANRE",
"http://www.uniprot.org/uniprot/PO5F1_PIG",
"http://www.uniprot.org/uniprot/PO5F1_PANTR",
"http://www.uniprot.org/uniprot/PO5F1_BOVIN",
"http://www.uniprot.org/uniprot/PO5F1_MOUSE",
"http://www.uniprot.org/uniprot/SOX2_CHICK",
"http://www.uniprot.org/uniprot/SOX2_DANRE",
"http://www.uniprot.org/uniprot/NANOG_HUMAN",
"http://www.uniprot.org/uniprot/NANOG_MUSMM",
"http://www.uniprot.org/uniprot/NANOG_BOVIN",
"http://www.uniprot.org/uniprot/NANOG_PANTR",
"http://www.uniprot.org/uniprot/NANOG_MACFA"
]
| []
| 56c85f675795f9a73e000013 | 25 |
yesno | Is there any linear-time and linear-space algorithm for the computation of avoided words in biological sequences? | ['yes'] | [
"yes"
]
| ['Yes. There is a linear-time and linear-space algorithm for the computation of avoided words of length k in a given sequence x.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28293277"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293277",
"endSection": "abstract",
"offsetInBeginSection": 1526,
"offsetInEndSection": 1979,
"text": "The systematic search for avoided words is particularly useful for biological sequence analysis. We present a linear-time and linear-space algorithm for the computation of avoided words of lengthkin a given sequencex. We suggest a modification to this algorithm so that it computes all avoided words ofx, irrespective of their length, within the same time complexity. We also present combinatorial results with regards to avoided words and absent words."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293277",
"endSection": "abstract",
"offsetInBeginSection": 365,
"offsetInEndSection": 468,
"text": "We present a linear-time and linear-space algorithm for the computation of avoided words of length <br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293277",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 364,
"text": "<b>BACKGROUND</b>: The deviation of the observed frequency of a word <br><b>RESULTS</b>: In this article, we propose an [Formula: see text]-time and [Formula: see text]-space algorithm to compute all [Formula: see text]-avoided words of length <br><b>CONCLUSIONS</b>: The systematic search for avoided words is particularly useful for biological sequence analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293277",
"endSection": "abstract",
"offsetInBeginSection": 338,
"offsetInEndSection": 436,
"text": "We present a linear-time and linear-space algorithm for the computation of avoided words of length"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293277",
"endSection": "abstract",
"offsetInBeginSection": 1647,
"offsetInEndSection": 1770,
"text": "We present a linear-time and linear-space algorithm for the computation of avoided words of length k in a given sequence x."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293277",
"endSection": "abstract",
"offsetInBeginSection": 608,
"offsetInEndSection": 943,
"text": "Hence, computing all such words naïvely can be a very time-consuming procedure, in particular for large k. RESULTS In this article, we propose an [Formula: see text]-time and [Formula: see text]-space algorithm to compute all [Formula: see text]-avoided words of length k in a given sequence of length n over a fixed-sized alphabet."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293277",
"endSection": "abstract",
"offsetInBeginSection": 944,
"offsetInEndSection": 1154,
"text": "We also present a time-optimal [Formula: see text]-time algorithm to compute all [Formula: see text]-avoided words (of any length) in a sequence of length n over an integer alphabet of size [Formula: see text]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293277",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1867,
"text": "the deviation of the observed frequency of a word from its expected frequency in a given sequence is used to determine whether or not the word is this concept is particularly useful in dna linguistic analysis the value of the deviation of denoted by formula see text effectively characterises the extent of a word by its edge contrast in the context in which it occurs a word of length formula see text is a formula see text avoided word in if formula see text for a given threshold formula see text notice that such a word may be completely from hence computing all such words naïvely can be a very time consuming procedure in particular for large in this article we propose an formula see text time and formula see text space algorithm to compute all formula see text avoided words of length in a given sequence of length over a fixed sized alphabet we also present a time optimal formula see text time algorithm to compute all formula see text avoided words of any length in a sequence of length over an integer alphabet of size formula see text in addition we provide a tight asymptotic upper bound for the number of formula see text avoided words over an integer alphabet and the expected length of the longest one we make available an implementation of our algorithm experimental results using both real and synthetic data show the efficiency and applicability of our implementation in biological sequence analysis the systematic search for avoided words is particularly useful for biological sequence analysis we present a linear time and linear space algorithm for the computation of avoided words of length in a given sequence we suggest a modification to this algorithm so that it computes all avoided words of irrespective of their length within the same time complexity we also present combinatorial results with regards to avoided words and absent words."
}
]
| 11 | BioASQ-training11b | null | null | 5a6d022ab750ff445500002a | 26 |
yesno | Is SARS virus interacting with ACE2 encoded protein? | ['yes'] | [
"yes"
]
| ['Yes,\nThe infection of target cells by the SARS CoV is mediated through the interaction of the viral Spike (S) protein (1255 amino acids) and its cellular receptor, angiotensin-converting enzyme 2 (ACE2).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26487711",
"http://www.ncbi.nlm.nih.gov/pubmed/27082314",
"http://www.ncbi.nlm.nih.gov/pubmed/29190287",
"http://www.ncbi.nlm.nih.gov/pubmed/30356097",
"http://www.ncbi.nlm.nih.gov/pubmed/30102747"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30102747",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 286,
"text": "The trimeric SARS coronavirus (SARS-CoV) surface spike (S) glycoprotein consisting of three S1-S2 heterodimers binds the cellular receptor angiotensin-converting enzyme 2 (ACE2) and mediates fusion of the viral and cellular membranes through a pre- to postfusion conformation transition"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30356097",
"endSection": "abstract",
"offsetInBeginSection": 133,
"offsetInEndSection": 369,
"text": "The viral spike glycoprotein (S) utilizes angiotensin-converting enzyme 2 (ACE2) as a host protein receptor and mediates fusion of the viral and host membranes, making S essential to viral entry into host cells and host species tropism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29190287",
"endSection": "abstract",
"offsetInBeginSection": 1538,
"offsetInEndSection": 1690,
"text": "Cell entry studies demonstrated that three newly identified SARSr-CoVs with different S protein sequences are all able to use human ACE2 as the receptor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27082314",
"endSection": "abstract",
"offsetInBeginSection": 837,
"offsetInEndSection": 1145,
"text": "Angiotensin-converting enzyme 2 (ACE2), a relatively new member of the RAS, has drawn extensive attention since 2003, because of the findings that ACE2 is the receptor for SARS Corona virus and that maintenance of normal ACE2 levels in the lung is beneficial for the host to combat inflammatory lung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26487711",
"endSection": "abstract",
"offsetInBeginSection": 147,
"offsetInEndSection": 345,
"text": "The infection of target cells by the SARS CoV is mediated through the interaction of the viral Spike (S) protein (1255 amino acids) and its cellular receptor, angiotensin-converting enzyme 2 (ACE2)."
}
]
| 11 | BioASQ-training11b | null | null | 5e80675d835f4e4777000026 | 27 |
End of preview. Expand
in Data Studio
README.md exists but content is empty.
- Downloads last month
- 26