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|---|---|---|---|---|---|---|---|---|---|---|---|---|
yesno
|
Is Semagacestat effective for treatment of Alzheimer's disease?
|
['no']
|
[
"no"
] |
['No. In clinical trial semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability. Semagacestat was associated with more adverse events, including skin cancers and infections.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27567808",
"http://www.ncbi.nlm.nih.gov/pubmed/23785331",
"http://www.ncbi.nlm.nih.gov/pubmed/23883379",
"http://www.ncbi.nlm.nih.gov/pubmed/23196551",
"http://www.ncbi.nlm.nih.gov/pubmed/24983746",
"http://www.ncbi.nlm.nih.gov/pubmed/25292430",
"http://www.ncbi.nlm.nih.gov/pubmed/21149978",
"http://www.ncbi.nlm.nih.gov/pubmed/28978478"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28978478",
"endSection": "abstract",
"offsetInBeginSection": 173,
"offsetInEndSection": 402,
"text": "However, a large phase 3 trial of semagacestat, a potential non-transition state analog (non-TSA) GSI, in patients with Alzheimer's disease (AD) was terminated due to unexpected aggravation of cognitive deficits and side effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27567808",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "BACKGROUND: In a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (semagacestat) was associated with poorer cognitive outcomes in Alzheimer's disease (AD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25292430",
"endSection": "abstract",
"offsetInBeginSection": 228,
"offsetInEndSection": 398,
"text": "A clinical trial with the wide-spectrum γ-secretase inhibitor semagacestat has, however, demonstrated that global inhibition of all γ-secretases causes serious toxicity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24983746",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "OBJECTIVE: Semagacestat, a γ-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with Alzheimer's disease (IDENTITY trials), and clinical development was halted. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23883379",
"endSection": "abstract",
"offsetInBeginSection": 2360,
"offsetInEndSection": 2626,
"text": "CONCLUSIONS: As compared with placebo, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability. Semagacestat was associated with more adverse events, including skin cancers and infections."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27567808",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "BACKGROUND\nIn a recent report, 76 weeks' treatment with a gamma-secretase inhibitor (semagacestat) was associated with poorer cognitive outcomes in Alzheimer's disease (AD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23883379",
"endSection": "abstract",
"offsetInBeginSection": 2539,
"offsetInEndSection": 2631,
"text": "Semagacestat was associated with more adverse events, including skin cancers and infections."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23883379",
"endSection": "abstract",
"offsetInBeginSection": 2366,
"offsetInEndSection": 2538,
"text": "CONCLUSIONS\nAs compared with placebo, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24983746",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 209,
"text": "OBJECTIVE\nSemagacestat, a γ-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with Alzheimer's disease (IDENTITY trials), and clinical development was halted."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23785331",
"endSection": "abstract",
"offsetInBeginSection": 436,
"offsetInEndSection": 640,
"text": "Recently disclosed Phase III findings on semagacestat indicated that Alzheimer's disease (AD) patients on this drug showed significantly worsened cognitive function compared to those treated with placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21149978",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "The recent failure of semagacestat in two large Phase III studies questions the value of γ-secretase inhibitors in treating Alzheimer's disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23883379",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 229,
"text": "A phase 3 trial of semagacestat for treatment of Alzheimer's disease.As compared with placebo, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23196551",
"endSection": "abstract",
"offsetInBeginSection": 754,
"offsetInEndSection": 983,
"text": "Preliminary results from Phase III studies showed that semagacestat failed to slow disease progression, and it was associated with worsening of clinical measures of cognition and the ability to perform activities of daily living. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27567808",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 287,
"text": "Changes in Neuropsychiatric Inventory Associated with Semagacestat Treatment of Alzheimer's Disease.In participants with mild to moderate AD, high dose semagacestat treatment was associated with greater severity and faster worsening of NPS in a pattern resembling an agitated depression. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23883379",
"endSection": "abstract",
"offsetInBeginSection": 1950,
"offsetInEndSection": 2164,
"text": "Patients treated with semagacestat lost more weight and had more skin cancers and infections, treatment discontinuations due to adverse events, and serious adverse events (P<0.001 for all comparisons with placebo)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24983746",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 217,
"text": "<b>OBJECTIVE</b>: Semagacestat, a γ-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with Alzheimer's disease (IDENTITY trials), and clinical development was halted."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24983746",
"endSection": "abstract",
"offsetInBeginSection": 898,
"offsetInEndSection": 1099,
"text": "Other relevant safety findings associated with semagacestat treatment included cognitive and functional worsening, skin-related TEAEs, renal and hepatic changes, increased QT interval, and weight loss."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23883379",
"endSection": "abstract",
"offsetInBeginSection": 1896,
"offsetInEndSection": 2113,
"text": "Patients treated with semagacestat lost more weight and had more skin cancers and infections, treatment discontinuations due to adverse events, and serious adverse events (P<0.001 for all comparisons with placebo)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24983746",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Semagacestat, a γ-secretase inhibitor, demonstrated an unfavorable risk-benefit profile in a Phase 3 study of patients with Alzheimer's disease (IDENTITY trials), and clinical development was halted."
}
] | 11 |
BioASQ-training11b
| null | null |
5c73acf27c78d6947100008a
| 324 |
yesno
|
Is Netrin-1 a secreted protein?
|
['yes']
|
[
"yes"
] |
['Yes,\nnetrin-1 is a secreted protein.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21303223",
"http://www.ncbi.nlm.nih.gov/pubmed/17174565",
"http://www.ncbi.nlm.nih.gov/pubmed/26039999",
"http://www.ncbi.nlm.nih.gov/pubmed/28174720",
"http://www.ncbi.nlm.nih.gov/pubmed/22046354",
"http://www.ncbi.nlm.nih.gov/pubmed/24174661"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21303223",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 109,
"text": "The axon guidance cues netrin-1 is a secreted protein overexpressed in many different cancer tissues"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24174661",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 229,
"text": "Netrin-1 is a secreted protein that directs long-range axon guidance during early stages of neural circuit formation and continues to be expressed in the mammalian forebrain during the postnatal period of peak synapse formation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26039999",
"endSection": "abstract",
"offsetInBeginSection": 292,
"offsetInEndSection": 384,
"text": " Netrin-1, a laminin-related secreted protein, displays proto-oncogenic activity in cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28174720",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 108,
"text": "Netrin-1, a multifunctional secreted protein, is up-regulated in cancer and inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22046354",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 135,
"text": "etrin-1 is a laminin-related secreted protein, is highly induced after tissue injury, and may serve as a marker of injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17174565",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Netrins are a family of secreted protein related to laminin and act as tropic cues directing axon growth and cell migration during neural development. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c89461675a4a5d219000013
| 325 |
yesno
|
Is Lennox-Gastaut Syndrome usually diagnosed in older adults?
|
['no']
|
[
"no"
] |
['Lennox-Gastaut syndrome (LGS) is a severe pediatric epilepsy syndrome characterized by mixed seizures, cognitive decline, and generalized slow (<3 Hz) spike wave discharges on electroencephalography.', 'lennox-gastaut syndrome (lgs) is a severe pediatric epilepsy syndrome characterized by mixed seizures, cognitive decline, and generalized slow (<3 hz) spike wave discharges on electroencephalography.', ' children with Lennox-Gastaut syndrome Lennox-Gastaut syndrome (LGS) is a severe pediatric epilepsy syndrome characterized by mixed seizures, cognitive decline, and generalized slow (<3 Hz) spike wave discharges on electroencephalography']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22576075",
"http://www.ncbi.nlm.nih.gov/pubmed/8029151",
"http://www.ncbi.nlm.nih.gov/pubmed/26166587",
"http://www.ncbi.nlm.nih.gov/pubmed/24659735",
"http://www.ncbi.nlm.nih.gov/pubmed/20542434",
"http://www.ncbi.nlm.nih.gov/pubmed/26945476",
"http://www.ncbi.nlm.nih.gov/pubmed/9400037",
"http://www.ncbi.nlm.nih.gov/pubmed/20518600"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26945476",
"endSection": "abstract",
"offsetInBeginSection": 583,
"offsetInEndSection": 729,
"text": "We studied 15 LGS patients (mean age ± 1 standard deviation [SD] = 28.7 ± 10.6 years) and 17 healthy controls (mean age ± 1 SD = 27.6 ± 6.6 years)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24659735",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 129,
"text": " children with Lennox-Gastaut syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26166587",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Lennox-Gastaut syndrome (LGS) is a severe pediatric epilepsy syndrome characterized by mixed seizures, cognitive decline, and generalized slow (<3 Hz) spike wave discharges on electroencephalography"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8029151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Clinical course and results of therapy were analysed in the group of 92 children, aged between 3 and 9 years, with diagnosed Lennox-Gastaut syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22576075",
"endSection": "abstract",
"offsetInBeginSection": 427,
"offsetInEndSection": 659,
"text": "We report the case of a 27-year-old man with a neurodevelopmental syndrome due to a 15q duplication, with intellectual disability, psychiatric disturbances, and an epileptic phenotype diagnosed as late-onset Lennox-Gastaut syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20518600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 247,
"text": "Lennox-Gastaut syndrome is a relatively rare epilepsy syndrome that usually begins in early-mid childhood and is characterized by multiple seizure types, particularly generalized seizures, which are often resistant to antiepileptic drug medication"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20542434",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "Lennox-Gastaut Syndrome is a severe childhood epilepsy syndrome characterised by the diagnostic triad of a slow spike and wave pattern on electroencephalogram, multiple seizure types and developmental delay"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22576075",
"endSection": "abstract",
"offsetInBeginSection": 427,
"offsetInEndSection": 660,
"text": "We report the case of a 27-year-old man with a neurodevelopmental syndrome due to a 15q duplication, with intellectual disability, psychiatric disturbances, and an epileptic phenotype diagnosed as late-onset Lennox-Gastaut syndrome.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9400037",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "The Lennox-Gastaut syndrome, a severe form of epilepsy that usually begins in early childhood, is difficult to treat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20518600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 248,
"text": "Lennox-Gastaut syndrome is a relatively rare epilepsy syndrome that usually begins in early-mid childhood and is characterized by multiple seizure types, particularly generalized seizures, which are often resistant to antiepileptic drug medication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19588340",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 400,
"text": "The Lennox-Gastaut syndrome is an age-specific disorder, characterised by epileptic seizures, a characteristic electroencephalogram (EEG), psychomotor delay and behaviour disorders. It occurs more frequently in males and onset is usually before the age of eight, with a peak between three and five years. Late cases occurring in adolescence and early adulthood have rarely been reported. "
}
] | 6 |
BioASQ-training6b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:0050561",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D065768"
] | null |
58dbb4f08acda3452900001a
| 326 |
yesno
|
Can Pentraxin 3 predict outcomes of sepsis?
|
['yes']
|
[
"yes"
] |
['Yes, Pentraxin 3 s an objective biochemical marker in diagnosis of sepsis; it is helpful in assessment of severity and prognosis of sepsis; it also has a certain clinical value in the assessment of sepsis cardiovascular function damage.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/15977234",
"http://www.ncbi.nlm.nih.gov/pubmed/25001601",
"http://www.ncbi.nlm.nih.gov/pubmed/25227610",
"http://www.ncbi.nlm.nih.gov/pubmed/26982005",
"http://www.ncbi.nlm.nih.gov/pubmed/27864924",
"http://www.ncbi.nlm.nih.gov/pubmed/26872435",
"http://www.ncbi.nlm.nih.gov/pubmed/24958171",
"http://www.ncbi.nlm.nih.gov/pubmed/23341967",
"http://www.ncbi.nlm.nih.gov/pubmed/20119647",
"http://www.ncbi.nlm.nih.gov/pubmed/22278372",
"http://www.ncbi.nlm.nih.gov/pubmed/26717657",
"http://www.ncbi.nlm.nih.gov/pubmed/11445697",
"http://www.ncbi.nlm.nih.gov/pubmed/25530683",
"http://www.ncbi.nlm.nih.gov/pubmed/25048752",
"http://www.ncbi.nlm.nih.gov/pubmed/25591437",
"http://www.ncbi.nlm.nih.gov/pubmed/24039869",
"http://www.ncbi.nlm.nih.gov/pubmed/21423699"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26872435",
"endSection": "abstract",
"offsetInBeginSection": 1447,
"offsetInEndSection": 1708,
"text": "As compared with low serum PTX3and sTWEAK cases, cirrhotic patients with high serum PTX3/sTWEAK levels a have higher probability of new severe infections, severe sepsis, septic shock, type 1 hepatorenal syndrome, in-hospital, and 3-month follow-up mortalities. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25048752",
"endSection": "abstract",
"offsetInBeginSection": 1350,
"offsetInEndSection": 1543,
"text": "Neonates with high nPTX3 concentrations also have lowered APGAR scores, increased rate of respiratory distress syndrome, clinical sepsis, IVH, necrotizing enterocolitis and prolonged NICU stay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26717657",
"endSection": "abstract",
"offsetInBeginSection": 3688,
"offsetInEndSection": 4106,
"text": "In terms of predicting the prognosis of sepsis with heart failure complications, the PTX3 value's area under ROC curve was larger than that of BNP (respectively 0. 844, 0. 472).CONCLUSION: The PTX3 is an objective biochemical marker in diagnosis of sepsis; it is helpful in assessment of severity and prognosis of sepsis; it also has a certain clinical value in the assessment of sepsis cardiovascular function damage."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25001601",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Severe Acinetobacter baumannii sepsis is associated with elevation of pentraxin 3."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25001601",
"endSection": "abstract",
"offsetInBeginSection": 1636,
"offsetInEndSection": 1755,
"text": "Together, these results suggest that elevation of PTX3 is associated with fulminant disease during A. baumannii sepsis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20119647",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Persisting high levels of plasma pentraxin 3 over the first days after severe sepsis and septic shock onset are associated with mortality."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20119647",
"endSection": "abstract",
"offsetInBeginSection": 231,
"offsetInEndSection": 332,
"text": "PTX3, as a mediator of inflammation, may represent an early marker of severity and outcome in sepsis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20119647",
"endSection": "abstract",
"offsetInBeginSection": 1413,
"offsetInEndSection": 1645,
"text": "CONCLUSIONS: Persisting high levels of circulating PTX3 over the first days from sepsis onset may be associated with mortality. PTX3 correlates with severity of sepsis and with sepsis-associated coagulation/fibrinolysis dysfunction."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27864924",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Pentraxin 3 in patients with severe sepsis or shock: the ALBIOS trial."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26982005",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Pentraxin 3: an immune modulator of infection and useful marker for disease severity assessment in sepsis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24958171",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Redox state of pentraxin 3 as a novel biomarker for resolution of inflammation and survival in sepsis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15977234",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 504,
"text": "The prototypic long pentraxin, pentraxin 3, is an acute phase protein that is structurally related but distinct from C-reactive protein which has proven to correlate with the severity of bacterial infection in critically ill patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11445697",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Circulating levels of the long pentraxin PTX3 correlate with severity of infection in critically ill patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23341967",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Pentraxin 3 (PTX3) is associated with severe sepsis and fatal disease in emergency room patients with suspected infection: a prospective cohort study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11445697",
"endSection": "abstract",
"offsetInBeginSection": 1074,
"offsetInEndSection": 1278,
"text": "In addition, high levels of PTX3 were associated with unfavorable outcome.CONCLUSIONS: The long pentraxin PTX3 is elevated in critically ill patients and correlates with severity of disease and infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20119647",
"endSection": "abstract",
"offsetInBeginSection": 222,
"offsetInEndSection": 323,
"text": "PTX3, as a mediator of inflammation, may represent an early marker of severity and outcome in sepsis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24958171",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Redox state of pentraxin 3 as a novel biomarker for resolution of inflammation and survival in sepsis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20119647",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Persisting high levels of plasma pentraxin 3 over the first days after severe sepsis and septic shock onset are associated with mortality."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23341967",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Pentraxin 3 (PTX3) is associated with severe sepsis and fatal disease in emergency room patients with suspected infection: a prospective cohort study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22278372",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "The proteomic profile of circulating pentraxin 3 (PTX3) complex in sepsis demonstrates the interaction with azurocidin 1 and other components of neutrophil extracellular traps."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018805",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000066891",
"http://www.biosemantics.org/jochem#4264880"
] | null |
5890eb22621ea6ff7e000006
| 327 |
yesno
|
Is there any role of the 'Greek islands' in olfactory receptor choice?
|
['yes']
|
[
"yes"
] |
["Yes. 'Greek islands' first contribute to the formation of olfactory receptor compartments and then form a multi-chromosomal super-enhancer that associates with the single active olfactory receptor gene. The Greek-island-bound transcription factor LHX2 and adaptor protein LDB1 regulate the assembly and maintenance of olfactory receptor compartments, Greek island hubs and olfactory receptor transcription, providing mechanistic insights into and functional support for the role of trans interactions in gene expression."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30626972"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30626972",
"endSection": "abstract",
"offsetInBeginSection": 367,
"offsetInEndSection": 1269,
"text": "Chromatin conformation capture using in situ Hi-C on fluorescence-activated cell-sorted olfactory sensory neurons and their progenitors shows that olfactory receptor gene clusters from 18 chromosomes make specific and robust interchromosomal contacts that increase with differentiation of the cells. These contacts are orchestrated by intergenic olfactory receptor enhancers, the 'Greek islands', which first contribute to the formation of olfactory receptor compartments and then form a multi-chromosomal super-enhancer that associates with the single active olfactory receptor gene. The Greek-island-bound transcription factor LHX2 and adaptor protein LDB1 regulate the assembly and maintenance of olfactory receptor compartments, Greek island hubs and olfactory receptor transcription, providing mechanistic insights into and functional support for the role of trans interactions in gene expression."
}
] | 11 |
BioASQ-training11b
| null | null |
620157bec9dfcb9c09000025
| 328 |
yesno
|
Is Nivolumab (Opdivo) a PD-L1 inhibitor?
|
['no']
|
[
"no"
] |
['No, Nivolumab (Opdivo) is a PD-1 inhibitor.', 'Fatal Myocarditis Following Treatment with the PD-1 Inhibitor Nivolumab']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30171077",
"http://www.ncbi.nlm.nih.gov/pubmed/27313464",
"http://www.ncbi.nlm.nih.gov/pubmed/28833116",
"http://www.ncbi.nlm.nih.gov/pubmed/26514815"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28833116",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Fatal Myocarditis Following Treatment with the PD-1 Inhibitor Nivolumab"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28833116",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 565,
"text": " PD-1 inhibitor nivolumab (Opdivo)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30171077",
"endSection": "abstract",
"offsetInBeginSection": 75,
"offsetInEndSection": 161,
"text": "programmed cell death protein 1 (PD-1)-blocking antibodies nivolumab or pembrolizumab "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27313464",
"endSection": "abstract",
"offsetInBeginSection": 123,
"offsetInEndSection": 332,
"text": "An improvement in the understanding of the role of the immune system in tumor immunosurveillance has led to the development of the programmed death-1 ( PD-1 ) immune checkpoint inhibitor nivolumab ( Opdivo) . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26514815",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 213,
"text": "Nivolumab (Opdivo(®); Nivolumab BMS™) was the first programmed death (PD)-1 immune checkpoint inhibitor to be approved for use in advanced, squamous non-small cell lung cancer (NSCLC) following prior chemotherapy."
}
] | 11 |
BioASQ-training11b
| null | null |
5e494cf96d0a277941000008
| 329 |
yesno
|
Do tumour-associated macrophages have a prognostic role in gliomas?
|
['yes']
|
[
"yes"
] |
['M2-like TAMs hold an unfavourable prognostic value in high-grade gliomas and may contribute to a pro-tumourigenic microenvironment.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28767130"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28767130",
"endSection": "abstract",
"offsetInBeginSection": 67,
"offsetInEndSection": 340,
"text": "Increasing evidence suggests that tumour-associated macrophages/microglia (TAMs) facilitate tumour progression by acquiring a M2-like phenotype. Our objective was to investigate the prognostic value of TAMs in gliomas using automated quantitative double immunofluorescence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28767130",
"endSection": "abstract",
"offsetInBeginSection": 1659,
"offsetInEndSection": 1932,
"text": "This is the first study to use automated quantitative immunofluorescence to determine the prognostic impact of TAMs. Our results suggest that M2-like TAMs hold an unfavourable prognostic value in high-grade gliomas and may contribute to a pro-tumourigenic microenvironment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28767130",
"endSection": "abstract",
"offsetInBeginSection": 941,
"offsetInEndSection": 1330,
"text": "Our data revealed that the amount of especially CD204+ TAMs increases with malignancy grade. In grade III-IV, high CD204 expression was associated with shorter survival, while high IBA-1 intensity correlated with a longer survival. In grade IV, CD204 showed independent prognostic value when adjusting for clinical data and the methylation status of O6-methylguanine-DNA methyltransferase."
}
] | 11 |
BioASQ-training11b
| null | null |
5c92159becadf2e73f000012
| 330 |
yesno
|
Do U6-associated proteins Lsm4 and Lsm6 interact with SMN?
|
['yes']
|
[
"yes"
] |
['SMN was found to interact with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6.', 'SMN interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6.', 'SMN interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6.', 'SMN was found to interact with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6.', 'yes']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"http://www.ncbi.nlm.nih.gov/pubmed/16087681",
"http://www.ncbi.nlm.nih.gov/pubmed/11720283",
"http://www.ncbi.nlm.nih.gov/pubmed/17178713",
"http://www.ncbi.nlm.nih.gov/pubmed/16003501",
"http://www.ncbi.nlm.nih.gov/pubmed/15526162",
"http://www.ncbi.nlm.nih.gov/pubmed/14962794",
"http://www.ncbi.nlm.nih.gov/pubmed/23334184"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"endSection": "abstract",
"offsetInBeginSection": 587,
"offsetInEndSection": 684,
"text": "SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"endSection": "abstract",
"offsetInBeginSection": 572,
"offsetInEndSection": 682,
"text": "Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16087681",
"endSection": "abstract",
"offsetInBeginSection": 1024,
"offsetInEndSection": 1115,
"text": "Furthermore, we present evidence for two separate binding sites in SMN for Sm/Lsm proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"endSection": "abstract",
"offsetInBeginSection": 572,
"offsetInEndSection": 682,
"text": "Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"endSection": "abstract",
"offsetInBeginSection": 572,
"offsetInEndSection": 684,
"text": "Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11720283",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Symmetrical dimethylation of arginine residues in spliceosomal Sm protein B/B' and the Sm-like protein LSm4, and their interaction with the SMN protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 790,
"text": "Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6. Furthermore, the carboxyl-terminal arginine- and glycine-rich domain of Lsm4 directly interacts with SMN."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 790,
"text": "Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6. Furthermore, the carboxyl-terminal arginine- and glycine-rich domain of Lsm4 directly interacts with SMN."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 790,
"text": "Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6. Furthermore, the carboxyl-terminal arginine- and glycine-rich domain of Lsm4 directly interacts with SMN."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 790,
"text": "Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6. Furthermore, the carboxyl-terminal arginine- and glycine-rich domain of Lsm4 directly interacts with SMN."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851237",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 790,
"text": "Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6. Furthermore, the carboxyl-terminal arginine- and glycine-rich domain of Lsm4 directly interacts with SMN."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17178713",
"endSection": "abstract",
"offsetInBeginSection": 175,
"offsetInEndSection": 311,
"text": "This entity promotes the binding of a set of factors, termed LSm/Sm proteins, onto snRNA to form the core structure of these particles. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16087681",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Toward an assembly line for U7 snRNPs: interactions of U7-specific Lsm proteins with PRMT5 and SMN complexes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16003501",
"endSection": "abstract",
"offsetInBeginSection": 770,
"offsetInEndSection": 1016,
"text": "In this report, we demonstrate that the coilin C-terminal domain binds directly to various Sm and Lsm proteins via their Sm motifs. We show that the region of coilin responsible for this binding activity is separable from that which binds to SMN."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16003501",
"endSection": "abstract",
"offsetInBeginSection": 1187,
"offsetInEndSection": 1454,
"text": "Thus, the ability to interact with free Sm (and Lsm) proteins as well as with intact snRNPs, indicates that coilin and CBs may facilitate the modification of newly formed snRNPs, the regeneration of 'mature' snRNPs, or the reclamation of unassembled snRNP components."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15526162",
"endSection": "abstract",
"offsetInBeginSection": 543,
"offsetInEndSection": 748,
"text": "Moreover this structure has important consequences for snRNP assembly that is mediated by two complexes containing the PRMT5 methyltransferase and the SMN (survival of motor neurons) protein, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14962794",
"endSection": "abstract",
"offsetInBeginSection": 1157,
"offsetInEndSection": 1372,
"text": "Arginine/glycine (RG)-rich domains in components of the SMN complex interact with Sm, like-Sm (LSm), fibrillarin, RNA helicase A (Gu), and coilin proteins, all of which are antigen targets in a variety of diseases. "
}
] | 5 |
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/LSM4_MOUSE",
"http://www.uniprot.org/uniprot/LSM6_MOUSE",
"http://www.uniprot.org/uniprot/LSM6_AJECN",
"http://www.uniprot.org/uniprot/LSM6_ASPCL",
"http://www.uniprot.org/uniprot/LSM6_LODEL",
"http://www.uniprot.org/uniprot/LSM6_DEBHA",
"http://www.uniprot.org/uniprot/LSM6_NEOFI",
"http://www.uniprot.org/uniprot/LSM6_CHAGB",
"http://www.uniprot.org/uniprot/LSM6_KLULA",
"http://www.uniprot.org/uniprot/LSM6_COPC7",
"http://www.uniprot.org/uniprot/LSM6_CRYNB",
"http://amigo.geneontology.org/amigo/term/GO:0034731",
"http://www.uniprot.org/uniprot/LSM4_HUMAN",
"http://www.uniprot.org/uniprot/LSM4_YEAST",
"http://www.uniprot.org/uniprot/LSM4_BOVIN",
"http://www.uniprot.org/uniprot/LSM6_PHANO"
] |
[] |
56cab4c75795f9a73e00001f
| 331 |
yesno
|
Are there any episignatures for Duchenne Muscular Dystrophy?
|
['yes']
|
[
"yes"
] |
['Yes, there is a DNA methylation episignature for Duchenne muscular dystrophy', 'Yes, there is an episignature for Duchenne Muscular Dystrophy (DMD).', 'Yes, a unique episignature for Duchenne Muscular Dystrophy (DMD) has been identified and its specificity has been confirmed in relation to other neurodevelopmental disorders with known episignatures.', 'Yes, a unique episignature for Duchenne Muscular Dystrophy (DMD) has been identified.', 'Yes, a unique episignature for Duchenne Muscular Dystrophy (DMD) has been discovered and its specificity has been confirmed in relation to other neurodevelopmental disorders with known episignatures.', 'Yes, there are episignatures for Duchenne Muscular Dystrophy', 'Yes, there have been identified episignatures for Duchenne Muscular Dystrophy.', 'Yes, there are episignatures for Duchenne Muscular Dystrophy.', 'Yes, a unique DNA methylation episignature for Duchenne muscular dystrophy (DMD) was identified and confirmed to be specific in relation to other neurodevelopmental disorders with known episignatures.']
|
[
"https://pubmed.ncbi.nlm.nih.gov/36572586/",
"http://www.ncbi.nlm.nih.gov/pubmed/36572586"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572586",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "The discovery of the DNA methylation episignature for Duchenne muscular dystrophy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572586",
"endSection": "abstract",
"offsetInBeginSection": 1174,
"offsetInEndSection": 1297,
"text": " we developed a new DMD episignature biomarker and provided novel insights into the molecular pathogenesis of this disorder"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572586",
"endSection": "abstract",
"offsetInBeginSection": 987,
"offsetInEndSection": 1140,
"text": "We identified a unique episignature for DMD that whose specificity was confirmed in relation other neurodevelopmental disorders with known episignatures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572586",
"endSection": "abstract",
"offsetInBeginSection": 1141,
"offsetInEndSection": 1387,
"text": "By modeling the DMD episignature, we developed a new DMD episignature biomarker and provided novel insights into the molecular pathogenesis of this disorder, which have the potential to advance more effective, personalized approaches to DMD care."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572586",
"endSection": "abstract",
"offsetInBeginSection": 744,
"offsetInEndSection": 1387,
"text": "To further investigate DMD pathophysiology, we assessed the genome-wide DNA methylation profiles of peripheral blood from 36 patients with DMD using the combination of Illumina Infinium Methylation EPIC bead chip array and EpiSign technology. We identified a unique episignature for DMD that whose specificity was confirmed in relation other neurodevelopmental disorders with known episignatures. By modeling the DMD episignature, we developed a new DMD episignature biomarker and provided novel insights into the molecular pathogenesis of this disorder, which have the potential to advance more effective, personalized approaches to DMD care."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572586",
"endSection": "abstract",
"offsetInBeginSection": 744,
"offsetInEndSection": 1140,
"text": "To further investigate DMD pathophysiology, we assessed the genome-wide DNA methylation profiles of peripheral blood from 36 patients with DMD using the combination of Illumina Infinium Methylation EPIC bead chip array and EpiSign technology. We identified a unique episignature for DMD that whose specificity was confirmed in relation other neurodevelopmental disorders with known episignatures."
}
] | 13 |
BioASQ-training13b
| null | null |
66301f5a187cba990d000028
| 332 |
yesno
|
Is Olaparib effective for prostate cancer?
|
['yes']
|
[
"yes"
] |
['Yes, olaparib was shown to be effective for treatment of prostate cancer. Olaparib led to stable disease or tumor regressions of prostate cancer patients.', 'Yes. Olaparib has antitumour activity against metastatic castration-resistant prostate cancer with DDR gene aberrations.', 'Treatment with the PARP inhibitor olaparib in patients whose prostate cancers were no longer responding to standard treatments and who had defects in DNA-repair genes led to a high response rate.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33012578",
"http://www.ncbi.nlm.nih.gov/pubmed/29880291",
"http://www.ncbi.nlm.nih.gov/pubmed/33044685",
"http://www.ncbi.nlm.nih.gov/pubmed/24789362",
"http://www.ncbi.nlm.nih.gov/pubmed/24225019",
"http://www.ncbi.nlm.nih.gov/pubmed/32343890",
"http://www.ncbi.nlm.nih.gov/pubmed/28895177",
"http://www.ncbi.nlm.nih.gov/pubmed/27317574",
"http://www.ncbi.nlm.nih.gov/pubmed/26658963",
"http://www.ncbi.nlm.nih.gov/pubmed/32955174",
"http://www.ncbi.nlm.nih.gov/pubmed/31075528",
"http://www.ncbi.nlm.nih.gov/pubmed/31404966",
"http://www.ncbi.nlm.nih.gov/pubmed/32293692",
"http://www.ncbi.nlm.nih.gov/pubmed/31501807",
"http://www.ncbi.nlm.nih.gov/pubmed/26510020",
"http://www.ncbi.nlm.nih.gov/pubmed/25616434",
"http://www.ncbi.nlm.nih.gov/pubmed/32814685",
"http://www.ncbi.nlm.nih.gov/pubmed/25583815",
"http://www.ncbi.nlm.nih.gov/pubmed/32982407",
"http://www.ncbi.nlm.nih.gov/pubmed/29465803",
"http://www.ncbi.nlm.nih.gov/pubmed/25127709",
"http://www.ncbi.nlm.nih.gov/pubmed/25366685",
"http://www.ncbi.nlm.nih.gov/pubmed/31806540",
"http://www.ncbi.nlm.nih.gov/pubmed/23847380",
"http://www.ncbi.nlm.nih.gov/pubmed/29979319",
"http://www.ncbi.nlm.nih.gov/pubmed/28069876",
"http://www.ncbi.nlm.nih.gov/pubmed/28280302",
"http://www.ncbi.nlm.nih.gov/pubmed/30514390"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26510020",
"endSection": "abstract",
"offsetInBeginSection": 122,
"offsetInEndSection": 496,
"text": "We hypothesized that metastatic, castration-resistant prostate cancers with DNA-repair defects would respond to poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibition with olaparib.METHODS: We conducted a phase 2 trial in which patients with metastatic, castration-resistant prostate cancer were treated with olaparib tablets at a dose of 400 mg twice a day. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26510020",
"endSection": "abstract",
"offsetInBeginSection": 2035,
"offsetInEndSection": 2244,
"text": "CONCLUSIONS: Treatment with the PARP inhibitor olaparib in patients whose prostate cancers were no longer responding to standard treatments and who had defects in DNA-repair genes led to a high response rate. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25616434",
"endSection": "abstract",
"offsetInBeginSection": 511,
"offsetInEndSection": 768,
"text": " In addition, phase III trials in breast, gastric and pancreatic cancer are underway/planned, and phase I/II investigation is being conducted in other malignancies, including prostate cancer, non-small cell lung cancer, Ewing's sarcoma and advanced cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25583815",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "In a phase II study, researchers found that the PARP inhibitor olaparib led to stable disease or tumor regressions in patients with advanced breast, ovarian, pancreatic, and prostate cancers who had germline mutations in BRCA1 or BRCA2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25366685",
"endSection": "abstract",
"offsetInBeginSection": 383,
"offsetInEndSection": 647,
"text": "Eligibility included ovarian cancer resistant to prior platinum; breast cancer with ≥ three chemotherapy regimens for metastatic disease; pancreatic cancer with prior gemcitabine treatment; or prostate cancer with progression on hormonal and one systemic therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25366685",
"endSection": "abstract",
"offsetInBeginSection": 825,
"offsetInEndSection": 1427,
"text": "The tumor response rate was 26.2% (78 of 298; 95% CI, 21.3 to 31.6) overall and 31.1% (60 of 193; 95% CI, 24.6 to 38.1), 12.9% (eight of 62; 95% CI, 5.7 to 23.9), 21.7% (five of 23; 95% CI, 7.5 to 43.7), and 50.0% (four of eight; 95% CI, 15.7 to 84.3) in ovarian, breast, pancreatic, and prostate cancers, respectively. Stable disease ≥ 8 weeks was observed in 42% of patients (95% CI, 36.0 to 47.4), including 40% (95% CI, 33.4 to 47.7), 47% (95% CI, 34.0 to 59.9), 35% (95% CI, 16.4 to 57.3), and 25% (95% CI, 3.2 to 65.1) of those with ovarian, breast, pancreatic, or prostate cancer, respectively. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24789362",
"endSection": "abstract",
"offsetInBeginSection": 698,
"offsetInEndSection": 1301,
"text": "It is increasingly clear that there are molecularly distinct subtypes of various common cancers, with different therapeutic approaches required for each subtype, for example, the use of the monoclonal antibodies (trastuzumab and cetuximab) in HER2-positive breast cancer and wild-type KRAS colorectal cancer; tyrosine kinase inhibitors (imatinib, gefitinib, erlotinib and crizotinib) in chronic myeloid leukaemia, gastrointestinal stromal tumours and non-small-cell lung cancer and intracellular agents (vemurafenib and olaparib) in metastatic malignant melanoma and ovarian, breast and prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24225019",
"endSection": "abstract",
"offsetInBeginSection": 512,
"offsetInEndSection": 703,
"text": "Olaparib, one of the most studied PARPis, has demonstrated activity in BRCA1/2(MUT+) and BRCA-like sporadic ovarian and breast cancers, and looks promising in prostate and pancreatic cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25127709",
"endSection": "abstract",
"offsetInBeginSection": 552,
"offsetInEndSection": 828,
"text": "Prostate cancer cells cotreated with the HDAC inhibitor, suberoylanilide hydroxamic acid (SAHA) and the PARPi, olaparib, demonstrated a synergistic decrease in cell viability compared with single-agent treatment (combination index<0.9), whereas normal prostatic cells did not."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26510020",
"endSection": "abstract",
"offsetInBeginSection": 2035,
"offsetInEndSection": 2243,
"text": "CONCLUSIONS: Treatment with the PARP inhibitor olaparib in patients whose prostate cancers were no longer responding to standard treatments and who had defects in DNA-repair genes led to a high response rate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24225019",
"endSection": "abstract",
"offsetInBeginSection": 512,
"offsetInEndSection": 704,
"text": "Olaparib, one of the most studied PARPis, has demonstrated activity in BRCA1/2(MUT+) and BRCA-like sporadic ovarian and breast cancers, and looks promising in prostate and pancreatic cancers. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26510020",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25127709",
"endSection": "abstract",
"offsetInBeginSection": 815,
"offsetInEndSection": 1093,
"text": "Prostate cancer cells cotreated with the HDAC inhibitor, suberoylanilide hydroxamic acid (SAHA) and the PARPi, olaparib, demonstrated a synergistic decrease in cell viability compared with single-agent treatment (combination index < 0.9), whereas normal prostatic cells did not."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26510020",
"endSection": "abstract",
"offsetInBeginSection": 305,
"offsetInEndSection": 501,
"text": "We hypothesized that metastatic, castration-resistant prostate cancers with DNA-repair defects would respond to poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibition with olaparib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23847380",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 303,
"text": "A phase II study of the PARP inhibitor olaparib (AstraZeneca) for cancer patients with inherited BRCA1 and BRCA2 gene mutations confirmed earlier results showing clinical benefit for advanced breast and ovarian cancers, and demonstrated evidence of effectiveness against pancreatic and prostate cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26510020",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 496,
"text": "BACKGROUND: Prostate cancer is a heterogeneous disease, but current treatments are not based on molecular stratification. We hypothesized that metastatic, castration-resistant prostate cancers with DNA-repair defects would respond to poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibition with olaparib.METHODS: We conducted a phase 2 trial in which patients with metastatic, castration-resistant prostate cancer were treated with olaparib tablets at a dose of 400 mg twice a day. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26510020",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 307,
"text": "Prostate cancer is a heterogeneous disease, but current treatments are not based on molecular stratification. We hypothesized that metastatic, castration-resistant prostate cancers with DNA-repair defects would respond to poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibition with olaparib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25127709",
"endSection": "abstract",
"offsetInBeginSection": 1398,
"offsetInEndSection": 1646,
"text": "Silencing RAD51 sensitized prostate cancer cells to SAHA and olaparib alone. Collectively, cotreatment with HDACi and PARPi downregulated HR-related protein expression and concomitantly increased DNA damage, resulting in prostate cancer cell death."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25127709",
"endSection": "abstract",
"offsetInBeginSection": 552,
"offsetInEndSection": 829,
"text": "Prostate cancer cells cotreated with the HDAC inhibitor, suberoylanilide hydroxamic acid (SAHA) and the PARPi, olaparib, demonstrated a synergistic decrease in cell viability compared with single-agent treatment (combination index<0.9), whereas normal prostatic cells did not. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26510020",
"endSection": "abstract",
"offsetInBeginSection": 1809,
"offsetInEndSection": 2244,
"text": "The specificity of the biomarker suite was 94%. Anemia (in 10 of the 50 patients [20%]) and fatigue (in 6 [12%]) were the most common grade 3 or 4 adverse events, findings that are consistent with previous studies of olaparib.CONCLUSIONS: Treatment with the PARP inhibitor olaparib in patients whose prostate cancers were no longer responding to standard treatments and who had defects in DNA-repair genes led to a high response rate. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25127709",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 822,
"text": "Prostate cancer cells cotreated with the HDAC inhibitor, suberoylanilide hydroxamic acid (SAHA) and the PARPi, olaparib, demonstrated a synergistic decrease in cell viability compared with single-agent treatment (combination index < 0.9), whereas normal prostatic cells did not."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25616434",
"endSection": "abstract",
"offsetInBeginSection": 512,
"offsetInEndSection": 768,
"text": "In addition, phase III trials in breast, gastric and pancreatic cancer are underway/planned, and phase I/II investigation is being conducted in other malignancies, including prostate cancer, non-small cell lung cancer, Ewing's sarcoma and advanced cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31806540",
"endSection": "abstract",
"offsetInBeginSection": 3329,
"offsetInEndSection": 3589,
"text": "INTERPRETATION: Olaparib has antitumour activity against metastatic castration-resistant prostate cancer with DDR gene aberrations, supporting the implementation of genomic stratification of metastatic castration-resistant prostate cancer in clinical practice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32343890",
"endSection": "abstract",
"offsetInBeginSection": 1966,
"offsetInEndSection": 2358,
"text": "CONCLUSIONS: In men with metastatic castration-resistant prostate cancer who had disease progression while receiving enzalutamide or abiraterone and who had alterations in genes with a role in homologous recombination repair, olaparib was associated with longer progression-free survival and better measures of response and patient-reported end points than either enzalutamide or abiraterone."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32293692",
"endSection": "abstract",
"offsetInBeginSection": 500,
"offsetInEndSection": 622,
"text": "Olaparib is an additional option for second- and third-line treatment in those with alterations in BRCA1, BRCA2, and ATM. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28895177",
"endSection": "abstract",
"offsetInBeginSection": 981,
"offsetInEndSection": 1319,
"text": "In this review, we describe current therapies for mCRPC, the rationale for anti-PARP therapies, the pharmacology of olaparib for prostate cancer, clinical trials of olaparib for mCRPC, our clinical experience with olaparib for prostate cancer at a comprehensive cancer center, and future directions of olaparib for the treatment of mCRPC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30514390",
"endSection": "abstract",
"offsetInBeginSection": 365,
"offsetInEndSection": 571,
"text": "Olaparib, a poly (ADP-ribose) polymerase inhibitor, has demonstrated an improvement in median progression-free survival (PFS) in select patients with metastatic castration-resistant prostate cancer (mCRPC)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30514390",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Activity of durvalumab plus olaparib in metastatic castration-resistant prostate cancer in men with and without DNA damage repair mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29880291",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "BACKGROUND: Patients with metastatic castration-resistant prostate cancer and homologous recombination repair (HRR) mutations have a better response to treatment with the poly(ADP-ribose) polymerase inhibitor olaparib than patients without HRR mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31075528",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 339,
"text": "The TOPARP-A clinical trial demonstrated that the PARP inhibitor olaparib may be an effective strategy for treating prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32814685",
"endSection": "abstract",
"offsetInBeginSection": 2299,
"offsetInEndSection": 2488,
"text": "MMARY: The poly(ADP-ribose) polymerase (PARP) inhibitors olaparib and rucaparib are now approved by the Food and Drug Administration for the treatment of advanced prostate cancer. Here, we "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32955174",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 408,
"text": "BACKGROUND: We previously reported that olaparib led to significantly longer imaging-based progression-free survival than the physician's choice of enzalutamide or abiraterone among men with metastatic castration-resistant prostate cancer who had qualifying alterations in homologous recombination repair genes and whose disease had progressed during previous treatment with a next-generation hormonal agent."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29465803",
"endSection": "abstract",
"offsetInBeginSection": 199,
"offsetInEndSection": 352,
"text": "Recent clinical studies show favorable results for the PARP inhibitor olaparib used as single agent for treatment of metastatic castration-resistant PCa."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33044685",
"endSection": "abstract",
"offsetInBeginSection": 884,
"offsetInEndSection": 1174,
"text": "The PROFOUND phase III trial, comparing olaparib with enzalutamide/abiraterone therapy, revealed increased radiological progression-free survival (rPFS) and overall survival (OS) among patients with metastatic castration-resistant prostate cancer (mCRPC) with BRCA1, BRCA2 or ATM mutations."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26658963",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Olaparib Targets Some Advanced Prostate Cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31501807",
"endSection": "abstract",
"offsetInBeginSection": 65,
"offsetInEndSection": 255,
"text": "The PARP inhibitor (PARPi) olaparib received FDA breakthrough designation for treatment of metastatic castration-resistant prostate cancers (CRPC) carrying mutations in BRCA1/2 or ATM genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32982407",
"endSection": "abstract",
"offsetInBeginSection": 461,
"offsetInEndSection": 617,
"text": " In prostate cancer, two PARPi, rucaparib and olaparib, have been FDA approved for the treatment of metastatic castration-resistant prostate cancer (mCRPC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28069876",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Olaparib is an FDA-approved PARP inhibitor (PARPi) that has shown promise as a synthetic lethal treatment approach for BRCA-mutant castration-resistant prostate cancer (CRPC) in clinical use"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28069876",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Targeting Plk1 to Enhance Efficacy of Olaparib in Castration-Resistant Prostate Cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29979319",
"endSection": "abstract",
"offsetInBeginSection": 473,
"offsetInEndSection": 649,
"text": "RECENT FINDINGS: The approval of several PARPi (olaparib, rucaparib, and niraparib) has driven the focus of anticancer treatment on synthetic lethality in prostate cancer too. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33012578",
"endSection": "abstract",
"offsetInBeginSection": 882,
"offsetInEndSection": 1111,
"text": "PATIENT SUMMARY: A large clinical study concluded that treatment with the PARP inhibitor olaparib benefits men with metastatic castration-resistant prostate cancer whose tumors harbor alterations in 15 different DNA repair genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31404966",
"endSection": "abstract",
"offsetInBeginSection": 760,
"offsetInEndSection": 853,
"text": " Among them, olaparib and rucaparib have breakthrough designations for BRCA1/2-mutated mCRPC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28280302",
"endSection": "abstract",
"offsetInBeginSection": 645,
"offsetInEndSection": 785,
"text": "In phase II clinical trials, including patients with advanced castration-resistant PC, olaparib seems to be efficacious and well tolerated. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27317574",
"endSection": "abstract",
"offsetInBeginSection": 1352,
"offsetInEndSection": 1547,
"text": "Of note is the recent U.S. Food and Drug Administration breakthrough therapy designation of olaparib for the treatment of BRCA1/2- or ATM-mutated metastatic castration-resistant prostate cancer. "
}
] | 11 |
BioASQ-training11b
|
[
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"http://www.disease-ontology.org/api/metadata/DOID:10286"
] |
[
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] |
602498cb1cb411341a00009e
| 334 |
yesno
|
Are Notch mutations related to T-cell Acute Lymphoblastic Leukemia (T-ALL)?
|
['yes']
|
[
"yes"
] |
['Yes, Notch1 is a transmembrane receptor that is frequently mutated in human T-cell acute lymphoblastic leukemia (T-ALL).T-cell acute lymphoblastic leukemia/lymphoma (T-ALL) is characterized by aberrant activation of NOTCH1 in over 60% of T-ALL cases.', 'Notch1 is a transmembrane receptor that is frequently mutated in human T-cell acute lymphoblastic leukemia (T-ALL). Activating mutations in NOTCH1, an essential regulator of T cell development, are frequently found in human T cell acute lymphoblastic leukemia (T-ALL). ', 'Notch1 is a transmembrane receptor that is frequently mutated in human T-cell acute lymphoblastic leukemia (T-ALL). Activating mutations in NOTCH1, an essential regulator of T cell development, are frequently found in human T cell acute lymphoblastic leukemia (T-ALL). ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20967796",
"http://www.ncbi.nlm.nih.gov/pubmed/18184405",
"http://www.ncbi.nlm.nih.gov/pubmed/24252593",
"http://www.ncbi.nlm.nih.gov/pubmed/24140475",
"http://www.ncbi.nlm.nih.gov/pubmed/24068942",
"http://www.ncbi.nlm.nih.gov/pubmed/23730497",
"http://www.ncbi.nlm.nih.gov/pubmed/23022380",
"http://www.ncbi.nlm.nih.gov/pubmed/18056171",
"http://www.ncbi.nlm.nih.gov/pubmed/21302811",
"http://www.ncbi.nlm.nih.gov/pubmed/25493453",
"http://www.ncbi.nlm.nih.gov/pubmed/16707600",
"http://www.ncbi.nlm.nih.gov/pubmed/17575125",
"http://www.ncbi.nlm.nih.gov/pubmed/20015880",
"http://www.ncbi.nlm.nih.gov/pubmed/21263446",
"http://www.ncbi.nlm.nih.gov/pubmed/20008221",
"http://www.ncbi.nlm.nih.gov/pubmed/23033986",
"http://www.ncbi.nlm.nih.gov/pubmed/21463127",
"http://www.ncbi.nlm.nih.gov/pubmed/24401270",
"http://www.ncbi.nlm.nih.gov/pubmed/24301524"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20967796",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 467,
"text": "Notch receptors participate in a highly conserved signalling pathway that regulates normal development and tissue homeostasis in a context- and dose-dependent manner. Deregulated Notch signalling has been implicated in many diseases, but the clearest example of a pathogenic role is found in T-cell lymphoblastic leukaemia/lymphoma (T-LL), in which the majority of human and murine tumours have acquired mutations that lead to aberrant increases in Notch1 signalling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18184405",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 351,
"text": "NOTCH proteins (NOTCH1, NOTCH2, NOTCH3 and NOTCH4) play crucial roles in embryonic development. Also, mounting evidence indicates that NOTCH contributes to the pathogenesis of hematopoietic and solid malignancies. Recent studies reported a high incidence of gain-of-function mutations of the NOTCH1 gene in T-cell acute lymphoblastic leukemias (ALL). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18184405",
"endSection": "abstract",
"offsetInBeginSection": 1126,
"offsetInEndSection": 1300,
"text": "Our data indicate that NOTCH1 is mutated in T-ALL, but not in other common human cancers, and that NOTCH2, NOTCH3 and NOTH4 genes are rarely mutated in common human cancers. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24252593",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 602,
"text": "The Notch signaling pathway plays a critical role in maintaining the balance between cell proliferation, differentiation and apoptosis, and is a highly conserved signaling pathway that regulates normal development in a context- and dose-dependent manner. Dysregulation of Notch signaling has been suggested to be key events in a variety of hematological malignancies. Notch1 signaling appears to be the central oncogenic trigger in T cell acute lymphoblastic leukemia (T-ALL), in which the majority of human malignancies have acquired mutations that lead to constitutive activation of Notch1 signaling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24140475",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 521,
"text": "T-cell acute lymphoblastic leukemia (T-ALL) is characterized as a high-risk stratified disease associated with frequent relapse, chemotherapy resistance, and a poorer prognostic outlook than B-precursor ALL. Many of the challenges in treating T-ALL reflect the lack of prognostic cytogenetic or molecular abnormalities on which to base therapy, including targeted therapy. Notch1 activating mutations were identified in more than 50% of T-ALL cases and can be therapeutically targeted with γ-secretase inhibitors (GSIs). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068942",
"endSection": "abstract",
"offsetInBeginSection": 180,
"offsetInEndSection": 296,
"text": "Notch1 is a transmembrane receptor that is frequently mutated in human T-cell acute lymphoblastic leukemia (T-ALL). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23730497",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 364,
"text": "T-cell acute lymphoblastic leukemia/lymphoma (T-ALL) is characterized by aberrant activation of NOTCH1 in over 60% of T-ALL cases. The high prevalence of activating NOTCH1 mutations highlights the critical role of NOTCH signaling in the pathogenesis of this disease and has prompted the development of therapeutic approaches targeting the NOTCH signaling pathway. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23022380",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Activating mutations in NOTCH1, an essential regulator of T cell development, are frequently found in human T cell acute lymphoblastic leukemia (T-ALL). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16707600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25493453",
"endSection": "abstract",
"offsetInBeginSection": 194,
"offsetInEndSection": 342,
"text": "Mutations in NOTCH1/FBXW7 activate NOTCH signaling and are of prognostic significance in patients with T-cell acute lymphoblastic leukemia (T-ALL)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21302811",
"endSection": "abstract",
"offsetInBeginSection": 79,
"offsetInEndSection": 207,
"text": "Gain-of-function mutations in Notch-1 have been reported in more than 50% of human T-cell acute lymphoblastic leukemia (T-ALL)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17575125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Notch signaling is of crucial importance in normal T-cell development and Notch 1 is frequently mutated in T-cell acute lymphoblastic leukemias (T-ALL), leading to aberrantly high Notch signaling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25493453",
"endSection": "abstract",
"offsetInBeginSection": 194,
"offsetInEndSection": 342,
"text": "Mutations in NOTCH1/FBXW7 activate NOTCH signaling and are of prognostic significance in patients with T-cell acute lymphoblastic leukemia (T-ALL)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17575125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Notch signaling is of crucial importance in normal T-cell development and Notch 1 is frequently mutated in T-cell acute lymphoblastic leukemias (T-ALL), leading to aberrantly high Notch signaling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21263446",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Activation of the Notch pathway occurs commonly in T acute lymphoblastic leukemia (T-ALL) because of mutations in Notch1 or Fbw7 and is involved in the regulation of cell proliferation and survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20015880",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "T-cell acute lymphoblastic leukemia (T-ALL) patients frequently display NOTCH1 activating mutations and Notch can transcriptionally down-regulate the tumor suppressor PTEN."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20008221",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "The identification of activating mutations in NOTCH1 in over 50% of T-cell acute lymphoblastic leukemias (T-ALL) has generated major interest in the elucidation of the mechanisms of transformation downstream of oncogenic NOTCH and in the targeting of the NOTCH signaling pathway in this disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23033986",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 263,
"text": "BACKGROUND: In T-cell acute lymphoblastic leukemia/lymphoma (T-ALL/LBL), activating mutations of NOTCH1 are observed in more than 50% of cases, whereas the t(7;9)(q34;q34) involving NOTCH1 at 9q34 and TRB@ at 7q34 is an extremely rare but recurrent translocation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20967796",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 467,
"text": "Notch receptors participate in a highly conserved signalling pathway that regulates normal development and tissue homeostasis in a context- and dose-dependent manner. Deregulated Notch signalling has been implicated in many diseases, but the clearest example of a pathogenic role is found in T-cell lymphoblastic leukaemia/lymphoma (T-LL), in which the majority of human and murine tumours have acquired mutations that lead to aberrant increases in Notch1 signalling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21263446",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Activation of the Notch pathway occurs commonly in T acute lymphoblastic leukemia (T-ALL) because of mutations in Notch1 or Fbw7 and is involved in the regulation of cell proliferation and survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21463127",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Activating mutations in NOTCH1 consitute the most prominent genetic abnormality in T-cell acute lymphoblastic leukemia (T-ALL)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24401270",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "T cell acute lymphoblastic leukemia (T-ALL) is an aggressive cancer that is frequently associated with activating mutations in NOTCH1 and dysregulation of MYC"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24301524",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "The Notch signaling pathway has been recognized as a key factor for the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL), because of the high incidence of activating mutations of Notch1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17575125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "Notch signaling is of crucial importance in normal T-cell development and Notch 1 is frequently mutated in T-cell acute lymphoblastic leukemias (T-ALL), leading to aberrantly high Notch signaling"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16707600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21302811",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 207,
"text": "Gain-of-function mutations in Notch-1 have been reported in more than 50% of human T-cell acute lymphoblastic leukemia (T-ALL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17575125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "Notch signaling is of crucial importance in normal T-cell development and Notch 1 is frequently mutated in T-cell acute lymphoblastic leukemias (T-ALL), leading to aberrantly high Notch signaling"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16707600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21302811",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 207,
"text": "Gain-of-function mutations in Notch-1 have been reported in more than 50% of human T-cell acute lymphoblastic leukemia (T-ALL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16707600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17575125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "Notch signaling is of crucial importance in normal T-cell development and Notch 1 is frequently mutated in T-cell acute lymphoblastic leukemias (T-ALL), leading to aberrantly high Notch signaling"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21302811",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 207,
"text": "Gain-of-function mutations in Notch-1 have been reported in more than 50% of human T-cell acute lymphoblastic leukemia (T-ALL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16707600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17575125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "Notch signaling is of crucial importance in normal T-cell development and Notch 1 is frequently mutated in T-cell acute lymphoblastic leukemias (T-ALL), leading to aberrantly high Notch signaling"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21302811",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 207,
"text": "Gain-of-function mutations in Notch-1 have been reported in more than 50% of human T-cell acute lymphoblastic leukemia (T-ALL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16707600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21302811",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 207,
"text": "Gain-of-function mutations in Notch-1 have been reported in more than 50% of human T-cell acute lymphoblastic leukemia (T-ALL)"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:5603"
] |
[] |
5522fadb7b523f2123000001
| 335 |
yesno
|
Can bergapten cause phototoxicity?
|
['yes']
|
[
"yes"
] |
['Yes, phototoxicity is a side effect of bergapten.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34347307"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34347307",
"endSection": "abstract",
"offsetInBeginSection": 739,
"offsetInEndSection": 841,
"text": "Furthermore, the phototoxicity of bergapten combined with ultraviolet light has always been mentioned."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34347307",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1236,
"text": "The phototoxicity of bergapten as a side effect should be further avoided. "
}
] | 11 |
BioASQ-training11b
| null | null |
620588f9c9dfcb9c09000033
| 336 |
yesno
|
Are there methods for generating highly multiplexed ChIP-seq libraries?
|
['yes']
|
[
"yes"
] |
['Yes. There are methods for generating highly multiplexed ChIP-seq libraries.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24885602"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24885602",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "A method for generating highly multiplexed ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24885602",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 817,
"text": "The barcoding of next generation sequencing libraries has become an essential part of the experimental design. Barcoding not only allows the sequencing of more than one sample per lane, but also reduces technical bias. However, current barcoding strategies impose significant limitations and/or technical barriers in their implementation for ChIP-sequencing.FINDINGS: Converting Y-shaped sequencing adapters to double stranded DNA prior to agarose gel size selection reduces adapter dimer contamination and quantitating the number of cycles required for amplification of the library with qPCR prior to library amplification eliminates library over-amplification.CONCLUSIONS: We describe an efficient and cost effective method for making barcoded ChIP-seq libraries for sequencing on the Illumina platform."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24885602",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "A method for generating highly multiplexed ChIP-seq libraries"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24885602",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "A method for generating highly multiplexed ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24885602",
"endSection": "abstract",
"offsetInBeginSection": 654,
"offsetInEndSection": 785,
"text": "We describe an efficient and cost effective method for making barcoded ChIP-seq libraries for sequencing on the Illumina platform.."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015698",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D047369",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D056656"
] | null |
589206fc49702f2e01000003
| 337 |
yesno
|
Is the number of described human nuclear mutations less than 50000?
|
['no']
|
[
"no"
] |
['No, The number of known mutations in human nuclear genes, underlying or associated with human inherited disease, has now exceeded 100,000 in more than 3700 different genes (Human Gene Mutation Database).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22948725",
"http://www.ncbi.nlm.nih.gov/pubmed/20569258",
"http://www.ncbi.nlm.nih.gov/pubmed/24077912"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20569258",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "The number of known mutations in human nuclear genes, underlying or associated with human inherited disease, has now exceeded 100,000 in more than 3700 different genes (Human Gene Mutation Database)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24077912",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 368,
"text": "The Human Gene Mutation Database (HGMD®) is a comprehensive collection of germline mutations in nuclear genes that underlie, or are associated with, human inherited disease. By June 2013, the database contained over 141,000 different lesions detected in over 5,700 different genes, with new mutation entries currently accumulating at a rate exceeding 10,000 per annum."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22948725",
"endSection": "abstract",
"offsetInBeginSection": 607,
"offsetInEndSection": 778,
"text": "By March 2012, the database contained in excess of 123,600 different lesions (HGMD Professional release 2012.1) detected in 4,514 different nuclear genes, with new entries"
}
] | 6 |
BioASQ-training6b
| null | null |
58e26ede6fddd3e83e000015
| 338 |
yesno
|
Are there enhancer RNAs (eRNAs)?
|
['yes']
|
[
"yes"
] |
['Yes. Active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs). eRNAs are distinct from long noncoding RNAs (lncRNAs), but these two species of noncoding RNAs may share a similar role in the activation of mRNA transcription.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"http://www.ncbi.nlm.nih.gov/pubmed/24674738",
"http://www.ncbi.nlm.nih.gov/pubmed/24525859",
"http://www.ncbi.nlm.nih.gov/pubmed/24480293",
"http://www.ncbi.nlm.nih.gov/pubmed/23877407",
"http://www.ncbi.nlm.nih.gov/pubmed/23728302",
"http://www.ncbi.nlm.nih.gov/pubmed/25404134",
"http://www.ncbi.nlm.nih.gov/pubmed/25263592",
"http://www.ncbi.nlm.nih.gov/pubmed/25810254",
"http://www.ncbi.nlm.nih.gov/pubmed/20393465",
"http://www.ncbi.nlm.nih.gov/pubmed/24135681"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "abstract",
"offsetInBeginSection": 34,
"offsetInEndSection": 293,
"text": "active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs). eRNAs are distinct from long noncoding RNAs (lncRNAs), but these two species of noncoding RNAs may share a similar role in the activation of mRNA transcription"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "abstract",
"offsetInBeginSection": 610,
"offsetInEndSection": 708,
"text": " eRNAs may then facilitate enhancer-promoter interaction or activate promoter-driven transcription"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Enhancer RNAs: a class of long noncoding RNAs synthesized at enhancers"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24674738",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 52,
"text": "Enhancer RNAs and regulated transcriptional programs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24674738",
"endSection": "abstract",
"offsetInBeginSection": 388,
"offsetInEndSection": 503,
"text": "enhancers have been found to be broadly transcribed, resulting in the production of enhancer-derived RNAs, or eRNAs"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24525859",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "The emerging roles of eRNAs in transcriptional regulatory networks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24525859",
"endSection": "abstract",
"offsetInBeginSection": 615,
"offsetInEndSection": 871,
"text": "we found certain enhancer RNAs (eRNAs) regulate chromatin accessibility of the transcriptional machinery at loci encoding master regulators of myogenesis (i.e., MyoD/MyoG), thus suggesting their significance and site-specific impact in cellular programming"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24480293",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 49,
"text": "Enhancer RNAs: the new molecules of transcription"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24480293",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 407,
"text": " the discovery that distal regulatory elements known as enhancers are transcribed and such enhancer-derived transcripts (eRNAs) serve a critical function in transcriptional activation has added a new dimension to transcriptional regulation"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23877407",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 38,
"text": "eRNAs reach the heart of transcription"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25404134",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Recent studies have disclosed the function of enhancer RNAs (eRNAs), which are long non-coding RNAs transcribed from gene enhancer regions, in transcriptional regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25810254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Since the discovery that many transcriptional enhancers are transcribed into long noncoding RNAs termed \"enhancer RNAs\" (eRNAs), their putative role in enhancer function has been debated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25263592",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers, whose function and action mechanism are yet to be firmly established."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25810254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Since the discovery that many transcriptional enhancers are transcribed into long noncoding RNAs termed \"enhancer RNAs\" (eRNAs), their putative role in enhancer function has been debated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25404134",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Recent studies have disclosed the function of enhancer RNAs (eRNAs), which are long non-coding RNAs transcribed from gene enhancer regions, in transcriptional regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25263592",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers, whose function and action mechanism are yet to be firmly established."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23728302",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 483,
"text": "In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25404134",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Recent studies have disclosed the function of enhancer RNAs (eRNAs), which are long non-coding RNAs transcribed from gene enhancer regions, in transcriptional regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25810254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Since the discovery that many transcriptional enhancers are transcribed into long noncoding RNAs termed \"enhancer RNAs\" (eRNAs), their putative role in enhancer function has been debated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25263592",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers, whose function and action mechanism are yet to be firmly established."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23728302",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 483,
"text": "In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23728302",
"endSection": "abstract",
"offsetInBeginSection": 94,
"offsetInEndSection": 290,
"text": "In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24135681",
"endSection": "abstract",
"offsetInBeginSection": 120,
"offsetInEndSection": 248,
"text": "A subset of enhancers are occupied by RNA polymerase II (RNAP II) and transcribed to produce long non-coding RNAs termed eRNAs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25810254",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 433,
"text": "Very recent evidence has indicted that some eRNAs play a role in initiating or activating transcription, possibly by helping recruit and/or stabilize binding of the general transcription machinery to the proximal promoter of their target genes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23728302",
"endSection": "abstract",
"offsetInBeginSection": 94,
"offsetInEndSection": 405,
"text": "In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). However, it has remained unclear whether these eRNAs are functional or merely a reflection of enhancer activation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23728302",
"endSection": "abstract",
"offsetInBeginSection": 94,
"offsetInEndSection": 290,
"text": "In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25810254",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 433,
"text": "Very recent evidence has indicted that some eRNAs play a role in initiating or activating transcription, possibly by helping recruit and/or stabilize binding of the general transcription machinery to the proximal promoter of their target genes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23728302",
"endSection": "abstract",
"offsetInBeginSection": 94,
"offsetInEndSection": 290,
"text": "In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25810254",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 433,
"text": "Very recent evidence has indicted that some eRNAs play a role in initiating or activating transcription, possibly by helping recruit and/or stabilize binding of the general transcription machinery to the proximal promoter of their target genes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20393465",
"endSection": "abstract",
"offsetInBeginSection": 440,
"offsetInEndSection": 877,
"text": "Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of histone H3 monomethylated at lysine 4. The level of eRNA expression at neuronal enhancers positively correlates with the level of messenger RNA synthesis at nearby genes, suggesting that eRNA synthesis occurs specifically at enhancers that are actively engaged in promoting mRNA synthesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20393465",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 626,
"text": "A function of CBP at enhancers may be to recruit RNA polymerase II (RNAPII), as we also observed activity-regulated RNAPII binding to thousands of enhancers. Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of histone H3 monomethylated at lysine 4."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25263592",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 413,
"text": " Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers, whose function and action mechanism are yet to be firmly established. Here we show that eRNAs facilitate the transition of paused RNA polymerase II (RNAPII) into productive elongation by acting as a decoy for the negative elongation factor (NELF) complex upon induction of immediate early genes (IEGs) in neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25404134",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Recent studies have disclosed the function of enhancer RNAs (eRNAs), which are long non-coding RNAs transcribed from gene enhancer regions, in transcriptional regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs). eRNAs are distinct from long noncoding RNAs (lncRNAs), but these two species of noncoding RNAs may share a similar role in the activation of mRNA transcription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20393465",
"endSection": "abstract",
"offsetInBeginSection": 440,
"offsetInEndSection": 877,
"text": "Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of histone H3 monomethylated at lysine 4. The level of eRNA expression at neuronal enhancers positively correlates with the level of messenger RNA synthesis at nearby genes, suggesting that eRNA synthesis occurs specifically at enhancers that are actively engaged in promoting mRNA synthesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25263592",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25404134",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Recent studies have disclosed the function of enhancer RNAs (eRNAs), which are long non-coding RNAs transcribed from gene enhancer regions, in transcriptional regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs). eRNAs are distinct from long noncoding RNAs (lncRNAs), but these two species of noncoding RNAs may share a similar role in the activation of mRNA transcription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20393465",
"endSection": "abstract",
"offsetInBeginSection": 440,
"offsetInEndSection": 877,
"text": "Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of histone H3 monomethylated at lysine 4. The level of eRNA expression at neuronal enhancers positively correlates with the level of messenger RNA synthesis at nearby genes, suggesting that eRNA synthesis occurs specifically at enhancers that are actively engaged in promoting mRNA synthesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25263592",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23728302",
"endSection": "abstract",
"offsetInBeginSection": 95,
"offsetInEndSection": 405,
"text": "In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). However, it has remained unclear whether these eRNAs are functional or merely a reflection of enhancer activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": " Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs). eRNAs are distinct from long noncoding RNAs (lncRNAs), but these two species of noncoding RNAs may share a similar role in the activation of mRNA transcription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20393465",
"endSection": "abstract",
"offsetInBeginSection": 440,
"offsetInEndSection": 877,
"text": "Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of histone H3 monomethylated at lysine 4. The level of eRNA expression at neuronal enhancers positively correlates with the level of messenger RNA synthesis at nearby genes, suggesting that eRNA synthesis occurs specifically at enhancers that are actively engaged in promoting mRNA synthesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25263592",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": " Recent studies have revealed that active enhancers are transcribed, producing a class of noncoding RNAs called enhancer RNAs (eRNAs). eRNAs are distinct from long noncoding RNAs (lncRNAs), but these two species of noncoding RNAs may share a similar role in the activation of mRNA transcription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20393465",
"endSection": "abstract",
"offsetInBeginSection": 440,
"offsetInEndSection": 877,
"text": "Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of histone H3 monomethylated at lysine 4. The level of eRNA expression at neuronal enhancers positively correlates with the level of messenger RNA synthesis at nearby genes, suggesting that eRNA synthesis occurs specifically at enhancers that are actively engaged in promoting mRNA synthesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25263592",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Enhancer RNAs (eRNAs) are a class of long noncoding RNAs (lncRNA) expressed from active enhancers,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23728302",
"endSection": "abstract",
"offsetInBeginSection": 95,
"offsetInEndSection": 405,
"text": "In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). However, it has remained unclear whether these eRNAs are functional or merely a reflection of enhancer activation."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004742",
"http://amigo.geneontology.org/amigo/term/GO:0035326"
] |
[] |
56a8adb0a17756b72f000003
| 339 |
yesno
|
Autophagy is the process where a virus obtains nutrients from it's host, yes or no?
|
['no']
|
[
"no"
] |
['No, autophagy is important in cellular homeostasis for the cell survival mechanism and is involved apoptosis.', 'Autophagy is a cellular survival pathway that is necessary for the degradation of cellular constituents such as long-lived proteins and damaged organelles.', 'Autophagy is important in cellular homeostasis for the cell survival mechanism.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29022289",
"http://www.ncbi.nlm.nih.gov/pubmed/22475795",
"http://www.ncbi.nlm.nih.gov/pubmed/24779013",
"http://www.ncbi.nlm.nih.gov/pubmed/30544615",
"http://www.ncbi.nlm.nih.gov/pubmed/28884441",
"http://www.ncbi.nlm.nih.gov/pubmed/28889353",
"http://www.ncbi.nlm.nih.gov/pubmed/31803515",
"http://www.ncbi.nlm.nih.gov/pubmed/24914338"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28884441",
"endSection": "abstract",
"offsetInBeginSection": 392,
"offsetInEndSection": 537,
"text": "In this study, we demonstrate that autophagy is a critical mediator of the viral degradation pathway and that this pathway is not HIV-1 specific."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28889353",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "Autophagy is important in cellular homeostasis for the cell survival mechanism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29022289",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Autophagy is a cellular survival pathway that is necessary for the degradation of cellular constituents such as long-lived proteins and damaged organelles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28889353",
"endSection": "abstract",
"offsetInBeginSection": 302,
"offsetInEndSection": 457,
"text": "Autophagy-related genes (ATGs) regulate the autophagy and also control the crosstalk with autophagy-associated cell death and apoptosis in some condition. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30544615",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "Autophagy is an evolutionarily conserved cellular process in which intracellular components are eliminated via lysosomal degradation to supply nutrients for organelle biogenesis and metabolic homeostasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24914338",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Autophagy is a lysosome-associated, degradative process that catabolizes cytosolic components to recycle nutrients for further use and maintain cell homeostasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31803515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Autophagy is a self-eating process, in which the damaged or excessed cell organelles and misfolded protein aggregates are removed from the cellular microenvironment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24914338",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Autophagy is a lysosome-associated, degradative process that catabolizes cytosolic components to recycle nutrients for further use and maintain cell homeostasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30544615",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "Autophagy is an evolutionarily conserved cellular process in which intracellular components are eliminated via lysosomal degradation to supply nutrients for organelle biogenesis and metabolic homeostasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22475795",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "Autophagy is a homeostatic process involved in the turnover or elimination of cytoplasmic components, damaged organelles, and protein aggregates via a lysosomal degradation mechanism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24779013",
"endSection": "abstract",
"offsetInBeginSection": 268,
"offsetInEndSection": 363,
"text": "Autophagy is known as a catabolic process for the recycling of the cytoplasmic macromolecules."
}
] | 11 |
BioASQ-training11b
| null | null |
5e3d8edf48dab47f26000003
| 340 |
yesno
|
Is SATB1 necessary for T-cell maturation?
|
['yes']
|
[
"yes"
] |
['Special AT-rich sequence binding protein 1 (SATB1) regulates gene expression essential in immune T-cell maturation and switching of fetal globin species, by binding to matrix attachment regions (MARs) of DNA and inducing a local chromatin remodeling.', 'Yes. SATB1 is an essential factor for the regulation of T-cell maturation.', 'Special AT-rich binding protein 1 (SATB1) nuclear protein, expressed predominantly in T cells, regulates genes through targeting chromatin remodeling during T-cell maturation. SATB1 is a transcriptional regulator controlling the gene expression that is essential in the maturation of the immune T-cell.', 'Special AT-rich binding protein 1 (SATB1) nuclear protein, expressed predominantly in T cells, regulates genes through targeting chromatin remodeling during T-cell maturation. the transcription factor SATB1 that regulates the T-cell maturation SATB1 is a transcriptional regulator controlling the gene expression that is essential in the maturation of the immune T-cell.', 'Yes, SATB1 is necessary for T-cell maturation.', 'Yes. SATB1 is an essential regulator of T-cell maturation.', 'Yes, SATB1 is required for T-cell maturation.', 'SATB1 is a transcriptional regulator controlling the gene expression that is essential in the maturation of the immune T-cell. Special AT-rich sequence binding protein 1 (SATB1) regulates gene expression essential in immune T-cell maturation and switching of fetal globin species, by binding to matrix attachment regions (MARs) of DNA and inducing a local chromatin remodeling.', 'Yes. SATB1 is associated with the late-M-to-early-G1 phase of T-cell maturation and its activation correlates with histone H3 hyperacetylation, DNA methylation, and chromatin reorganization at the transcriptional level, while it is involved in the early stages of T cell differentiation into the erythroid lineage.', 'yes, SATB1 is a transcriptional regulator controlling the gene expression that is essential in the maturation of the immune T-cell. ', 'Special AT-rich binding protein 1 (SATB1) nuclear protein, expressed predominantly in T cells, regulates genes through targeting chromatin remodeling during T-cell maturation.', 'Special AT-rich binding protein 1 (SATB1) nuclear protein, expressed predominantly in T cells, regulates genes through targeting chromatin remodeling during T-cell maturation. the transcription factor SATB1 that regulates the T-cell maturation', 'the transcription factor SATB1 that regulates the T-cell maturation. SATB1 is a transcriptional regulator controlling the gene expression that is essential in the maturation of the immune T-cell.', 'Special AT-rich binding protein 1 (SATB1) nuclear protein, expressed predominantly in T cells, regulates genes through targeting chromatin remodeling during T-cell maturation. Special AT-rich sequence binding protein 1 (SATB1) regulates gene expression essential in immune T-cell maturation and switching of fetal globin species, by binding to matrix attachment regions (MARs) of DNA and inducing a local chromatin remodeling.', 'the transcription factor SATB1 that regulates the T-cell maturation Special AT-rich sequence binding protein 1 (SATB1) regulates gene expression essential in immune T-cell maturation and switching of fetal globin species, by binding to matrix attachment regions (MARs) of DNA and inducing a local chromatin remodeling.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17652321",
"http://www.ncbi.nlm.nih.gov/pubmed/16371359",
"http://www.ncbi.nlm.nih.gov/pubmed/15618465"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15618465",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Special AT-rich binding protein 1 (SATB1) nuclear protein, expressed predominantly in T cells, regulates genes through targeting chromatin remodeling during T-cell maturation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16371359",
"endSection": "title",
"offsetInBeginSection": 90,
"offsetInEndSection": 157,
"text": "the transcription factor SATB1 that regulates the T-cell maturation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16371359",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "SATB1 is a transcriptional regulator controlling the gene expression that is essential in the maturation of the immune T-cell. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17652321",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 251,
"text": "Special AT-rich sequence binding protein 1 (SATB1) regulates gene expression essential in immune T-cell maturation and switching of fetal globin species, by binding to matrix attachment regions (MARs) of DNA and inducing a local chromatin remodeling. "
}
] | 11 |
BioASQ-training11b
| null | null |
5d36b4817bc3fee31f000007
| 341 |
yesno
|
Is Cryptococcus neoformans a frequent cause of isolated skin infections in immunocompromised individuals
|
['no']
|
[
"no"
] |
['Primary cutaneous cryptococcosis (PCC) without systemic infection is rare.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26246081",
"http://www.ncbi.nlm.nih.gov/pubmed/12602722",
"http://www.ncbi.nlm.nih.gov/pubmed/27852678",
"http://www.ncbi.nlm.nih.gov/pubmed/12219115"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26246081",
"endSection": "abstract",
"offsetInBeginSection": 10,
"offsetInEndSection": 284,
"text": " Cryptococcus is an opportunistic yeast with a worldwide distribution that primarily causes significant infections in immunocompromised individuals, generally by affecting the respiratory tract. But primary cutaneous cryptococcosis (PCC) without systemic infection is rare. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27852678",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Cryptococcus is a ubiquitous fungus and is known for causing meningitis and cutaneous infections in immunocompromised individuals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12602722",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "Cryptococcus neoformans is an encapsulated yeast that can cause primary pulmonary infections or disseminate and cause infections of the central nervous system, meninges, skin, and bone in the immunocompromised host."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12219115",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "The authors report a male patient, a seller with no detected immunosuppression, with an extensive ulcerated skin lesion localized on the left forearm, caused by Cryptococcus neoformans var."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003453",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012874",
"http://www.disease-ontology.org/api/metadata/DOID:12053",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003455",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003454"
] |
[
{
"o": "http://linkedlifedata.com/resource/umls/label/A18683550",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0010414"
},
{
"o": "cryptococcus neoformans",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A18683550"
},
{
"o": "Cryptococcus neoformans",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0010416"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0043970",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0010416"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8355137",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0010414"
},
{
"o": "Infection by Cryptococcus neoformans",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8355137"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0560486",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0010414"
},
{
"o": "Infection by Cryptococcus neoformans",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0560486"
}
] |
58e120036fddd3e83e00000d
| 342 |
yesno
|
Is the gene SLC6A2 associated with orthostatic intolerance?
|
['yes']
|
[
"yes"
] |
['Yes, variants of the SLC6A2 (or NET) gene are associated with orthostatic intolerance.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12391111",
"http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"http://www.ncbi.nlm.nih.gov/pubmed/15894713",
"http://www.ncbi.nlm.nih.gov/pubmed/23580201",
"http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"http://www.ncbi.nlm.nih.gov/pubmed/12589229",
"http://www.ncbi.nlm.nih.gov/pubmed/11458707"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12391111",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Orthostatic intolerance is a debilitating syndrome characterized by tachycardia on assumption of upright posture. The norepinephrine (NE) transporter (NET) has been implicated in a genetic form of the disorder. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12391111",
"endSection": "abstract",
"offsetInBeginSection": 1185,
"offsetInEndSection": 1324,
"text": "Thus attenuated baroreflex function and reduced sympathetic outflow may contribute to the orthostatic intolerance of severe NET deficiency."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 334,
"text": " Recently, our laboratory reported a polymorphism in the human NET (hNET) gene A457P in an individual with the autonomic disorder orthostatic intolerance (OI). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15894713",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 578,
"text": "Nonsynonymous single nucleotide polymorphisms (SNPs) in the human NET (hNET) gene that influence transporter function can contribute to disease, such as the nonfunctional transporter, A457P, identified in orthostatic intolerance. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12589229",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Orthostatic intolerance is not necessarily related to a specific mutation (Ala457Pro) in the human norepinephrine transporter gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12589229",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Orthostatic intolerance is not necessarily related to a specific mutation (Ala457Pro) in the human norepinephrine transporter gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": -1,
"offsetInEndSection": 117,
"text": "We propose that chromatin-modifying events associated with SLC6A2 gene suppression may constitute a mechanism of POTS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 457,
"text": "The goal of the present study was to further characterize the role and regulation of the SLC6A2 gene in POTS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 1114,
"offsetInEndSection": 1383,
"text": "In the absence of altered SLC6A2 gene sequence or promoter methylation, this reduced expression was directly correlated with chromatin modifications. We propose that chromatin-modifying events associated with SLC6A2 gene suppression may constitute a mechanism of POTS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 458,
"text": "A coding mutation in the norepinephrine transporter gene (SLC6A2) sequence has been reported in 1 family kindred only. The goal of the present study was to further characterize the role and regulation of the SLC6A2 gene in POTS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 1114,
"offsetInEndSection": 1383,
"text": "In the absence of altered SLC6A2 gene sequence or promoter methylation, this reduced expression was directly correlated with chromatin modifications. We propose that chromatin-modifying events associated with SLC6A2 gene suppression may constitute a mechanism of POTS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 458,
"text": "A coding mutation in the norepinephrine transporter gene (SLC6A2) sequence has been reported in 1 family kindred only. The goal of the present study was to further characterize the role and regulation of the SLC6A2 gene in POTS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 1114,
"offsetInEndSection": 1383,
"text": "In the absence of altered SLC6A2 gene sequence or promoter methylation, this reduced expression was directly correlated with chromatin modifications. We propose that chromatin-modifying events associated with SLC6A2 gene suppression may constitute a mechanism of POTS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 458,
"text": "A coding mutation in the norepinephrine transporter gene (SLC6A2) sequence has been reported in 1 family kindred only. The goal of the present study was to further characterize the role and regulation of the SLC6A2 gene in POTS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 1114,
"offsetInEndSection": 1383,
"text": "In the absence of altered SLC6A2 gene sequence or promoter methylation, this reduced expression was directly correlated with chromatin modifications. We propose that chromatin-modifying events associated with SLC6A2 gene suppression may constitute a mechanism of POTS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 458,
"text": "A coding mutation in the norepinephrine transporter gene (SLC6A2) sequence has been reported in 1 family kindred only. The goal of the present study was to further characterize the role and regulation of the SLC6A2 gene in POTS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805287",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "A mutation in the human norepinephrine transporter gene (SLC6A2) associated with orthostatic intolerance disrupts surface expression of mutant and wild-type transporters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 1114,
"offsetInEndSection": 1383,
"text": "In the absence of altered SLC6A2 gene sequence or promoter methylation, this reduced expression was directly correlated with chromatin modifications. We propose that chromatin-modifying events associated with SLC6A2 gene suppression may constitute a mechanism of POTS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22723437",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 458,
"text": "A coding mutation in the norepinephrine transporter gene (SLC6A2) sequence has been reported in 1 family kindred only. The goal of the present study was to further characterize the role and regulation of the SLC6A2 gene in POTS."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054971"
] |
[] |
56d8ba1851531f7e33000005
| 343 |
yesno
|
Is Tako-Tsubo syndrome is an irreversible form of an acute stress-related cardiomyopathy?
|
['no']
|
[
"no"
] |
['No, Tako-Tsubo syndrome is a recognized clinical syndrome characterized by reversible cardiomyopathy', 'no, Tako-Tsubo syndrome, also known as Takotsubo cardiomyopathy, is a reversible form of cardiomyopathy.', 'No, Takotsubo syndrome is a reversible form of an acute stress-related cardiomyopathy.', 'No, Tako-Tsubo syndrome, also known as Takotsubo cardiomyopathy, is a reversible form of acute stress-related cardiomyopathy characterized by transient left ventricular dysfunction.', 'No, Tako-Tsubo cardiomyopathy (TC) is a recognized clinical syndrome characterized by reversible cardiomyopathy with a distinctive left ventricular apical ballooning appearance.', 'No, Tako-Tsubo syndrome is a reversible form of an acute stress-related cardiomyopathy.', 'No, Tako-Tsubo syndrome is not an irreversible form of an acute stress-related cardiomyopathy.', 'No, Tako-Tsubo syndrome is a reversible condition.', 'Tako-Tsubo syndrome, also known as stress cardiomyopathy, is typically reversible.', 'No', 'No. Tako-Tsubo syndrome is a reversible form of an acute stress-related cardiomyopathy.', 'Tako-Tsubo syndrome is an reversible form of an acute stress-related cardiomyopathy', 'Takotsubo cardiomyopathy is a reversible cardiomyopathy with a distinctive left ventricular apical ballooning appearance. It is a rare cause of acute left ventricular dysfunction in the absence of obstructive coronary disease.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19185360",
"http://www.ncbi.nlm.nih.gov/pubmed/16829194",
"http://www.ncbi.nlm.nih.gov/pubmed/26904708",
"http://www.ncbi.nlm.nih.gov/pubmed/21949534",
"http://www.ncbi.nlm.nih.gov/pubmed/36268377",
"http://www.ncbi.nlm.nih.gov/pubmed/22942784",
"http://www.ncbi.nlm.nih.gov/pubmed/18407362",
"http://www.ncbi.nlm.nih.gov/pubmed/32693809",
"http://www.ncbi.nlm.nih.gov/pubmed/20091403",
"http://www.ncbi.nlm.nih.gov/pubmed/25788945",
"http://www.ncbi.nlm.nih.gov/pubmed/17403953",
"http://www.ncbi.nlm.nih.gov/pubmed/29122235",
"http://www.ncbi.nlm.nih.gov/pubmed/27638018",
"http://www.ncbi.nlm.nih.gov/pubmed/20455042",
"http://www.ncbi.nlm.nih.gov/pubmed/18688681",
"http://www.ncbi.nlm.nih.gov/pubmed/24815525",
"http://www.ncbi.nlm.nih.gov/pubmed/31752657",
"http://www.ncbi.nlm.nih.gov/pubmed/31818146",
"http://www.ncbi.nlm.nih.gov/pubmed/23765730",
"http://www.ncbi.nlm.nih.gov/pubmed/16387374",
"http://www.ncbi.nlm.nih.gov/pubmed/21503250",
"http://www.ncbi.nlm.nih.gov/pubmed/28967342",
"http://www.ncbi.nlm.nih.gov/pubmed/25380951",
"http://www.ncbi.nlm.nih.gov/pubmed/20131190",
"http://www.ncbi.nlm.nih.gov/pubmed/22427775",
"http://www.ncbi.nlm.nih.gov/pubmed/24222823",
"http://www.ncbi.nlm.nih.gov/pubmed/35198223",
"http://www.ncbi.nlm.nih.gov/pubmed/38090463",
"http://www.ncbi.nlm.nih.gov/pubmed/21769261",
"http://www.ncbi.nlm.nih.gov/pubmed/18597972",
"http://www.ncbi.nlm.nih.gov/pubmed/31423403"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38090463",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Takotsubo cardiomyopathy (TC) is a recognized clinical syndrome characterized by reversible cardiomyopathy with a distinctive left ventricular apical ballooning appearance"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25788945",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "Tako-Tsubo cardiomyopathy (TTC) is a reversible cardiomyopathy characterized by acute left ventricular segmental dysfunction, whose clinical presentation resembles that of acute myocardial infarction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31752657",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 178,
"text": "Takotsubo Cardiomyopathy (TTC) is an uncommon cause of acute reversible ventricular systolic dysfunction in the absence of obstructive Coronary Artery Disease (CAD). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22942784",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 104,
"text": "Tako-Tsubo syndrome is a reversible form of an acute stress-related cardiomyopathy that was reported"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18407362",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 201,
"text": "GROUND: The Tako-Tsubo Syndrome is a clinical entity characterized by acute but rapidly reversible left ventricular systolic dysfunction and triggered by emotional or psychological stress. The aim "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597972",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "The etiology of a novel cardiac syndrome called \"tako-tsubo\" cardiomyopathy, otherwise known as \"acute onset and reversible"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25380951",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "BACKGROUND: The etiology of tako-tsubo cardiomyopathy, defined as a transient left ventricular dysfunction in"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22942784",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "The Tako-Tsubo syndrome is a reversible form of an acute stress-related cardiomyopathy that was reported during the last decade."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21503250",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Tako-tsubo cardiomyopathy (transient left ventricular apical ballooning) is a reversible form of cardiomyopathy of unknown etiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17403953",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 267,
"text": "Tako-tsubo syndrome (TTS) or stress-related acute reversible ventricular apical dysfunction is an emerging but seemingly under-recognised cardiomyopathy mimicking acute ST elevation myocardial infarction (STEMI) without concomitant epicardial coronary artery disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21949534",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Tako-Tsubo cardiomyopathy (TTC), also known as transient left ventricular apical ballooning syndrome or stress-induced cardiomyopathy, is a novel reversible cardiomyopathy mimicking acute myocardial infarction without epicardial coronary artery disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20091403",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Tako-tsubo cardiomyopathy is a form of reversible left ventricular dysfunction, with a clinical and electrocardiographic picture of acute myocardial infarction in the absence of significant coronary disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16829194",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 225,
"text": "Tako-Tsubo's syndrome (apical ballooning or broken heart syndrome) is a reversible left ventricular dysfunction due to apical asynergy that occurs typically after sudden emotional stress in a subject without coronary disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20131190",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 327,
"text": "Tako-tsubo cardiomyopathy, also known as stress-induced cardiomyopathy, is a temporary left ventricular dysfunction characterised by acute retrosternal rest pain, ST - segment elevation, slight elevation of cardiac necrosis markers, preferential apical akinesia or hypokinesia with basal hypercontractility in echocardiography."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31423403",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Takotsubo cardiomyopathy (TTC) is reversible stress-induced cardiomyopathy featuring symptoms of acute myocardial infarction without significant coronary artery abnormalities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24815525",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "BACKGROUND AND OBJECTIVE: The Tako-tsubo syndrome (TS) is a reversible acute cardiomyopathy simulating an infarction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21769261",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Tako-Tsubo cardiomyopathy (TTC) is an acute reversible cause of segmental myocardial dysfunction that is poorly understood and cannot be explained by the occlusion of a single coronary vessel."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36268377",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 422,
"text": "Introduction: Takotsubo cardiomyopathy is a transient type of acute heart failure with distinct wall motion abnormalities and unclear pathophysiology. This review focuses on the proposed pathophysiological mechanisms that could be involved in the occurrence takotsubo cardiomyopathy.Main body: Acute stress and subsequent excessive activation of the sympathetic nervous system are major factors in the pathophysiology of t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31818146",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 279,
"text": "Takotsubo cardiomyopathy or stress cardiomyopathy is a transient reversible cardiomyopathy characterized by regional wall motion abnormalities that usually extend beyond a single epicardial vascular distribution. It is often precipitated by acute physical or emotional stressors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26904708",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 175,
"text": "Stress cardiomyopathy, or takotsubo cardiomyopathy, is an acute, reversible left ventricular dysfunction usually initiated by a psychological or physical stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16387374",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Tako-tsubo syndrome appears to be an apparently reversible form of the cardiomyopathy, but little is known about the long term risk even with normalization of ventricular function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19185360",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Tako-Tsubo cardiomyopathy is characterized by a transient and reversible left ventricular dysfunction possibly due to a catecholamine-mediated myocardial stunning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23765730",
"endSection": "abstract",
"offsetInBeginSection": 130,
"offsetInEndSection": 239,
"text": "This reversible cardiomyopathy without epicardial coronary artery disease mimics acute myocardial infarction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29122235",
"endSection": "abstract",
"offsetInBeginSection": 511,
"offsetInEndSection": 832,
"text": "TURE REVIEW: Tako-tsubo cardiomyopathy is characterized by a reversible left ventricular dysfunction and wall movement abnormalities, without any compromise of the coronary arteries, associated to high plasma levels of catecholamines which in most cases correlates with an acute stress of emotional or physical type.CONCL"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28967342",
"endSection": "abstract",
"offsetInBeginSection": 206,
"offsetInEndSection": 389,
"text": "colleagues. Takotsubo cardiomyopathy is an increasingly recognized syndrome characterized by transient and reversible systolic dysfunction of the apical and middle segments of the lef"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597972",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 312,
"text": "The etiology of a novel cardiac syndrome called \"tako-tsubo\" cardiomyopathy, otherwise known as \"acute onset and reversible left ventricular apical wall motion abnormality (ballooning),\" is very similar to that of acute myocardial infarction; however, it may also be associated with emotional or physical stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20455042",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Tako-tsubo cardiomyopathy is characterized by a transient and reversible left ventricular dysfunction and shows clinical similarities with the acute coronary syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18407362",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 104,
"text": "GROUND: The Tako-Tsubo Syndrome is a clinical entity characterized by acute but rapidly reversible l"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597972",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 197,
"text": "The etiology of a novel cardiac syndrome called \"tako-tsubo\" cardiomyopathy, otherwise known as \"acute onset and reversible left ventricular apical wall motion abnormality (ballooning),\" is very si"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20091403",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Tako-tsubo cardiomyopathy is a form of reversible left ventricular dysfunction, with a clinical and electroca"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32693809",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 384,
"text": "BACKGROUND: Takotsubo cardiomyopathy is characterized by transient dysfunction of the medial to apical segment of the left ventricle. Recurrence within a few months or years has been reported and serious complications, including arrhythmia, acute cardiac shock and cardiac rupture, can arise; however, recurrence is rare and takotsubo cardiomyopathy is typically a reversible function"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18688681",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "BACKGROUND: Takotsubo cardiomyopathy is a novel, yet well-described, reversible cardiomyopathy triggered by profound psychological or physical stress with a female p"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35198223",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 213,
"text": "Takotsubo cardiomyopathy is considered a benign syndrome that presented by transient characteristic left ventricular dysfunction with a variety of wall-motion abnormalities that resolve completely after few weeks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27638018",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Takotsubo syndrome is typically characterized by acute reversible impairment of apical and mid -left ventricular systolic function. "
}
] | 13 |
BioASQ-training13b
| null | null |
6609827afdcbea915f000011
| 344 |
yesno
|
Are there any R packages that help with visualizing data on spirals?
|
['yes']
|
[
"yes"
] |
['Yes. Spiralize is an R package for visualizing data on spirals.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34849585"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34849585",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "spiralize: an R package for Visualizing Data on Spirals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34849585",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 584,
"text": "Spiral layout has two major advantages for data visualization. First, it is able to visualize data with long axes, which greatly improves the resolution of visualization. Second, it is efficient for time series data to reveal periodic patterns. Here we present the R package spiralize that provides a general solution for visualizing data on spirals. spiralize implements numerous graphics functions so that self-defined high-level graphics can be easily implemented by users. The flexibility and power of spiralize are demonstrated by five examples from real-world datasets."
}
] | 11 |
BioASQ-training11b
| null | null |
621e62c33a8413c653000050
| 345 |
yesno
|
Does PCSK9 (Proprotein convertase subtilisin/kexin type 9) binds with HDL-receptor (HDL-R)?
|
['no']
|
[
"no"
] |
['No, Proprotein Convertase Subtilisin Kexin 9 (PCSK9) binds with LDL-receptor (LDL-R) causing its degradation in the lysosome with the result of LDL-C accumulating in the blood.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27284008",
"http://www.ncbi.nlm.nih.gov/pubmed/26040332",
"http://www.ncbi.nlm.nih.gov/pubmed/20529551",
"http://www.ncbi.nlm.nih.gov/pubmed/23675525",
"http://www.ncbi.nlm.nih.gov/pubmed/26318398",
"http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"http://www.ncbi.nlm.nih.gov/pubmed/25649668",
"http://www.ncbi.nlm.nih.gov/pubmed/26256967",
"http://www.ncbi.nlm.nih.gov/pubmed/22683370",
"http://www.ncbi.nlm.nih.gov/pubmed/23690465",
"http://www.ncbi.nlm.nih.gov/pubmed/24164109",
"http://www.ncbi.nlm.nih.gov/pubmed/21692990",
"http://www.ncbi.nlm.nih.gov/pubmed/23974119",
"http://www.ncbi.nlm.nih.gov/pubmed/21122852",
"http://www.ncbi.nlm.nih.gov/pubmed/23261172",
"http://www.ncbi.nlm.nih.gov/pubmed/25679794",
"http://www.ncbi.nlm.nih.gov/pubmed/26495026",
"http://www.ncbi.nlm.nih.gov/pubmed/24094767",
"http://www.ncbi.nlm.nih.gov/pubmed/18436719",
"http://www.ncbi.nlm.nih.gov/pubmed/21497351",
"http://www.ncbi.nlm.nih.gov/pubmed/22580899",
"http://www.ncbi.nlm.nih.gov/pubmed/17702855",
"http://www.ncbi.nlm.nih.gov/pubmed/20716520",
"http://www.ncbi.nlm.nih.gov/pubmed/26056005",
"http://www.ncbi.nlm.nih.gov/pubmed/23141813",
"http://www.ncbi.nlm.nih.gov/pubmed/22300679",
"http://www.ncbi.nlm.nih.gov/pubmed/25463543",
"http://www.ncbi.nlm.nih.gov/pubmed/24685817",
"http://www.ncbi.nlm.nih.gov/pubmed/25905719",
"http://www.ncbi.nlm.nih.gov/pubmed/26548330",
"http://www.ncbi.nlm.nih.gov/pubmed/24603306",
"http://www.ncbi.nlm.nih.gov/pubmed/22907332",
"http://www.ncbi.nlm.nih.gov/pubmed/26088304",
"http://www.ncbi.nlm.nih.gov/pubmed/19828345",
"http://www.ncbi.nlm.nih.gov/pubmed/26364362",
"http://www.ncbi.nlm.nih.gov/pubmed/23106476",
"http://www.ncbi.nlm.nih.gov/pubmed/26023080",
"http://www.ncbi.nlm.nih.gov/pubmed/17493938",
"http://www.ncbi.nlm.nih.gov/pubmed/22176652",
"http://www.ncbi.nlm.nih.gov/pubmed/25744035",
"http://www.ncbi.nlm.nih.gov/pubmed/25070550",
"http://www.ncbi.nlm.nih.gov/pubmed/26195630",
"http://www.ncbi.nlm.nih.gov/pubmed/25971287",
"http://www.ncbi.nlm.nih.gov/pubmed/24144304"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25679794",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 747,
"text": "Recently it was revealed that the secreted Proprotein Convertase Subtilisin Kexin 9 (PCSK9) binds with LDL-receptor (LDL-R) causing its degradation in the lysosome with the result of LDL-C accumulating in the blood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25679794",
"endSection": "abstract",
"offsetInBeginSection": 1066,
"offsetInEndSection": 1296,
"text": "The major goal of this study is to identify peptide/s from the catalytic domain of hPCSK9 that can block the binding of hPCSK9 and LDL-R and therefore can reduce LDL-R degradation leading to the clearance of LDL-C from the plasma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24603306",
"endSection": "abstract",
"offsetInBeginSection": 1112,
"offsetInEndSection": 1324,
"text": "In vitro administration of SRT3025 to cultured AML12 hepatocytes attenuated Pcsk9 secretion and its binding to Ldlr, thereby reducing Pcsk9-mediated Ldlr degradation and increasing Ldlr expression and LDL uptake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26056005",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 246,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9), which involves in low-density lipoprotein cholesterol (LDL-C) metabolism by interacting with the LDL receptor, is considered as a potent therapeutic target for treating hypercholesterolemia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26056005",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 1030,
"text": "Taken together, these results suggested that the IgG1-PA4 can be served as a potential candidate for the treatment of hypercholesterolemia by inhibiting PCSK9-mediated degradation of cell surface LDLRs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26088304",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to the low-density lipoprotein receptor, escorting it to its destruction in the lysosome and thereby preventing the recirculation of the low-density lipoprotein receptor to the hepatocyte cell surface. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26318398",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 447,
"text": "However, statins have low efficiency because they also increase PCSK9 which targets LDLR for degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26364362",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 316,
"text": "Inhibition of the enzyme PCSK9 (proprotein convertase subtilisin/kexin type 9), which is involved in depletion of the LDL-receptor, is a new pharmacologic approach. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26495026",
"endSection": "abstract",
"offsetInBeginSection": 389,
"offsetInEndSection": 510,
"text": "Proprotein convertase subtilisin kexin type 9 (PCSK9) modulates LDL-c through post-translational degradation of the LDLR."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26495026",
"endSection": "abstract",
"offsetInBeginSection": 1656,
"offsetInEndSection": 1837,
"text": "Mechanistically, hepatic S1P KD was shown to decrease the liver and plasma levels of the protein proprotein convertase subtilisin/kexin type 9 (PCSK9), which degrades LDLR protein. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27284008",
"endSection": "abstract",
"offsetInBeginSection": 229,
"offsetInEndSection": 376,
"text": "We report here the development of sdAbs targeting human PCSK9 (proprotein convertase subtilisin/kexin type 9) as an alternative to anti-PCSK9 mAbs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24164109",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "PCSK9 proprotein convertase subtilisin/kexin type (PCSK9) protein plays an important role in LDL cholesterol (LDL-C) metabolism, due to its role in the degradation of the LDL receptor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24094767",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to LDL receptors, leading to their degradation"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Low density lipoprotein binds to proprotein convertase subtilisin/kexin type-9 (PCSK9) in human plasma and inhibits PCSK9-mediated low density lipoprotein receptor degradation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 217,
"text": "Proprotein convertase subtilisin/kexin type-9 (PCSK9) is a secreted protein that binds to the epidermal growth factor-like-A domain of the low density lipoprotein receptor (LDLR) and mediates LDLR degradation in liver"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23141813",
"endSection": "abstract",
"offsetInBeginSection": 86,
"offsetInEndSection": 191,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds LDL receptors, targeting them for degradation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26023080",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 233,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9), which binds the low-density lipoprotein receptor and targets it for degradation, has emerged as an important regulator of serum cholesterol levels and cardiovascular disease risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22683370",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "Secreted proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to the low-density lipoprotein receptor (LDLR) at the cell surface and disrupts the normal recycling of the LDLR"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20716520",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 250,
"text": "Proprotein convertase, subtilisin/kexin type 9 (PCSK9), a key regulator of plasma LDL-cholesterol (LDL-c) and cardiovascular risk, is produced in liver and secreted into plasma where it binds hepatic LDL receptors (LDLR), leading to their degradation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25744035",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes the degradation of the hepatic low-density lipoprotein receptor (LDL-R) and is therefore a prominent therapeutic target for reducing LDL-cholesterol"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20529551",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 862,
"text": "In the present study we scanned the related gene of a clinically diagnosed autosomal genetic hypercholesterolemia family for the possible mutations and established eukaryotic expression vector of mutation of proprotein convertase subtilisin/kexin type 9 (PCSK9) gene with gene recombination technique to investigate the contributions of the variation on low density lipoprotein receptor (LDL-R) metabolism and function alternation.Mutation detection was conducted for LDL-R, apolipoprotein B(100) (apoB(100)) and PCSK9 gene with nucleotide sequencing in a Chinese FH family"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22300679",
"endSection": "abstract",
"offsetInBeginSection": 172,
"offsetInEndSection": 304,
"text": "Proprotein convertase subtilisin-kexin type 9 (PCSK9) provides a key step in LDL metabolism by stimulating LDL receptor degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23261172",
"endSection": "abstract",
"offsetInBeginSection": 176,
"offsetInEndSection": 323,
"text": "The proprotein convertase subtilisin-kexin type 9 (PCSK9) pathway plays a key role in lipoprotein metabolism by promoting LDL-receptor degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21122852",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 237,
"text": "Proprotein convertase subtilisin-kexin type 9 (PCSK9) plays a key role in LDL receptor processing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18436719",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 353,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes the degradation of the LDL receptor (LDLr) in hepatocytes, and its expression in mouse liver has been shown to decrease with fenofibrate treatment.We developed a sandwich ELISA using recombinant human PCSK9 protein and 2 affinity-purified polyclonal antibodies directed against human PCSK9."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25463543",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 413,
"text": "Proprotein convertase subtilisin kexin type 9 (PCSK9) enhances the degradation of the LDLR and modulates liver CD81 levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23106476",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 299,
"text": "Low-density lipoprotein (LDL) metabolism is governed by proprotein convertase subtilisin-kexin type 9 (PCSK9), which down-regulates LDL receptor expression, resulting in higher LDL cholesterol (LDL-C)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17702855",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Proprotein convertase subtilisin kexin type 9 (PCSK9) is gaining attention as a key regulator of serum LDL-cholesterol (LDLC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25649668",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 270,
"text": "The proprotein convertase subtilisin/kexin type 9 (PCSK9) gene regulates cholesterol homoeostasis by accelerating low-density lipoprotein receptor (LDLR) degradation resulting in the decreased catabolism of low-density lipoprotein (LDL) leading to hypercholesterolaemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Low density lipoprotein binds to proprotein convertase subtilisin/kexin type-9 (PCSK9) in human plasma and inhibits PCSK9-mediated low density lipoprotein receptor degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400816",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 218,
"text": "Proprotein convertase subtilisin/kexin type-9 (PCSK9) is a secreted protein that binds to the epidermal growth factor-like-A domain of the low density lipoprotein receptor (LDLR) and mediates LDLR degradation in liver."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24685817",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a regulator of LDL-cholesterol receptor homeostasis and emerges as a therapeutic target in the prevention of cardiovascular (CV) disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21497351",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 392,
"text": "The present study was conducted to investigate the role of plasma proprotein convertase subtilisin kexin type 9 (PCSK9) levels, a regulator of LDL-receptor expression, in the occurrence of diabetic dyslipidemia."
}
] | 6 |
BioASQ-training6b
|
[
"http://www.uniprot.org/uniprot/PCSK9_SAIBB",
"http://www.uniprot.org/uniprot/PCSK9_MACMU",
"http://www.uniprot.org/uniprot/PCSK9_PANTR",
"http://www.uniprot.org/uniprot/PCSK9_COLGU",
"http://www.uniprot.org/uniprot/PCSK9_CALJA",
"http://www.uniprot.org/uniprot/PCSK9_LAGLA",
"http://www.uniprot.org/uniprot/PCSK9_SAGLB",
"http://www.uniprot.org/uniprot/PCSK9_HUMAN",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D043484",
"http://www.uniprot.org/uniprot/PCSK9_PONPY",
"http://amigo.geneontology.org/amigo/term/GO:1990666",
"http://www.uniprot.org/uniprot/PCSK9_MACNE",
"http://www.uniprot.org/uniprot/PCSK9_RAT",
"http://www.uniprot.org/uniprot/PCSK9_ATEGE",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000071449",
"http://www.uniprot.org/uniprot/PCSK9_PANPA",
"http://www.uniprot.org/uniprot/PCSK9_PLEMO"
] |
[
{
"o": "PCSK9",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1426592"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A20814698",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1426592"
},
{
"o": "proprotein convertase subtilisin/kexin type 9",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A20814698"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A19343187",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C2611277"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8395721",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0062151"
},
{
"o": "high density lipoprotein receptors",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8395721"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A16773852",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0062151"
},
{
"o": "high density lipoprotein receptors",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16773852"
}
] |
58db9aa28acda34529000018
| 346 |
yesno
|
Are there canonical marks of active chromatin in developmentally regulated genes?
|
['no']
|
[
"no"
] |
['No. The transcription of genes temporally regulated during fly and worm development occurs in the absence of canonically active histone modifications. Conversely, strong chromatin marking is related to transcriptional and post-transcriptional stability, an association also observed in mammals. Consequently, chromatin marking is associated with the stable production of RNA, whereas unmarked chromatin would permit rapid gene activation and deactivation during development. In the latter case, regulation by transcription factors would have a comparatively more important regulatory role than chromatin marks.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26280901"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26280901",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Absence of canonical marks of active chromatin in developmentally regulated genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26280901",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 823,
"text": "The interplay of active and repressive histone modifications is assumed to have a key role in the regulation of gene expression. In contrast to this generally accepted view, we show that the transcription of genes temporally regulated during fly and worm development occurs in the absence of canonically active histone modifications. Conversely, strong chromatin marking is related to transcriptional and post-transcriptional stability, an association that we also observe in mammals. Our results support a model in which chromatin marking is associated with the stable production of RNA, whereas unmarked chromatin would permit rapid gene activation and deactivation during development. In the latter case, regulation by transcription factors would have a comparatively more important regulatory role than chromatin marks."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26280901",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Absence of canonical marks of active chromatin in developmentally regulated genes"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26280901",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Absence of canonical marks of active chromatin in developmentally regulated genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26280901",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 333,
"text": "In contrast to this generally accepted view, we show that the transcription of genes temporally regulated during fly and worm development occurs in the absence of canonically active histone modifications."
}
] | 6 |
BioASQ-training6b
|
[
"http://amigo.geneontology.org/amigo/term/GO:0035327",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018507"
] | null |
588383172305cd7e21000004
| 347 |
yesno
|
Is cabozantinib effective for Hepatocellular Carcinoma?
|
['yes']
|
[
"yes"
] |
['Yes, cabozantinib is approved as second line agent for treatment of Hepatocellular Carcinoma.', 'Yes, cabozantinib effective for hepatocellular carcinoma. Cabozantinib is useful second-line therapy after the failure of sorafenib.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27638856",
"http://www.ncbi.nlm.nih.gov/pubmed/29505843",
"http://www.ncbi.nlm.nih.gov/pubmed/29059635",
"http://www.ncbi.nlm.nih.gov/pubmed/29807383",
"http://www.ncbi.nlm.nih.gov/pubmed/30308081",
"http://www.ncbi.nlm.nih.gov/pubmed/29283440",
"http://www.ncbi.nlm.nih.gov/pubmed/30317696",
"http://www.ncbi.nlm.nih.gov/pubmed/28426123",
"http://www.ncbi.nlm.nih.gov/pubmed/30039640",
"http://www.ncbi.nlm.nih.gov/pubmed/30087805",
"http://www.ncbi.nlm.nih.gov/pubmed/29253194",
"http://www.ncbi.nlm.nih.gov/pubmed/28703624",
"http://www.ncbi.nlm.nih.gov/pubmed/29913090",
"http://www.ncbi.nlm.nih.gov/pubmed/29783126",
"http://www.ncbi.nlm.nih.gov/pubmed/24700742",
"http://www.ncbi.nlm.nih.gov/pubmed/28862760",
"http://www.ncbi.nlm.nih.gov/pubmed/29972759"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28862760",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 373,
"text": "However, clinical trials of nonselective kinase inhibitors with c-Met activity (tivantinib, cabozantinib, foretinib, and golvatinib) in patients with HCC have failed so far to demonstrate significant efficacy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29283440",
"endSection": "abstract",
"offsetInBeginSection": 396,
"offsetInEndSection": 604,
"text": "Rationale for use, clinical trial data, and current recommendations for cabozantinib in renal cell cancer, thyroid cancer, prostate cancer, hepatocellular cancer, and lung cancer are detailed in this article."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29253194",
"endSection": "abstract",
"offsetInBeginSection": 854,
"offsetInEndSection": 964,
"text": "More recently, promising outcomes have also been reported with new agents, such as nivolumab and cabozantinib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29505843",
"endSection": "abstract",
"offsetInBeginSection": 279,
"offsetInEndSection": 509,
"text": "Positive results in recent phase III clinical trials have confirmed the high value of anti-angiogenic therapies for HCC in both first (sorafenib and lenvatinib) and second line (regorafenib and cabozantinib) treatment modalities. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29783126",
"endSection": "abstract",
"offsetInBeginSection": 213,
"offsetInEndSection": 488,
"text": "More recently, regorafenib and nivolumab have received approval in the second-line setting after sorafenib, with further positive phase 3 studies emerging in the first line (lenvatinib non-inferior to sorafenib) and second line versus placebo (cabozantinib and ramucirumab). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29783126",
"endSection": "abstract",
"offsetInBeginSection": 1070,
"offsetInEndSection": 1459,
"text": "The rapidly changing treatment landscape due to the emergence of new treatment options (sorafenib and lenvatinib equally effective in first line; regorafenib, cabozantinib, and ramucirumab showing OS benefit in second line with nivolumab approved by the FDA based on response rate) underscores the importance of re-assessing the role of the first approved systemic agent in HCC, sorafenib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29807383",
"endSection": "abstract",
"offsetInBeginSection": 797,
"offsetInEndSection": 917,
"text": "Positive phase III-study data have been published for lenvatinib as first-line and cabozantinib as second-line therapy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29972759",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Cabozantinib in Patients with Advanced and Progressing Hepatocellular Carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29972759",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 303,
"text": "BACKGROUND: Cabozantinib inhibits tyrosine kinases, including vascular endothelial growth factor receptors 1, 2, and 3, MET, and AXL, which are implicated in the progression of hepatocellular carcinoma and the development of resistance to sorafenib, the standard initial treatment for advanced disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29972759",
"endSection": "abstract",
"offsetInBeginSection": 1925,
"offsetInEndSection": 2119,
"text": "CONCLUSIONS: Among patients with previously treated advanced hepatocellular carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29913090",
"endSection": "abstract",
"offsetInBeginSection": 700,
"offsetInEndSection": 971,
"text": "Expert opinion: Based on favorable phase III clinical trial data, sorafenib and lenvatinib are considered promising agents for HCC as first-line systemic chemotherapy. Moreover, regorafenib and cabozantinib are useful second-line therapies after the failure of sorafenib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29972759",
"endSection": "abstract",
"offsetInBeginSection": 1925,
"offsetInEndSection": 2120,
"text": "CONCLUSIONS: Among patients with previously treated advanced hepatocellular carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29972759",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "Cabozantinib in Patients with Advanced and Progressing Hepatocellular Carcinoma.Among patients with previously treated advanced hepatocellular carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29972759",
"endSection": "abstract",
"offsetInBeginSection": 1899,
"offsetInEndSection": 2080,
"text": "Among patients with previously treated advanced hepatocellular carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29972759",
"endSection": "abstract",
"offsetInBeginSection": 1126,
"offsetInEndSection": 1559,
"text": "Median overall survival was 10.2 months with cabozantinib and 8.0 months with placebo (hazard ratio for death, 0.76; 95% confidence interval [CI], 0.63 to 0.92; P=0.005). Median progression-free survival was 5.2 months with cabozantinib and 1.9 months with placebo (hazard ratio for disease progression or death, 0.44; 95% CI, 0.36 to 0.52; P<0.001), and the objective response rates were 4% and less than 1%, respectively (P=0.009)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29972759",
"endSection": "abstract",
"offsetInBeginSection": 1704,
"offsetInEndSection": 2159,
"text": "The most common high-grade events were palmar-plantar erythrodysesthesia (17% with cabozantinib vs. 0% with placebo), hypertension (16% vs. 2%), increased aspartate aminotransferase level (12% vs. 7%), fatigue (10% vs. 4%), and diarrhea (10% vs. 2%).<br><b>CONCLUSIONS</b>: Among patients with previously treated advanced hepatocellular carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29972759",
"endSection": "abstract",
"offsetInBeginSection": 1931,
"offsetInEndSection": 2124,
"text": "CONCLUSIONS Among patients with previously treated advanced hepatocellular carcinoma, treatment with cabozantinib resulted in longer overall survival and progression-free survival than placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30039640",
"endSection": "abstract",
"offsetInBeginSection": 1122,
"offsetInEndSection": 1399,
"text": "CONCLUSIONS The tyrosine kinase inhibitors sorafenib (first line) and regorafenib (second line) have been approved for hepatocellular carcinoma, and the immune checkpoint inhibitor nivolumab obtained conditional approval for sorafenib-experienced patients in the United States."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30317696",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 282,
"text": "The principal advancements in the treatment of hepatocellular carcinoma (HCC) are the use of new systemic treatments such as lenvatinib in first-line treatment and regorafenib, cabozantinib and ramucirumab in second-line treatment due to their benefits in terms of overall survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308081",
"endSection": "abstract",
"offsetInBeginSection": 1308,
"offsetInEndSection": 1527,
"text": "Recently, a few systemic chemotherapies proved to be effective for advanced stage HCC in phase III studies: lenvatinib as the first line of therapy, and regorafenib, cabozantinib, and ramucirumab as second-line therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30039640",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 270,
"text": "<b>BACKGROUND</b>: The approval of the tyrosine kinase inhibitor sorafenib in 2007 marked a milestone in the treatment of hepatocellular carcinoma, as sorafenib was the first systemic therapy to show a survival benefit in patients with advanced hepatocellular carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30039640",
"endSection": "abstract",
"offsetInBeginSection": 1002,
"offsetInEndSection": 1443,
"text": "We also elaborate the unmet need of biomarkers to guide treatment decisions and discuss the emerging field of immunotherapy in hepatocellular carcinoma.<br><b>CONCLUSIONS</b>: The tyrosine kinase inhibitors sorafenib (first line) and regorafenib (second line) have been approved for hepatocellular carcinoma, and the immune checkpoint inhibitor nivolumab obtained conditional approval for sorafenib-experienced patients in the United States."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28703624",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 58,
"text": "Cabozantinib in the treatment of hepatocellular carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30039640",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 251,
"text": "The approval of the tyrosine kinase inhibitor sorafenib in 2007 marked a milestone in the treatment of hepatocellular carcinoma, as sorafenib was the first systemic therapy to show a survival benefit in patients with advanced hepatocellular carcinoma."
}
] | 11 |
BioASQ-training11b
| null | null |
5c6b7a9e7c78d69471000029
| 348 |
yesno
|
Does radiotherapy for Hodgkin disease increases risk for lung cancer?
|
['yes']
|
[
"yes"
] |
['Yes, radiotherapy for Hodgkin disease is associated with increased risk for lung cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/11830608",
"http://www.ncbi.nlm.nih.gov/pubmed/2754447",
"http://www.ncbi.nlm.nih.gov/pubmed/11045784",
"http://www.ncbi.nlm.nih.gov/pubmed/23053567",
"http://www.ncbi.nlm.nih.gov/pubmed/27913498",
"http://www.ncbi.nlm.nih.gov/pubmed/25104066",
"http://www.ncbi.nlm.nih.gov/pubmed/25025999",
"http://www.ncbi.nlm.nih.gov/pubmed/7563187",
"http://www.ncbi.nlm.nih.gov/pubmed/2981984",
"http://www.ncbi.nlm.nih.gov/pubmed/25615851",
"http://www.ncbi.nlm.nih.gov/pubmed/1428226",
"http://www.ncbi.nlm.nih.gov/pubmed/25754634",
"http://www.ncbi.nlm.nih.gov/pubmed/26530956"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27913498",
"endSection": "abstract",
"offsetInBeginSection": 871,
"offsetInEndSection": 965,
"text": "Risks of lung, breast, and gastrointestinal (GI) cancers increase with higher radiation dose. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26530956",
"endSection": "abstract",
"offsetInBeginSection": 1133,
"offsetInEndSection": 1513,
"text": "CONCLUSIONS: RT treatment, especially with doses higher than 42 Gy, and smoking increase the risk of SN after HL. In this series, LC patients with early stages had a shorter elapsed time from HL diagnosis and longer OS, therefore the role of LC screening in HL survivors should be prospectively evaluated and smoking cessation counseling ought to be a key aspect during follow-up."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25025999",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "BACKGROUND: Long-term Hodgkin lymphoma (HL) survivors have an increased risk of late cardiac morbidity and secondary lung cancer after chemotherapy and mediastinal radiotherapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25754634",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "PURPOSE: Hodgkin lymphoma (HL) survivors have an increased risk of cardiovascular disease (CD), lung cancer, and breast cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25615851",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Lung cancer (LC) represents the most common solid tumor in survivors of Hodgkin's disease (HD), and the assessment of the mutational status of oncogenic driver mutations in LC is now standard. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25104066",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "PURPOSE: Hodgkin lymphoma (HL) survivors face an increased risk of treatment-related lung cancer. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23053567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Increased risk of second lung cancer in Hodgkin's lymphoma survivors: a meta-analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23053567",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "BACKGROUND: Patients treated for Hodgkin's lymphoma (HL) have a higher risk of developing second lung cancer (SLC) compared with the general population. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23053567",
"endSection": "abstract",
"offsetInBeginSection": 766,
"offsetInEndSection": 939,
"text": "The pooled relative risk (RR) of SLC was 4.62 (95 % confidence interval [CI], 3.18-6.70], I (2) = 98 %), with a median absolute excess rate of 10.4 per 10,000 person-years. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23053567",
"endSection": "abstract",
"offsetInBeginSection": 1762,
"offsetInEndSection": 1869,
"text": "CONCLUSIONS: The current meta-analysis provided a detailed estimate of the risk of SLC among HL survivors. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7563187",
"endSection": "abstract",
"offsetInBeginSection": 2195,
"offsetInEndSection": 2370,
"text": "CONCLUSIONS\n\nThe excess risk of lung cancer in Hodgkin's disease patients treated with radiotherapy is related to the radiation dose received by the affected area of the lung."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11830608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "BACKGROUND\n\nLung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and smoking are not well described."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11830608",
"endSection": "abstract",
"offsetInBeginSection": 1807,
"offsetInEndSection": 1998,
"text": "CONCLUSIONS\n\nPast treatments with alkylating agents and radiation therapy for Hodgkin's disease were associated with an increased risk of lung cancer in a dose-dependent and additive fashion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7563187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "BACKGROUND\n\nSeveral studies have shown that survivors of Hodgkin's disease have increased risk of lung cancer, but the factors responsible for this excess risk are not well known."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7563187",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 356,
"text": "PURPOSE\n\nThis study was undertaken to investigate the effects of radiation dose, chemotherapy, and smoking on the risk of lung cancer following treatment of Hodgkin's disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2754447",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Increased risk of lung cancer, non-Hodgkin's lymphoma, and leukemia following Hodgkin's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1428226",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "It is recognized that survivors of Hodgkin's disease are at a substantially increased risk of lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11045784",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "The risk of lung and breast cancer is significantly increased after therapy for Hodgkin 's disease ( HD) , but there are few data that describe the molecular profiles of these tumors . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25754634",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Hodgkin lymphoma ( HL ) survivors have an increased risk of cardiovascular disease ( CD) , lung cancer , and breast cancer . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11830608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "BACKGROUND\nLung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and smoking are not well described."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11830608",
"endSection": "abstract",
"offsetInBeginSection": 1807,
"offsetInEndSection": 1998,
"text": "CONCLUSIONS\nPast treatments with alkylating agents and radiation therapy for Hodgkin's disease were associated with an increased risk of lung cancer in a dose-dependent and additive fashion."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2981984",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Lung cancer in Hodgkin's disease: association with previous radiotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2981984",
"endSection": "abstract",
"offsetInBeginSection": 651,
"offsetInEndSection": 788,
"text": "Twenty-eight (94%) of 30 patients developing metachronous lung cancer received supradiaphragmatic irradiation as primary therapy for HD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2981984",
"endSection": "abstract",
"offsetInBeginSection": 93,
"offsetInEndSection": 216,
"text": "The risk ratio for the development of lung cancer among HD patients was 5.6 times that expected in the general population."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2981984",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 93,
"text": "Seven cases of lung cancer were observed in patients with Hodgkin's disease (HD) since 1970."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7563187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "BACKGROUND\nSeveral studies have shown that survivors of Hodgkin's disease have increased risk of lung cancer, but the factors responsible for this excess risk are not well known."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7563187",
"endSection": "abstract",
"offsetInBeginSection": 2152,
"offsetInEndSection": 2314,
"text": "The excess risk of lung cancer in Hodgkin's disease patients treated with radiotherapy is related to the radiation dose received by the affected area of the lung."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11830608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 169,
"text": "Lung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and smoking are not well described."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11830608",
"endSection": "abstract",
"offsetInBeginSection": 1774,
"offsetInEndSection": 1952,
"text": "Past treatments with alkylating agents and radiation therapy for Hodgkin's disease were associated with an increased risk of lung cancer in a dose-dependent and additive fashion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7563187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Several studies have shown that survivors of Hodgkin's disease have increased risk of lung cancer, but the factors responsible for this excess risk are not well known."
}
] | 11 |
BioASQ-training11b
| null | null |
5e33904afbd6abf43b00005f
| 349 |
yesno
|
Is tretinoin effective for photoaging?
|
['yes']
|
[
"yes"
] |
['Yes, Tretinoin is commonly used topically in the treatment of photoaging.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/7544967",
"http://www.ncbi.nlm.nih.gov/pubmed/28762645",
"http://www.ncbi.nlm.nih.gov/pubmed/8435921",
"http://www.ncbi.nlm.nih.gov/pubmed/26885791",
"http://www.ncbi.nlm.nih.gov/pubmed/2186790",
"http://www.ncbi.nlm.nih.gov/pubmed/25603890",
"http://www.ncbi.nlm.nih.gov/pubmed/28293257",
"http://www.ncbi.nlm.nih.gov/pubmed/3336176",
"http://www.ncbi.nlm.nih.gov/pubmed/16724545",
"http://www.ncbi.nlm.nih.gov/pubmed/10790815",
"http://www.ncbi.nlm.nih.gov/pubmed/27050699",
"http://www.ncbi.nlm.nih.gov/pubmed/11535421",
"http://www.ncbi.nlm.nih.gov/pubmed/9703125",
"http://www.ncbi.nlm.nih.gov/pubmed/1552056",
"http://www.ncbi.nlm.nih.gov/pubmed/9486677",
"http://www.ncbi.nlm.nih.gov/pubmed/25141855",
"http://www.ncbi.nlm.nih.gov/pubmed/24734193",
"http://www.ncbi.nlm.nih.gov/pubmed/9589209"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293257",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Background. Tretinoin has been shown to improve photoaged skin. This study was designed to evaluate the efficacy and tolerability of a 5% retinoic acid peel combined with microdermabrasion for facial photoaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293257",
"endSection": "abstract",
"offsetInBeginSection": 1113,
"offsetInEndSection": 1296,
"text": ".Conclusion. This study demonstrated that 5% retinoic acid peel cream combined with microdermabrasion was safe and effective in the treatment of photoaging in the Iranian population. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28762645",
"endSection": "abstract",
"offsetInBeginSection": 1490,
"offsetInEndSection": 1717,
"text": "CONCLUSIONS: Treatment with a double-conjugate retinoid cream demonstrated early reductions in photodamage and improvements in Hydration. AHA-Ret induced less Erythema vs retinol and was more tolerable vs retinol and tretinoin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26885791",
"endSection": "abstract",
"offsetInBeginSection": 769,
"offsetInEndSection": 939,
"text": "These comparative products include prescription tretinoin, physician strength idebenone, kinetin, polyhydroxy, lactic and glycolic acids in reversing signs of photoaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27050699",
"endSection": "abstract",
"offsetInBeginSection": 1888,
"offsetInEndSection": 2073,
"text": "CONCLUSION: Either topical tretinoin (0.25%) or retinol (0.25%) can be used safely and effectively when applied in office immediately after SA peeling to ameliorate signs of photoaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25603890",
"endSection": "abstract",
"offsetInBeginSection": 1423,
"offsetInEndSection": 1596,
"text": "CONCLUSION: The treatment outcome of Retinol 0.2%/LR2412 2% cream does not differ from the one of tretinoin 0.025% cream. Clinical results were not statistically different. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25603890",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "INTRODUCTION: Topical tretinoin is considered the gold standard to treat photoaged skin, but it is associated with side effects and only available upon prescription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24734193",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 372,
"text": "Tretinoin is commonly used topically for acne treatment and in the treatment of photoaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9486677",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "BACKGROUND: Topical tretinoin is effective treatment for both acne and photoaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16724545",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "The efficacy of tretinoin is well established in the treatment of acne and photoaged skin, however as a typical side effect of tretinoin treatment most patients develop a low-grade irritant dermatitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9703125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Topical tretinoin is established as an effective treatment for photoaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9486677",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "BACKGROUND Topical tretinoin is effective treatment for both acne and photoaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8435921",
"endSection": "abstract",
"offsetInBeginSection": 222,
"offsetInEndSection": 319,
"text": "Tretinoin is the only pharmacologic compound shown to partially reverse some signs of photoaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9589209",
"endSection": "abstract",
"offsetInBeginSection": 90,
"offsetInEndSection": 214,
"text": "Although once considered an irreversible process, it is now established that photoaging can be treated by topical tretinoin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11535421",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 754,
"text": "Moreover, studies that have elucidated photoaging pathophysiology have produced significant evidence that topical tretinoin (all-trans retinoic acid), the only agent approved so far for the treatment of photoaging, also works to prevent it."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7544967",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "BACKGROUND AND DESIGN The efficacy of topical tretinoin (all-trans-retinoic acid) in treating photoaging is well established."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25141855",
"endSection": "abstract",
"offsetInBeginSection": 293,
"offsetInEndSection": 404,
"text": "MAJOR CONCLUSIONS Tretinoin can be used for photoaging treatment or combined treatment by different mechanisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25141855",
"endSection": "abstract",
"offsetInBeginSection": 220,
"offsetInEndSection": 290,
"text": "Tretinoin is still the best tested retinoid to reverse photoaged skin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7544967",
"endSection": "abstract",
"offsetInBeginSection": 1872,
"offsetInEndSection": 2036,
"text": "The separation between clinical improvement and irritation suggests that mechanisms other than irritation dominate tretinoin-induced repair of photoaging in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10790815",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "* A cream containing 0.05% tretinoin (Retinova((R)) is approved for treatment of sun-induced skin damage (\"photoaging\")."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2186790",
"endSection": "abstract",
"offsetInBeginSection": 544,
"offsetInEndSection": 656,
"text": "Randomized, controlled trials have shown that topical tretinoin is effective in the treatment of photoaged skin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28293257",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 63,
"text": "Tretinoin has been shown to improve photoaged skin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9486677",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Topical tretinoin is effective treatment for both acne and photoaging."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2186790",
"endSection": "abstract",
"offsetInBeginSection": 544,
"offsetInEndSection": 657,
"text": "Randomized, controlled trials have shown that topical tretinoin is effective in the treatment of photoaged skin.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1552056",
"endSection": "abstract",
"offsetInBeginSection": 1636,
"offsetInEndSection": 1740,
"text": "Tretinoin emollient cream 0.05% appears to be safe and effective in the treatment of photodamaged skin.."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3336176",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Topical tretinoin improves photoaged skin. A double-blind vehicle-controlled study."
}
] | 11 |
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D014212"
] | null |
5a68f2bab750ff4455000017
| 350 |
yesno
|
Can enhancer-promoter interactions form independently of genomic distance?
|
['yes']
|
[
"yes"
] |
['Yes, enhancer-promoter interactions can form independently of genomic distance. A study in Drosophila embryos found that a significant proportion of enhancer-promoter interactions are established across Topologically Associating Domains (TAD) boundaries, which are regions of the genome that are thought to facilitate and constrain enhancer-promoter interactions. However, the study also found that developmental genes are enriched in intra-TAD but not inter-TAD interactions, suggesting that there may be specific mechanisms that facilitate intra-TAD interactions for these genes. Furthermore, the formation of inter-TAD enhancer-promoter interactions is not solely driven by genomic distance, with distal interactions sometimes favored over proximal ones. This indicates that there may be other general mechanisms at play that establish and maintain specific enhancer-promoter interactions across large distances, regardless of genomic distance.', 'Yes, enhancer-promoter interactions can form independently of genomic distance. While Topologically Associating Domains (TADs) have been suggested to facilitate and constrain these interactions, recent studies show that a significant proportion of enhancer-promoter interactions are established across TAD boundaries in Drosophila embryos. However, developmental genes are enriched in intra-TAD but not inter-TAD interactions, suggesting topological constraints on the functionality of these interactions. The formation of inter-TAD enhancer-promoter interactions is not solely driven by genomic distance, with distal interactions sometimes favored over proximal ones, indicating the existence of other general mechanisms to establish and maintain specific enhancer-promoter interactions across large distances.', 'Topologically Associating Domains (TADs) have been suggested to facilitate and constrain enhancer-promoter interactions. A significant proportion of enhancer-promoter interactions are established across TAD boundaries in Drosophila embryos, but developmental genes are strikingly enriched in intra- but not inter-TAD interactions. Furthermore, contrary to intra-TAD interactions, the formation of inter-TAD enhancer-promoter interactions is not solely driven by genomic distance, with distal interactions sometimes favored over proximal ones. This suggests that other general mechanisms must exist to establish and maintain specific enhancer-promoter interactions across large distances']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27932455",
"http://www.ncbi.nlm.nih.gov/pubmed/37511131",
"http://www.ncbi.nlm.nih.gov/pubmed/11742093",
"http://www.ncbi.nlm.nih.gov/pubmed/37858706",
"http://www.ncbi.nlm.nih.gov/pubmed/36717694",
"http://www.ncbi.nlm.nih.gov/pubmed/27799341",
"http://www.ncbi.nlm.nih.gov/pubmed/30395328",
"http://www.ncbi.nlm.nih.gov/pubmed/36824960",
"http://www.ncbi.nlm.nih.gov/pubmed/23045397",
"http://www.ncbi.nlm.nih.gov/pubmed/35418676",
"http://www.ncbi.nlm.nih.gov/pubmed/35691341",
"http://www.ncbi.nlm.nih.gov/pubmed/38084924",
"http://www.ncbi.nlm.nih.gov/pubmed/31829768",
"http://www.ncbi.nlm.nih.gov/pubmed/36769179",
"https://pubmed.ncbi.nlm.nih.gov/38084924/",
"http://www.ncbi.nlm.nih.gov/pubmed/37451823",
"http://www.ncbi.nlm.nih.gov/pubmed/35168174",
"http://www.ncbi.nlm.nih.gov/pubmed/11190466",
"http://www.ncbi.nlm.nih.gov/pubmed/24600469"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38084924",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Enhancer-promoter interactions can form independently of genomic distance and be functional across TAD boundaries"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38084924",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 453,
"text": "Topologically Associating Domains (TADs) have been suggested to facilitate and constrain enhancer-promoter interactions. However, the role of TAD boundaries in effectively restricting these interactions remains unclear. Here, we show that a significant proportion of enhancer-promoter interactions are established across TAD boundaries in Drosophila embryos, but that developmental genes are strikingly enriched in intra- but not inter-TAD interactions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38084924",
"endSection": "abstract",
"offsetInBeginSection": 827,
"offsetInEndSection": 1196,
"text": "Furthermore, contrary to intra-TAD interactions, the formation of inter-TAD enhancer-promoter interactions is not solely driven by genomic distance, with distal interactions sometimes favored over proximal ones. These observations suggest that other general mechanisms must exist to establish and maintain specific enhancer-promoter interactions across large distances."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38084924",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Enhancer-promoter interactions can form independently of genomic distance and be functional across TAD boundaries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37858706",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Enhancers activate their cognate promoters over huge distances but how enhancer/promoter interactions become established is not completely understood"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37511131",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "In higher eukaryotes, distance enhancer-promoter interactions are organized by topologically associated domains, tethering elements, and chromatin insulators/boundaries"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37451823",
"endSection": "abstract",
"offsetInBeginSection": 595,
"offsetInEndSection": 832,
"text": "We show that active regulatory elements, independent of cohesin and polycomb, interact with each other across distances of tens of megabases in vertebrate and invertebrate genomes and that interactions correlate and change with activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30395328",
"endSection": "abstract",
"offsetInBeginSection": 407,
"offsetInEndSection": 610,
"text": "TADs are also functional blocks of chromosomes as enhancers and their cognate promoters are normally located in the same TAD, even if their genomic distance from each other can be as large as a megabase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38084924",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Topologically Associating Domains (TADs) have been suggested to facilitate and constrain enhancer-promoter interactions. However, the role of TAD boundaries in effectively restricting these interactions remains unclear."
}
] | 13 |
BioASQ-training13b
| null | null |
662edc6f187cba990d00000c
| 351 |
yesno
|
Is cadherin a plasma membrane marker?
|
['yes']
|
[
"yes"
] |
['Yes,\ncadherin is a plasma membrane protein marker.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31838186",
"http://www.ncbi.nlm.nih.gov/pubmed/32044971",
"http://www.ncbi.nlm.nih.gov/pubmed/32939719",
"http://www.ncbi.nlm.nih.gov/pubmed/32239671"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32939719",
"endSection": "abstract",
"offsetInBeginSection": 966,
"offsetInEndSection": 1010,
"text": "the plasma membrane-bound E-cadherin protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31838186",
"endSection": "abstract",
"offsetInBeginSection": 933,
"offsetInEndSection": 1013,
"text": "VE-cadherin protein levels were also increased in the plasma membrane fraction. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32044971",
"endSection": "abstract",
"offsetInBeginSection": 649,
"offsetInEndSection": 698,
"text": " recycling of VE-cadherin to the plasma membrane,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32239671",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "E-cadherin, a central component of the adherens junction (AJ), is a single-pass transmembrane protein "
}
] | 11 |
BioASQ-training11b
| null | null |
6060c7c094d57fd879000046
| 352 |
yesno
|
Are deletions of chromosomal regulatory boundaries associated with congenital disease?
|
['yes']
|
[
"yes"
] |
['Yes. Enhancer adoption caused by deletions of regulatory boundaries may contribute to a substantial minority of copy-number variation phenotypes and should thus be taken into account in their medical interpretation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25315429"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25315429",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Deletions of chromosomal regulatory boundaries are associated with congenital disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25315429",
"endSection": "abstract",
"offsetInBeginSection": 1404,
"offsetInEndSection": 1638,
"text": "Our results suggest that enhancer adoption caused by deletions of regulatory boundaries may contribute to a substantial minority of copy-number variation phenotypes and should thus be taken into account in their medical interpretation"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25315429",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Deletions of chromosomal regulatory boundaries are associated with congenital disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25315429",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "Deletions of chromosomal regulatory boundaries are associated with congenital disease."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002872",
"http://www.disease-ontology.org/api/metadata/DOID:1086",
"http://www.disease-ontology.org/api/metadata/DOID:0080014"
] | null |
587f56c392a5b8ad44000001
| 353 |
yesno
|
Is tocilizumab a csDMARD?
|
['no']
|
[
"no"
] |
['No, tocilizumab is a biological DMARD (bDMARD).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31969328"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31969328",
"endSection": "abstract",
"offsetInBeginSection": 730,
"offsetInEndSection": 1251,
"text": "The task force agreed on 5 overarching principles and 12 recommendations concerning use of conventional synthetic (cs) DMARDs (methotrexate (MTX), leflunomide, sulfasalazine); glucocorticoids (GCs); biological (b) DMARDs (tumour necrosis factor inhibitors (adalimumab, certolizumab pegol, etanercept, golimumab, infliximab), abatacept, rituximab, tocilizumab, sarilumab and biosimilar (bs) DMARDs) and targeted synthetic (ts) DMARDs (the Janus kinase (JAK) inhibitors tofacitinib, baricitinib, filgotinib, upadacitinib). "
}
] | 11 |
BioASQ-training11b
| null | null |
60259fe91cb411341a0000b3
| 354 |
yesno
|
Does chromatin accessibility affect CRISPR-Cas9 efficiency?
|
['yes']
|
[
"yes"
] |
['Yes, chromatin accessibility significantly affects CRISPR-Cas9 efficiency. The abstracts collectively demonstrate that gene editing is more efficient in euchromatin (open chromatin) than in heterochromatin (closed chromatin). This correlation is observed in various cell lines and organisms, including HEK293T cells, HeLa cells, human fibroblasts, and zebrafish embryos. The studies show that chromatin openness positively correlates with CRISPR-Cas9 mutagenesis efficiency, whereas closed chromatin regions exhibit reduced editing efficiency. These findings are consistent across different experimental settings, including in vitro and in vivo systems. Furthermore, modulating chromatin accessibility using transactivation or targeting proximal dsgRNAs can enhance Cas9 editing efficiency in vivo. Therefore, considering chromatin accessibility is crucial for optimizing CRISPR-Cas9 gene editing outcomes.', 'While many studies consider DNA sequences of CRISPR target sites as the primary determinant for CRISPR-Cas9 mutagenesis efficiency and mutation profiles, increasing evidence reveals the substantial role of chromatin context. Indeed, results across different organisms have shown that Cas9-mediated editing is more efficient in open chromatin regions (euchromatin) than in closed ones (heterochromatin).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28580607",
"http://www.ncbi.nlm.nih.gov/pubmed/31672284",
"http://www.ncbi.nlm.nih.gov/pubmed/36727449",
"http://www.ncbi.nlm.nih.gov/pubmed/37162994",
"http://www.ncbi.nlm.nih.gov/pubmed/27280977",
"http://www.ncbi.nlm.nih.gov/pubmed/37985205",
"http://www.ncbi.nlm.nih.gov/pubmed/30413470",
"http://www.ncbi.nlm.nih.gov/pubmed/31349852",
"http://www.ncbi.nlm.nih.gov/pubmed/36374245",
"http://www.ncbi.nlm.nih.gov/pubmed/31799598",
"http://www.ncbi.nlm.nih.gov/pubmed/29684067",
"http://www.ncbi.nlm.nih.gov/pubmed/33659408",
"http://www.ncbi.nlm.nih.gov/pubmed/26987018",
"http://www.ncbi.nlm.nih.gov/pubmed/30189348",
"http://www.ncbi.nlm.nih.gov/pubmed/37456665",
"http://www.ncbi.nlm.nih.gov/pubmed/31967103",
"http://www.ncbi.nlm.nih.gov/pubmed/35689624",
"http://www.ncbi.nlm.nih.gov/pubmed/30201707",
"http://www.ncbi.nlm.nih.gov/pubmed/28303677",
"http://www.ncbi.nlm.nih.gov/pubmed/30540740",
"http://www.ncbi.nlm.nih.gov/pubmed/28800611"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28580607",
"endSection": "abstract",
"offsetInBeginSection": 457,
"offsetInEndSection": 621,
"text": "Our study indicates that gene editing is more efficient in euchromatin than in heterochromatin, and we validate this finding in HeLa cells and in human fibroblasts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29684067",
"endSection": "abstract",
"offsetInBeginSection": 1183,
"offsetInEndSection": 1280,
"text": "We found a correlation between chromatin openness and the efficiency of CRISPR-Cas9 mutagenesis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31349852",
"endSection": "abstract",
"offsetInBeginSection": 100,
"offsetInEndSection": 220,
"text": "We show that Cas9-mediated editing is more efficient in open chromatin regions than in closed chromatin regions in rice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35689624",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 343,
"text": "While many studies consider DNA sequences of CRISPR target sites as the primary determinant for CRISPR mutagenesis efficiency and mutation profiles, increasing evidence reveals the substantial role of chromatin context"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35689624",
"endSection": "abstract",
"offsetInBeginSection": 1350,
"offsetInEndSection": 1550,
"text": "Our findings provide strong evidence that specific chromatin features could have substantial and lasting impacts on both CRISPR-Cas9 mutagenesis efficiency and DNA double-strand break repair outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28303677",
"endSection": "abstract",
"offsetInBeginSection": 1469,
"offsetInEndSection": 1571,
"text": "Furthermore, we demonstrate that DNA target site accessibility influences the activity of CRISPR/Cas9."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36374245",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 374,
"text": "In this study, we show that chromatin open status is a pivotal determinant of the Cas9 editing activity in mammalian cells, and increasing chromatin accessibility can efficiently improve Cas9 genome editing"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28580607",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Chromatin accessibility and guide sequence secondary structure affect CRISPR-Cas9 gene editing efficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29684067",
"endSection": "abstract",
"offsetInBeginSection": 1183,
"offsetInEndSection": 1394,
"text": "We found a correlation between chromatin openness and the efficiency of CRISPR-Cas9 mutagenesis. These results indicate that CRISPR-Cas9 mutagenesis is influenced by chromatin accessibility in zebrafish embryos."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28800611",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1294,
"text": "Our study demonstrated that chromatin accessibility showed positive correlation with CRISPR/Cas9 efficiency, but we did not observe a clear correlation between nucleosome organization and CRISPR/Cas9 efficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28800611",
"endSection": "abstract",
"offsetInBeginSection": 363,
"offsetInEndSection": 497,
"text": "Besides the sequence features, local chromatin structures may have effects on CRISPR/Cas9 efficiency, which remain largely unexplored."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29684067",
"endSection": "abstract",
"offsetInBeginSection": 951,
"offsetInEndSection": 1394,
"text": "In order to further inspect the effect of chromatin on CRISPR-Cas9 mutagenesis, we analysed the relationship of selected chromatin features on CRISPR-Cas9 mutagenesis efficiency using publicly available data from zebrafish embryos. We found a correlation between chromatin openness and the efficiency of CRISPR-Cas9 mutagenesis. These results indicate that CRISPR-Cas9 mutagenesis is influenced by chromatin accessibility in zebrafish embryos."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29684067",
"endSection": "abstract",
"offsetInBeginSection": 951,
"offsetInEndSection": 1279,
"text": "In order to further inspect the effect of chromatin on CRISPR-Cas9 mutagenesis, we analysed the relationship of selected chromatin features on CRISPR-Cas9 mutagenesis efficiency using publicly available data from zebrafish embryos. We found a correlation between chromatin openness and the efficiency of CRISPR-Cas9 mutagenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28800611",
"endSection": "abstract",
"offsetInBeginSection": 363,
"offsetInEndSection": 700,
"text": "Besides the sequence features, local chromatin structures may have effects on CRISPR/Cas9 efficiency, which remain largely unexplored. In the only related study in zebrafish, nucleosome organization was not found to have an effect on CRISPR/Cas9 efficiency, which is inconsistent with recent studies in vitro and in mammalian cell lines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36374245",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 375,
"text": "In this study, we show that chromatin open status is a pivotal determinant of the Cas9 editing activity in mammalian cells, and increasing chromatin accessibility can efficiently improve Cas9 genome editing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30189348",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 377,
"text": "Recent studies indicate that heterochromatin can negatively affect Cas9 binding and functioning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30540740",
"endSection": "abstract",
"offsetInBeginSection": 1171,
"offsetInEndSection": 1452,
"text": "Combined, our data show that heterochromatin imposes a permeable barrier that influences the kinetics, but not the endpoint, of CRISPR-Cas9 genome editing and suggest that therapeutic applications involving low-level Cas9 exposure will be particularly affected by chromatin status."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29684067",
"endSection": "abstract",
"offsetInBeginSection": 1280,
"offsetInEndSection": 1394,
"text": "These results indicate that CRISPR-Cas9 mutagenesis is influenced by chromatin accessibility in zebrafish embryos."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29684067",
"endSection": "abstract",
"offsetInBeginSection": 1183,
"offsetInEndSection": 1279,
"text": "We found a correlation between chromatin openness and the efficiency of CRISPR-Cas9 mutagenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37162994",
"endSection": "abstract",
"offsetInBeginSection": 387,
"offsetInEndSection": 717,
"text": "We found that both regional constitutive heterochromatin and local nucleosome occlusion of target sites impede editing, while position-specific G/C nucleotides in the primer binding site (PBS) and reverse transcription (RT) template regions of PE guide-RNA (pegRNA) yield high editing efficiency, especially for short PBS designs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37456665",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 93,
"text": "Chromatin structure and context-dependent sequence features control prime editing efficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31799598",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 307,
"text": "Despite the rapid development of CRISPR/Cas9-mediated gene editing technology, the gene editing potential of CRISPR/Cas9 is hampered by low efficiency, especially for clinical applications. One of the major challenges is that chromatin compaction inevitably limits the Cas9 protein access to the target DNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33659408",
"endSection": "abstract",
"offsetInBeginSection": 132,
"offsetInEndSection": 467,
"text": "Different intracellular environments (dependent on cell type or cell cycle state for example) may affect sgRNA efficiency by altering accessibility of genomic DNA through DNA modifications such as epigenetic marks and DNA-binding proteins (e.g., histones) as well as alteration of the chromatin state of genomic DNA within the nucleus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35689624",
"endSection": "abstract",
"offsetInBeginSection": 730,
"offsetInEndSection": 877,
"text": "Our results indicated that DNA methylation and chromatin features could lead to substantial variations in mutagenesis efficiency by up to 250-fold."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31672284",
"endSection": "abstract",
"offsetInBeginSection": 54,
"offsetInEndSection": 1501,
"text": "CRISPR/Cas9 has been a major research focus. Whereas sequence complementarity between guide RNA and target DNA substantially dictates cleavage efficiency, DNA accessibility of the targeted loci has also been hypothesized to be an important factor. In this study, functional data from two genome-wide assays, genome-wide, unbiased identification of DSBs enabled by sequencing (GUIDE-seq) and circularization for in vitro reporting of cleavage effects by sequencing (CIRCLE-seq), have been computationally analyzed in conjunction with DNA accessibility determined via DNase I-hypersensitive sequencing from the Encyclopedia of DNA Elements (ENCODE) Database and transcriptome from the Sequence Read Archive to determine whether cellular factors influence CRISPR-induced cleavage efficiency. CIRCLE-seq and GUIDE-seq datasets were selected to represent the absence and presence of cellular factors, respectively. Data analysis revealed that correlations between sequence similarity and CRISPR-induced cleavage frequency were altered by the presence of cellular factors that modulated the level of DNA accessibility. The above-mentioned correlation was abolished when cleavage sites were located in less accessible regions. Furthermore, CRISPR-mediated edits were permissive even at regions that were insufficient for most endogenous genes to be expressed. These results provide a strong basis to dissect the contribution of local chromatin modulation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31349852",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "The CRISPR/Cas9 system is unable to edit all targetable genomic sites with full efficiency in vivo. We show that Cas9-mediated editing is more efficient in open chromatin regions than in closed chromatin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30413470",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 535,
"text": "To investigate whether and how CRISPR-Cas9 on-target and off-target activities are affected by chromatin in eukaryotic cells, we first identified a series of identical endogenous DNA sequences present in both open and closed chromatin regions and then measured mutation frequencies at these sites in human cells using Cas9 complexed with matched or mismatched sgRNAs. Unlike matched sgRNAs, mismatched sgRNAs were highly sensitive to chromatin states, suggesting that off-target but not on-target DNA cleavage is hindered by chromatin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27280977",
"endSection": "abstract",
"offsetInBeginSection": 809,
"offsetInEndSection": 981,
"text": "By using these systems, we demonstrate that TALENs and CRISPR/Cas9 nucleases are both significantly affected by the high-order epigenetic context of their target sequences."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26987018",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 810,
"text": "In vitro experiments demonstrated that nucleosomes in fact directly impede Cas9 binding and cleavage, while chromatin remodeling can restore Cas9 access."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30540740",
"endSection": "abstract",
"offsetInBeginSection": 730,
"offsetInEndSection": 967,
"text": "We found that heterochromatin can impede mutagenesis, but to a degree that depends on other key experimental parameters. Mutagenesis was impeded by up to 7-fold when Cas9 exposure was brief and when intracellular Cas9 expression was low."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31349852",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "The CRISPR/Cas9 system is unable to edit all targetable genomic sites with full efficiency in vivo. We show that Cas9-mediated editing is more efficient in open chromatin regions than in closed chromatin regions in rice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26987018",
"endSection": "abstract",
"offsetInBeginSection": 530,
"offsetInEndSection": 656,
"text": "We observed that highly active sgRNAs for Cas9 and dCas9 were found almost exclusively in regions of low nucleosome occupancy."
}
] | 13 |
BioASQ-training13b
| null | null |
661c413f48a2c27714000006
| 355 |
yesno
|
Can untranslated regions (UTRs) regulate gene expression?
|
['yes']
|
[
"yes"
] |
['Although UTRs are not part of the protein-coding region of genes, they can control gene expression in various ways because they contain various elements important for the regulation of mRNA stability or translation.', "Yes, untranslated regions (UTRs) can regulate gene expression by controlling mRNA stability and translation. The 5'-UTRs control transcriptional initiation and mRNA stability, while the 3'-UTRs play a key role in post-transcriptional regulation by harboring cis-acting elements that bind to RNA-binding proteins and microRNAs, thereby affecting mRNA stability and translation rates.", "Yes, untranslated regions (UTRs) can regulate gene expression. UTRs are located at the ends of a gene's coding sequence and contain regulatory elements that can control the expression of the gene. These elements can affect the stability of the mRNA, the rate of translation, and the amount of protein produced. UTRs can also contain binding sites for transcription factors, which can further regulate gene expression."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28229978",
"http://www.ncbi.nlm.nih.gov/pubmed/27208003",
"http://www.ncbi.nlm.nih.gov/pubmed/10977083",
"http://www.ncbi.nlm.nih.gov/pubmed/15608165",
"http://www.ncbi.nlm.nih.gov/pubmed/36399486",
"http://www.ncbi.nlm.nih.gov/pubmed/26386038",
"http://www.ncbi.nlm.nih.gov/pubmed/24067953",
"http://www.ncbi.nlm.nih.gov/pubmed/22538991",
"http://www.ncbi.nlm.nih.gov/pubmed/18631145",
"http://www.ncbi.nlm.nih.gov/pubmed/30120519",
"http://www.ncbi.nlm.nih.gov/pubmed/28867199",
"http://www.ncbi.nlm.nih.gov/pubmed/28985357",
"http://www.ncbi.nlm.nih.gov/pubmed/7662369",
"http://www.ncbi.nlm.nih.gov/pubmed/20720301",
"http://www.ncbi.nlm.nih.gov/pubmed/21543795",
"http://www.ncbi.nlm.nih.gov/pubmed/21075793",
"http://www.ncbi.nlm.nih.gov/pubmed/16430990",
"http://www.ncbi.nlm.nih.gov/pubmed/19880380",
"http://www.ncbi.nlm.nih.gov/pubmed/28287067",
"http://www.ncbi.nlm.nih.gov/pubmed/20037631",
"http://www.ncbi.nlm.nih.gov/pubmed/22846368",
"http://www.ncbi.nlm.nih.gov/pubmed/22614827",
"http://www.ncbi.nlm.nih.gov/pubmed/30961831",
"http://www.ncbi.nlm.nih.gov/pubmed/34287278"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22538991",
"endSection": "abstract",
"offsetInBeginSection": 175,
"offsetInEndSection": 582,
"text": "Previously dismissed as \"junk DNA\", it is the non-coding regions of the genome that are responsible for regulation, facilitating complex temporal and spatial gene expression through the combinatorial effect of numerous mechanisms and interactions working together to fine-tune gene expression. The major regions involved in regulation of a particular gene are the 5' and 3' untranslated regions and introns."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18631145",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Post-transcriptional regulation, via 5'-UTRs (5'-untranslated regions), plays an important role in the control of eukaryotic gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28287067",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 320,
"text": "Eukaryotic gene expression is precisely regulated at all points between transcription and translation. In this review, we focus on translational control mediated by the 3'-untranslated regions (UTRs) of mRNAs. mRNA 3'-UTRs contain cis-acting elements that function in the regulation of protein translation or mRNA decay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27208003",
"endSection": "abstract",
"offsetInBeginSection": 123,
"offsetInEndSection": 378,
"text": "Now, we are beginning to better appreciate the role of 3'-UTR (untranslated region) cis-elements which harbor not only microRNA but also RNA-binding protein (RBP) binding sites that have significant effect on the stability and translational rate of mRNAs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28985357",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Many studies using reporter assays have demonstrated that 3' untranslated regions (3'-UTRs) regulate gene expression by controlling mRNA stability and translation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16430990",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "The untranslated regions of mRNAs can determine gene expression by influencing mRNA stability and translational efficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28229978",
"endSection": "abstract",
"offsetInBeginSection": 449,
"offsetInEndSection": 623,
"text": "In higher eukaryotes, untranslated regions (UTRs) of transcripts are one of the crucial regulators of gene expression (influencing mRNA stability and translation efficiency)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21075793",
"endSection": "abstract",
"offsetInBeginSection": 821,
"offsetInEndSection": 1063,
"text": "Our results suggest that 3'UTR sequences can function not only in cis to regulate protein expression, but also intrinsically and independently in trans, likely as noncoding RNAs, a conclusion supported by a number of previous genetic studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21075793",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "The 3' untranslated regions (3'UTRs) of eukaryotic genes regulate mRNA stability, localization and translation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36399486",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 272,
"text": "The 5' and 3' untranslated regions of eukaryotic mRNAs (UTRs) play crucial roles in the post-transcriptional regulation of gene expression through the modulation of nucleo-cytoplasmic mRNA transport, translation efficiency, subcellular localization, and message stability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24067953",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "3' untranslated regions (UTRs) are known to play an important role in posttranscriptional regulation of gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7662369",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "The 3' untranslated region (3' UTR) can control gene expression by affecting the localization, stability and translation of mRNAs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28229978",
"endSection": "abstract",
"offsetInBeginSection": 448,
"offsetInEndSection": 623,
"text": " In higher eukaryotes, untranslated regions (UTRs) of transcripts are one of the crucial regulators of gene expression (influencing mRNA stability and translation efficiency)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10977083",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Untranslated regions (UTR) play important roles in the posttranscriptional regulation of mRNA processing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34287278",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "Untranslated gene regions (UTRs) play an important role in controlling gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28867199",
"endSection": "abstract",
"offsetInBeginSection": 120,
"offsetInEndSection": 197,
"text": " The untranslated regions (UTRs) of mRNA are hotspots for regulatory control."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22846368",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Untranslated regions (UTRs) in eukaryotes play a significant role in the regulation of translation and mRNA half-life, as well as interacting with specific RNA-binding proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20720301",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Untranslated regions (UTRs) of eukaryotic mRNAs play crucial roles in post-transcriptional regulation of gene expression via the modulation of nucleocytoplasmic mRNA transport, translation efficiency, subcellular localization, and message stability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30961831",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 364,
"text": "The 5' and 3' untranslated regions (UTRs) regulate crucial aspects of post-transcriptional gene regulation that are necessary for the maintenance of cellular homeostasis. When these processes go awry through mutation or misexpression of certain regulatory elements, the subsequent deregulation of oncogenic gene expression can drive or enhance cancer pathogenesis."
}
] | 12 |
BioASQ-training12b
| null | null |
6428d7da690f196b51000050
| 356 |
yesno
|
Is osteocrin expressed exclusively in the bone?
|
['no']
|
[
"no"
] |
['No, Osteocrin (Ostn) has been detected in the bones and the brain.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/15923362",
"http://www.ncbi.nlm.nih.gov/pubmed/14523025",
"http://www.ncbi.nlm.nih.gov/pubmed/27830782",
"http://www.ncbi.nlm.nih.gov/pubmed/17951249"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27830782",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Evolution of Osteocrin as an activity-regulated factor in the primate brain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27830782",
"endSection": "abstract",
"offsetInBeginSection": 390,
"offsetInEndSection": 601,
"text": "Here we use transcriptional profiling of human fetal brain cultures to identify an activity-dependent secreted factor, Osteocrin (OSTN), that is induced by membrane depolarization of human but not mouse neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17951249",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Osteocrin (Ostn) is a recently discovered secreted protein produced by cells of the osteoblast lineage that shows a well conserved homology with members of the natriuretic peptide (NP) family. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15923362",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Osteocrin (Ostn), a bone-active molecule, has been shown in animals to be highly expressed in cells of the osteoblast lineage. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14523025",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Osteocrin, a novel bone-specific secreted protein that modulates the osteoblast phenotype."
}
] | 6 |
BioASQ-training6b
| null | null |
58df73bd38f7f3e93a000001
| 357 |
yesno
|
Are there any desmins present in plants?
|
['No.']
|
[
"No."
] |
['No. Desmins are type III intermediate filament (IF) proteins that have been identified to date only in metazoa (human, Danio rerio, bovine). Desmins are also associated with severe forms of skeletal, cardiac and myofibrillar myopathies.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20171226",
"http://www.ncbi.nlm.nih.gov/pubmed/19026658",
"http://www.ncbi.nlm.nih.gov/pubmed/18033728",
"http://www.ncbi.nlm.nih.gov/pubmed/12529857",
"http://www.ncbi.nlm.nih.gov/pubmed/10929203",
"http://www.ncbi.nlm.nih.gov/pubmed/8752741",
"http://www.ncbi.nlm.nih.gov/pubmed/1694790",
"http://www.ncbi.nlm.nih.gov/pubmed/2659540",
"http://www.ncbi.nlm.nih.gov/pubmed/7460905"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20171226",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Inherited mutations in the gene coding for the intermediate filament protein desmin have been demonstrated to cause severe skeletal and cardiac myopathies."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19026658",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Mutations in the intermediate filament (IF) protein desmin cause severe forms of myofibrillar myopathy characterized by partial aggregation of the extrasarcomeric desmin cytoskeleton and structural disorganization of myofibrils."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18033728",
"endSection": "sections.0",
"offsetInBeginSection": 135,
"offsetInEndSection": 479,
"text": "The family of 70 intermediate filament genes (including those encoding keratins, desmins, and lamins) is now known to be associated with a wide range of diverse diseases, at least 72 distinct human pathologies, including skin blistering, muscular dystrophy, cardiomyopathy, premature aging syndromes, neurodegenerative disorders, and cataract. "
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12529857",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Mutations in desmin have been associated with a subset of human myopathies."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10929203",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Characterization of a zebrafish (Danio rerio) desmin cDNA: an early molecular marker of myogenesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12529857",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 93,
"text": "Acute effects of desmin mutations on cytoskeletal and cellular integrity in cardiac myocytes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10929203",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 293,
"text": "Desmin is a muscle-specific protein and a constitutive subunit of the intermediate filaments (IF) in skeletal, cardiac and smooth muscles. It is an early marker of skeletal muscle myogenesis. We have characterized a clone of desmin cDNA from an embryonic zebrafish (Danio rerio) cDNA library. "
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8752741",
"endSection": "sections.0",
"offsetInBeginSection": 1055,
"offsetInEndSection": 1246,
"text": "Immunohistochemical investigation showed a positive reaction for smooth muscle actin and desmins in the spindle cells proliferated in the lymph nodes; no cytokeratin positivity was detected. "
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1694790",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "We have raised monoclonal antibodies (Mab) to the Mr 55,000 desmin polypeptide, electrophoretically purified from cytoskeletal preparations of isolated bovine heart Purkinje fibers. "
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2659540",
"endSection": "sections.0",
"offsetInBeginSection": 237,
"offsetInEndSection": 409,
"text": "Mesothelial and ovarian carcinoma cells could not be distinguished by (intermediate) filament typing, using monoclonal antibodies (MAbs) to keratins, vimentins and desmins."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7460905",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "A fast and convenient procedure for the purification of polymerization-competent smooth-muscle desmin is described. Desmin from chicken gizzard and hog stomach were compared by fingerprint techniques. "
}
] | 5 |
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/DESM_CHICK",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0045098"
] |
[
{
"o": "http://linkedlifedata.com/resource/geneontology/id/GO:0005882",
"p": "http://www.w3.org/2004/02/skos/core#broader",
"s": "http://linkedlifedata.com/resource/geneontology/id/GO:0045098"
}
] |
5162e011298dcd4e51000049
| 358 |
yesno
|
Do cells undergoing necroptosis show disruption of their cell membranes?
|
['yes']
|
[
"yes"
] |
['Necroptosis is a form of caspase-independent programmed cell death that arises from disruption of cell membranes', 'Yes, cells undergoing necroptosis show disruption of their cell membranes due to the activation of the MLKL pseudokinase by upstream kinases, leading to membrane rupture and cell death.', 'Yes, cells undergoing necroptosis show disruption of their cell membranes, leading to the release of intracellular contents.', 'Yes, cells undergoing necroptosis show disruption of their cell membranes, which is a key feature of this type of programmed cell death.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33848465",
"http://www.ncbi.nlm.nih.gov/pubmed/27158445",
"http://www.ncbi.nlm.nih.gov/pubmed/31138766",
"http://www.ncbi.nlm.nih.gov/pubmed/35365636",
"http://www.ncbi.nlm.nih.gov/pubmed/30709919",
"http://www.ncbi.nlm.nih.gov/pubmed/28388412",
"http://www.ncbi.nlm.nih.gov/pubmed/30148498",
"http://www.ncbi.nlm.nih.gov/pubmed/31766571",
"http://www.ncbi.nlm.nih.gov/pubmed/30344099",
"http://www.ncbi.nlm.nih.gov/pubmed/32839552",
"http://www.ncbi.nlm.nih.gov/pubmed/31490656",
"http://www.ncbi.nlm.nih.gov/pubmed/29076500",
"http://www.ncbi.nlm.nih.gov/pubmed/28388403",
"http://www.ncbi.nlm.nih.gov/pubmed/30341907"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35365636",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 314,
"text": "Necroptosis is a form of caspase-independent programmed cell death that arises from disruption of cell membranes by the mixed lineage kinase domain-like (MLKL) pseudokinase after its activation by the upstream kinases, receptor interacting protein kinase (RIPK)-1 and RIPK3, within a complex known as the necrosome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31138766",
"endSection": "abstract",
"offsetInBeginSection": 677,
"offsetInEndSection": 814,
"text": "Thus, cells undergoing necroptosis need to overcome these independent suppressive mechanisms before plasma membrane disruption can occur."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31490656",
"endSection": "abstract",
"offsetInBeginSection": 1263,
"offsetInEndSection": 1556,
"text": "Taken together, these results confirm the active role of VLCFAs during necroptosis and point to multiple potential mechanisms of membrane disruption including direct permeabilization via bilayer disruption and permeabilization by targeting of proteins to cellular membranes by fatty acylation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35365636",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 315,
"text": "Necroptosis is a form of caspase-independent programmed cell death that arises from disruption of cell membranes by the mixed lineage kinase domain-like (MLKL) pseudokinase after its activation by the upstream kinases, receptor interacting protein kinase (RIPK)-1 and RIPK3, within a complex known as the necrosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31490656",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Necroptosis is a form of regulated cell death which results in loss of plasma membrane integrity, release of intracellular contents, and an associated inflammatory response."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28388412",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 385,
"text": "Here, we show that, during necroptosis, MLKL-dependent calcium (Ca2+) influx and phosphatidylserine (PS) exposure on the outer leaflet of the plasma membrane preceded loss of PM integrity."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31490656",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Membrane Disruption by Very Long Chain Fatty Acids during Necroptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28388412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "The activation of mixed lineage kinase-like (MLKL) by receptor-interacting protein kinase-3 (RIPK3) results in plasma membrane (PM) disruption and a form of regulated necrosis, called necroptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28388403",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Necroptosis is a highly inflammatory form of programmed cell death that results from MLKL-mediated disruption of the cell membrane."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32839552",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 283,
"text": "Necroptosis, a form of programmed cell death, is characterized by the loss of membrane integrity and release of intracellular contents, the execution of which depends on the membrane-disrupting activity of the Mixed Lineage Kinase Domain-Like protein (MLKL) upon its phosphorylation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30344099",
"endSection": "abstract",
"offsetInBeginSection": 324,
"offsetInEndSection": 556,
"text": "Here we report that, following sciatic nerve injury, MLKL, a pseudokinase known to rupture cell membranes during necroptotic cell death, is induced and targets the myelin sheath membrane of Schwann cells to promote myelin breakdown."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28388412",
"endSection": "abstract",
"offsetInBeginSection": 689,
"offsetInEndSection": 794,
"text": "Under conditions of necroptotic cell death, ESCRT-III controls the duration of plasma membrane integrity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31766571",
"endSection": "abstract",
"offsetInBeginSection": 108,
"offsetInEndSection": 198,
"text": "Necroptosis induction leads to cell membrane disruption, inflammation and vascularization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30341907",
"endSection": "abstract",
"offsetInBeginSection": 464,
"offsetInEndSection": 657,
"text": " Both necrosis and necroptosis show similar morphological features and are characterized by an increase in cell volume, cell membrane permeabilization, and rupture that lead to cellular demise."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31138766",
"endSection": "abstract",
"offsetInBeginSection": 676,
"offsetInEndSection": 814,
"text": " Thus, cells undergoing necroptosis need to overcome these independent suppressive mechanisms before plasma membrane disruption can occur."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27158445",
"endSection": "abstract",
"offsetInBeginSection": 905,
"offsetInEndSection": 1055,
"text": "chanisms by which the essential, and possibly terminal, necroptotic effector, MLKL, triggers the disruption of cellular membranes to cause cell lysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33848465",
"endSection": "abstract",
"offsetInBeginSection": 484,
"offsetInEndSection": 634,
"text": "uring necroptosis. We show that MLKL and phosphoMLKL, key for membrane permeabilization, are exclusively acylated during necroptosis. Reducing the lev"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30709919",
"endSection": "abstract",
"offsetInBeginSection": 235,
"offsetInEndSection": 385,
"text": "anslocates to and disrupts the plasma membrane, thereby causing necroptotic cell lysis. Herein, we show that activation of necroptosis in mouse dermal"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30148498",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 260,
"text": "Necroptosis is a programmed cell death pathway triggered by activation of receptor interacting protein kinase 3 (RIPK3), which phosphorylates and activates the mixed lineage kinase-like domain pseudokinase, MLKL, to rupture or permeabilize the plasma membrane."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29076500",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 410,
"text": " non-inflammatory process while necrosis triggers inflammation. Recent studies on necroptosis and pyroptosis, two types of programmed necrosis, revealed that plasma membrane rupture is mediated by MLKL channels during necroptosis but depen"
}
] | 12 |
BioASQ-training12b
| null | null |
641357bc201352f04a000039
| 359 |
yesno
|
Are there roles for cohesin mutations in AML?
|
['yes']
|
[
"yes"
] |
['Yes. Several landmark studies have shown that cohesin mutations perturb the balance between self-renewal and differentiation of hematopoietic stem and progenitor cells (HSPC). Emerging data now begin to uncover the molecular mechanisms that underpin this phenotype. Among these mechanisms is a role for cohesin in the control of inflammatory responses in HSPCs and myeloid cells. Inflammatory signals limit HSPC self-renewal and drive HSPC differentiation. Consistent with this, cohesin mutations promote resistance to inflammatory signals, and may provide a selective advantage for AML progression.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31552185"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31552185",
"endSection": "abstract",
"offsetInBeginSection": 741,
"offsetInEndSection": 1336,
"text": "Several landmark studies have shown that cohesin mutations perturb the balance between self-renewal and differentiation of hematopoietic stem and progenitor cells (HSPC). Emerging data now begin to uncover the molecular mechanisms that underpin this phenotype. Among these mechanisms is a role for cohesin in the control of inflammatory responses in HSPCs and myeloid cells. Inflammatory signals limit HSPC self-renewal and drive HSPC differentiation. Consistent with this, cohesin mutations promote resistance to inflammatory signals, and may provide a selective advantage for AML progression. "
}
] | 11 |
BioASQ-training11b
| null | null |
621e9aa13a8413c653000053
| 360 |
yesno
|
Is adenosine methylation an epigenetic modification?
|
['yes']
|
[
"yes"
] |
['Adenosine methylation is the most common mammalian epigenetic modification of mRNAs that is directed by a large methyltransferase complex containing Mettl3.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36196023",
"http://www.ncbi.nlm.nih.gov/pubmed/31243897",
"http://www.ncbi.nlm.nih.gov/pubmed/34850126",
"http://www.ncbi.nlm.nih.gov/pubmed/23453015",
"http://www.ncbi.nlm.nih.gov/pubmed/29082271",
"http://www.ncbi.nlm.nih.gov/pubmed/33839323",
"http://www.ncbi.nlm.nih.gov/pubmed/36314059",
"http://www.ncbi.nlm.nih.gov/pubmed/33630241",
"http://www.ncbi.nlm.nih.gov/pubmed/32245489",
"http://www.ncbi.nlm.nih.gov/pubmed/35696004",
"http://www.ncbi.nlm.nih.gov/pubmed/33999093",
"http://www.ncbi.nlm.nih.gov/pubmed/32513173",
"http://www.ncbi.nlm.nih.gov/pubmed/32867812",
"http://www.ncbi.nlm.nih.gov/pubmed/35406663",
"http://www.ncbi.nlm.nih.gov/pubmed/31801551",
"http://www.ncbi.nlm.nih.gov/pubmed/29036602",
"http://www.ncbi.nlm.nih.gov/pubmed/35095893",
"http://www.ncbi.nlm.nih.gov/pubmed/34130310",
"http://www.ncbi.nlm.nih.gov/pubmed/34039354",
"http://www.ncbi.nlm.nih.gov/pubmed/31188932",
"http://www.ncbi.nlm.nih.gov/pubmed/35032318",
"http://www.ncbi.nlm.nih.gov/pubmed/35752056",
"http://www.ncbi.nlm.nih.gov/pubmed/36407103",
"http://www.ncbi.nlm.nih.gov/pubmed/35748227"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36196023",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 405,
"text": "Epigenetic modifications have received increasing attention and have been shown to be extensively involved in kidney development and disease progression. Among them, the most common RNA modification, N6 -methyladenosine (m6 A), has been shown to dynamically and reversibly exert its functions in multiple ways, including splicing, export, decay and translation initiation efficiency to regulate mRNA fate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36314059",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 311,
"text": "N6-methyladenosine (m6A) methylation is the most abundant mammalian mRNA modification. m6A regulates RNA processing, splicing, nucleation, translation and stability by transferring, removing and recognizing m6A methylation sites, which are critical for cancer initiation, progression, metabolism and metastasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34130310",
"endSection": "abstract",
"offsetInBeginSection": 10,
"offsetInEndSection": 259,
"text": "The methyltransferase-like 3 (Mettl3) is a key component of the large N6-adenosine-methyltransferase complex in mammalian responsible for RNA N6-methyladenosine (m6A) modification, which plays an important role in gene post-transcription modulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31188932",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 223,
"text": "Methylation of the N6 position of adenosine (m6A) is a post-transcriptional epigenetic modification of RNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35032318",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 260,
"text": "N6-methyladenosine (m6A) is a dynamic reversible methylation modification of the adenosine N6 position and is the most common chemical epigenetic modification among mRNA post-transcriptional modifications, including methylation, demethylation, and recognition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35748227",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 298,
"text": "N6-adenosine methylation (m6A) is one of the most common modifications on mRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31801551",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "N6-methyladenosine (m6A) is methylation that occurs in the N6-position of adenosine, which is the most prevalent internal modification on eukaryotic mRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32867812",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 362,
"text": "The N6-methyl adenosine (m6A) is an important epigenetic modification primarily present on mRNA that controls the levels of transcripts and efficiency of translation in eukaryotes."
}
] | 12 |
BioASQ-training12b
| null | null |
6429eb8457b1c7a31500000a
| 361 |
yesno
|
Can Isradipine slow progression of Early Parkinson Disease?
|
['no']
|
[
"no"
] |
['No. In a multicenter, randomized, parallel-group, double-blind, placebo-controlled trial Isradipine did not slow progression of Early Parkinson Disease.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32227247",
"http://www.ncbi.nlm.nih.gov/pubmed/34766657",
"http://www.ncbi.nlm.nih.gov/pubmed/33460320",
"http://www.ncbi.nlm.nih.gov/pubmed/33716705"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32227247",
"endSection": "abstract",
"offsetInBeginSection": 1255,
"offsetInEndSection": 1569,
"text": "Adjusted least-squares mean changes in total UPDRS score in the antiparkinson medication ON state over 36 months for isradipine and placebo recipients were 2.99 (95% CI, 0.95 to 5.03) points versus 3.26 (CI, 1.25 to 5.26) points, respectively, with a treatment effect of -0.27 (CI, -3.02 to 2.48) point (P = 0.85)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32227247",
"endSection": "abstract",
"offsetInBeginSection": 1924,
"offsetInEndSection": 2046,
"text": "Conclusion: Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage PD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34766657",
"endSection": "abstract",
"offsetInBeginSection": 1511,
"offsetInEndSection": 1727,
"text": "ONS: These results are consistent with the recent secondary analysis of the STEADY-PD III clinical trial-suggesting that clinically attainable brain exposure to isradipine may slow early-stage PD progression. © 2021 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34766657",
"endSection": "abstract",
"offsetInBeginSection": 314,
"offsetInEndSection": 404,
"text": "These findings suggest that greater exposure to isradipine might slow disease progression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32227247",
"endSection": "abstract",
"offsetInBeginSection": 1942,
"offsetInEndSection": 2064,
"text": "erm treatment with immediate-release isradipine did not slow the clinical progression of early-stage PD.Primary Funding So"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34766657",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 304,
"text": "BACKGROUND: Recent examination of the STEADY-PD III isradipine clinical trial data concluded that early-stage Parkinson's disease (PD) participants who had longer exposure to isradipine had a significant delay in their need for symptomatic medication, as well as a lower medication burden at the end of t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33460320",
"endSection": "abstract",
"offsetInBeginSection": 985,
"offsetInEndSection": 1233,
"text": "RESULTS: Isradipine exposures did not correlate with the primary clinical outcome, changes in the antiparkinson therapy-adjusted Unified Parkinson's Disease Rating Scale parts I-III score over 36 months (Spearman rank correlation coefficient, rs : "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34766657",
"endSection": "abstract",
"offsetInBeginSection": 313,
"offsetInEndSection": 402,
"text": " These findings suggest that greater exposure to isradipine might slow disease progressio"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32227247",
"endSection": "abstract",
"offsetInBeginSection": 1924,
"offsetInEndSection": 2044,
"text": "Conclusion: Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage P"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33716705",
"endSection": "abstract",
"offsetInBeginSection": 943,
"offsetInEndSection": 1160,
"text": "However, in a recently completed phase 3 clinical trial, the dihydropyridine (DHP) LTCC inhibitor isradipine failed to slow disease progression in early PD patients, questioning the feasibility of DHPs for PD therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34766657",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 301,
"text": "BACKGROUND: Recent examination of the STEADY-PD III isradipine clinical trial data concluded that early-stage Parkinson's disease (PD) participants who had longer exposure to isradipine had a significant delay in their need for symptomatic medication, as well as a lower medication burden at the end o"
}
] | 11 |
BioASQ-training11b
| null | null |
61f93c38882a024a1000004b
| 362 |
yesno
|
Is nivolumab used for treatment of Non–Small-Cell Lung Cancer?
|
['yes']
|
[
"yes"
] |
['Yes, nivolumab used for treatment of Non–Small-Cell Lung Cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26028407",
"http://www.ncbi.nlm.nih.gov/pubmed/24685885",
"http://www.ncbi.nlm.nih.gov/pubmed/25897158",
"http://www.ncbi.nlm.nih.gov/pubmed/25704439",
"http://www.ncbi.nlm.nih.gov/pubmed/25496336",
"http://www.ncbi.nlm.nih.gov/pubmed/24402925",
"http://www.ncbi.nlm.nih.gov/pubmed/25965365"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028407",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 428,
"text": "BACKGROUND: Patients with advanced squamous-cell non-small-cell lung cancer (NSCLC) who have disease progression during or after first-line chemotherapy have limited treatment options. This randomized, open-label, international, phase 3 study evaluated the efficacy and safety of nivolumab, a fully human IgG4 programmed death 1 (PD-1) immune-checkpoint-inhibitor antibody, as compared with docetaxel in this patient population."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028407",
"endSection": "abstract",
"offsetInBeginSection": 1610,
"offsetInEndSection": 1855,
"text": "CONCLUSIONS: Among patients with advanced, previously treated squamous-cell NSCLC, overall survival, response rate, and progression-free survival were significantly better with nivolumab than with docetaxel, regardless of PD-L1 expression level."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24685885",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 741,
"text": "Agents currently in active clinical development for lung cancer include ipilimumab, which modulates the cytotoxic T-lymphocyte-associated antigen 4 pathway, and multiple agents targeting the programmed death protein 1 (PD-1) pathway, both anti-PD-1 compounds (nivolumab, pembrolizumab [MK-3475]) and those that target programmed death ligand 1 (PD-L1), a key ligand for PD-1 (BMS-936559, MPDL3280A)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25897158",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Overall Survival and Long-Term Safety of Nivolumab (Anti-Programmed Death 1 Antibody, BMS-936558, ONO-4538) in Patients With Previously Treated Advanced Non-Small-Cell Lung Cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25897158",
"endSection": "abstract",
"offsetInBeginSection": 318,
"offsetInEndSection": 666,
"text": "We report overall survival (OS), response durability, and long-term safety in patients with non-small-cell lung cancer (NSCLC) receiving nivolumab in this trial.PATIENTS AND METHODS: Patients (N = 129) with heavily pretreated advanced NSCLC received nivolumab 1, 3, or 10 mg/kg intravenously once every 2 weeks in 8-week cycles for up to 96 weeks. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25897158",
"endSection": "abstract",
"offsetInBeginSection": 1545,
"offsetInEndSection": 1752,
"text": "CONCLUSION: Nivolumab monotherapy produced durable responses and encouraging survival rates in patients with heavily pretreated NSCLC. Randomized clinical trials with nivolumab in advanced NSCLC are ongoing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24402925",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "Two PD-1 inhibitors, Bristol-Myers Squibb's nivolumab and Merck's MK-3475, both demonstrated positive results in phase I trials of previously treated patients with non-small cell lung cancer, reported at the World Conference on Lung Cancer in Sydney, Australia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25496336",
"endSection": "abstract",
"offsetInBeginSection": 718,
"offsetInEndSection": 923,
"text": "Recently, many trials addressed the role of such therapies for metastatic NSCLC treatment: ipilimumab, tremelimumab, nivolumab and lambrolizumab are immunotherapeutic agents of main interest in this field."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24402925",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "Two PD-1 inhibitors, Bristol-Myers Squibb's nivolumab and Merck's MK-3475, both demonstrated positive results in phase I trials of previously treated patients with non-small cell lung cancer, reported at the World Conference on Lung Cancer in Sydney, Australia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25496336",
"endSection": "abstract",
"offsetInBeginSection": 718,
"offsetInEndSection": 923,
"text": "Recently, many trials addressed the role of such therapies for metastatic NSCLC treatment: ipilimumab, tremelimumab, nivolumab and lambrolizumab are immunotherapeutic agents of main interest in this field."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24402925",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 270,
"text": "Two PD-1 inhibitors, Bristol-Myers Squibb's nivolumab and Merck's MK-3475, both demonstrated positive results in phase I trials of previously treated patients with non-small cell lung cancer, reported at the World Conference on Lung Cancer in Sydney, Australia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25965365",
"endSection": "abstract",
"offsetInBeginSection": 677,
"offsetInEndSection": 936,
"text": "Nivolumab, pembrolizumab (formerly known as MK-3475 and lambrolizumab), and pidilizumab are anti-PD-1 antibodies in clinical development for melanoma, non-small cell lung cancer, renal cell carcinoma, head and neck cancers, lymphoma, and several other cancers"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028407",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Nivolumab versus Docetaxel in Advanced Squamous-Cell Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25897158",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Overall Survival and Long-Term Safety of Nivolumab (Anti-Programmed Death 1 Antibody, BMS-936558, ONO-4538) in Patients With Previously Treated Advanced Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25704439",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Activity and safety of nivolumab, an anti-PD-1 immune checkpoint inhibitor, for patients with advanced, refractory squamous non-small-cell lung cancer (CheckMate 063): a phase 2, single-arm trial."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028407",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Nivolumab versus Docetaxel in Advanced Squamous-Cell Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25897158",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Overall Survival and Long-Term Safety of Nivolumab (Anti-Programmed Death 1 Antibody, BMS-936558, ONO-4538) in Patients With Previously Treated Advanced Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25704439",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Activity and safety of nivolumab, an anti-PD-1 immune checkpoint inhibitor, for patients with advanced, refractory squamous non-small-cell lung cancer (CheckMate 063): a phase 2, single-arm trial."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028407",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Nivolumab versus Docetaxel in Advanced Squamous-Cell Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25897158",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Overall Survival and Long-Term Safety of Nivolumab (Anti-Programmed Death 1 Antibody, BMS-936558, ONO-4538) in Patients With Previously Treated Advanced Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25704439",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Activity and safety of nivolumab, an anti-PD-1 immune checkpoint inhibitor, for patients with advanced, refractory squamous non-small-cell lung cancer (CheckMate 063): a phase 2, single-arm trial."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028407",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Nivolumab versus Docetaxel in Advanced Squamous-Cell Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25897158",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Overall Survival and Long-Term Safety of Nivolumab (Anti-Programmed Death 1 Antibody, BMS-936558, ONO-4538) in Patients With Previously Treated Advanced Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25704439",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Activity and safety of nivolumab, an anti-PD-1 immune checkpoint inhibitor, for patients with advanced, refractory squamous non-small-cell lung cancer (CheckMate 063): a phase 2, single-arm trial."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028407",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Nivolumab versus Docetaxel in Advanced Squamous-Cell Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25897158",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Overall Survival and Long-Term Safety of Nivolumab (Anti-Programmed Death 1 Antibody, BMS-936558, ONO-4538) in Patients With Previously Treated Advanced Non-Small-Cell Lung Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25704439",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Activity and safety of nivolumab, an anti-PD-1 immune checkpoint inhibitor, for patients with advanced, refractory squamous non-small-cell lung cancer (CheckMate 063): a phase 2, single-arm trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25704439",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 290,
"text": " Patients with squamous non-small-cell lung cancer that is refractory to multiple treatments have poor outcomes. We assessed the activity of nivolumab, a fully human IgG4 PD-1 immune checkpoint inhibitor antibody, for patients with advanced, refractory, squamous non-small-cell lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25704439",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 290,
"text": " Patients with squamous non-small-cell lung cancer that is refractory to multiple treatments have poor outcomes. We assessed the activity of nivolumab, a fully human IgG4 PD-1 immune checkpoint inhibitor antibody, for patients with advanced, refractory, squamous non-small-cell lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25704439",
"endSection": "abstract",
"offsetInBeginSection": 1708,
"offsetInEndSection": 2011,
"text": " Nivolumab has clinically meaningful activity and a manageable safety profile in previously treated patients with advanced, refractory, squamous non-small cell lung cancer. These data support the assessment of nivolumab in randomised, controlled, phase 3 studies of first-line and second-line treatment."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002289",
"http://www.disease-ontology.org/api/metadata/DOID:3908"
] |
[] |
56bb68a5ac7ad1001900000a
| 363 |
yesno
|
Does ghrelin play a role in ischemic stroke?
|
['yes']
|
[
"yes"
] |
['Yes. It has been shown that serum ghrelin levels are reduced after ischemic stroke and ghrelin is associated with stroke type. Ghrelin can be a useful marker for the prediction of stoke after cardiopulmonary bypass. Ghrelin may be neuroprotective after injury in animal models of cerebral ischemia by inhibiting apoptotic processes, inflammation, nNOS activity and modulating gastrointestinal motility.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23576609",
"http://www.ncbi.nlm.nih.gov/pubmed/22190447",
"http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"http://www.ncbi.nlm.nih.gov/pubmed/20720512",
"http://www.ncbi.nlm.nih.gov/pubmed/19352052",
"http://www.ncbi.nlm.nih.gov/pubmed/15613277",
"http://www.ncbi.nlm.nih.gov/pubmed/24961317",
"http://www.ncbi.nlm.nih.gov/pubmed/24768795"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23576609",
"endSection": "abstract",
"offsetInBeginSection": 96,
"offsetInEndSection": 213,
"text": "Recent evidence suggests that ghrelin may also be neuroprotective after injury in animal models of cerebral ischemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23576609",
"endSection": "abstract",
"offsetInBeginSection": 1573,
"offsetInEndSection": 1840,
"text": "Overall, these experiments point to a neurodegenerative but antiapoptotic effect of endogenous ghrelin in this model of global ischemia, highlighting that further research is essential before we can apply ghrelin treatments to neurodegenerative insults in the clinic."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22190447",
"endSection": "abstract",
"offsetInBeginSection": 981,
"offsetInEndSection": 1084,
"text": " The serum ghrelin level was higher in the MCAO group when compared with the control group (P < 0.05). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22190447",
"endSection": "abstract",
"offsetInBeginSection": 1435,
"offsetInEndSection": 1587,
"text": "Our results showed that higher level of serum ghrelin decreased gastrointestinal motility and damage to the intestinal mucosa existed in rats with MCAO."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Leptin, adiponectin and ghrelin, new potential mediators of ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 723,
"text": "RESULTS: Significantly higher levels of leptin and lower levels of adiponectin and ghrelin were confirmed in the stroke group."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 873,
"offsetInEndSection": 983,
"text": "Ghrelin levels correlated mildly with triglyceride levels, and were dominant in men with cardioembolic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1133,
"offsetInEndSection": 1291,
"text": "CONCLUSIONS: Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20720512",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Ghrelin suppresses inflammation and neuronal nitric oxide synthase in focal cerebral ischemia via the vagus nerve."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20720512",
"endSection": "abstract",
"offsetInBeginSection": 851,
"offsetInEndSection": 1026,
"text": "Compared with vehicle treatment, human ghrelin treatment in vagus nerve-intact rats after MCAO showed marked reduction in neurological deficit by 57% and infarct size by 25%. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20720512",
"endSection": "abstract",
"offsetInBeginSection": 1213,
"offsetInEndSection": 1498,
"text": "Human ghrelin treatment in vagus nerve-intact rats significantly decreased the above measurements. Human ghrelin treatment also improved 7-day survival and significantly decreased neurological deficit over the entire 7 days after MCAO in vagus nerve-intact rats compared with vehicle. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20720512",
"endSection": "abstract",
"offsetInBeginSection": 1671,
"offsetInEndSection": 1825,
"text": "Human ghrelin is thus a neuroprotective agent that inhibits inflammation, nNOS activity, and apoptosis in focal cerebral ischemia through a vagal pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19352052",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Ghrelin is known to promote neuronal defense and survival against ischemic injury by inhibiting apoptotic processes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19352052",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1104,
"text": "Our data indicate that des-acyl ghrelin, as well as ghrelin, protect cortical neurons against ischemic injury through the inhibition of Par-4 expression and apoptotic molecules in mitochondrial pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15613277",
"endSection": "abstract",
"offsetInBeginSection": 958,
"offsetInEndSection": 1083,
"text": "In conclusion, it is considered that ghrelin as well as S-100B can be a useful marker for the prediction of stoke after CPB. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1092,
"offsetInEndSection": 1237,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Leptin, adiponectin and ghrelin, new potential mediators of ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24961317",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 311,
"text": "In this review we discuss pre-clinical evidence suggesting ghrelin may be a useful therapeutic in protecting the brain against injury after ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19352052",
"endSection": "abstract",
"offsetInBeginSection": 367,
"offsetInEndSection": 450,
"text": "Both ghrelin and des-acyl ghrelin protected cortical neurons from ischemic injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19352052",
"endSection": "abstract",
"offsetInBeginSection": 895,
"offsetInEndSection": 1098,
"text": "Our data indicate that des-acyl ghrelin, as well as ghrelin, protect cortical neurons against ischemic injury through the inhibition of Par-4 expression and apoptotic molecules in mitochondrial pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1092,
"offsetInEndSection": 1237,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Leptin, adiponectin and ghrelin, new potential mediators of ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24961317",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 311,
"text": "In this review we discuss pre-clinical evidence suggesting ghrelin may be a useful therapeutic in protecting the brain against injury after ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1092,
"offsetInEndSection": 1237,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Leptin, adiponectin and ghrelin, new potential mediators of ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24961317",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 311,
"text": "In this review we discuss pre-clinical evidence suggesting ghrelin may be a useful therapeutic in protecting the brain against injury after ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1092,
"offsetInEndSection": 1237,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Leptin, adiponectin and ghrelin, new potential mediators of ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24961317",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 311,
"text": "In this review we discuss pre-clinical evidence suggesting ghrelin may be a useful therapeutic in protecting the brain against injury after ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1133,
"offsetInEndSection": 1291,
"text": "CONCLUSIONS: Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23576609",
"endSection": "abstract",
"offsetInBeginSection": 96,
"offsetInEndSection": 213,
"text": "Recent evidence suggests that ghrelin may also be neuroprotective after injury in animal models of cerebral ischemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23576609",
"endSection": "abstract",
"offsetInBeginSection": 1573,
"offsetInEndSection": 1840,
"text": "Overall, these experiments point to a neurodegenerative but antiapoptotic effect of endogenous ghrelin in this model of global ischemia, highlighting that further research is essential before we can apply ghrelin treatments to neurodegenerative insults in the clinic."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Leptin, adiponectin and ghrelin, new potential mediators of ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24961317",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 310,
"text": "In this review we discuss pre-clinical evidence suggesting ghrelin may be a useful therapeutic in protecting the brain against injury after ischemic stroke"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20720512",
"endSection": "abstract",
"offsetInBeginSection": 1672,
"offsetInEndSection": 1825,
"text": "Human ghrelin is thus a neuroprotective agent that inhibits inflammation, nNOS activity, and apoptosis in focal cerebral ischemia through a vagal pathway"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19352052",
"endSection": "abstract",
"offsetInBeginSection": 369,
"offsetInEndSection": 450,
"text": "Both ghrelin and des-acyl ghrelin protected cortical neurons from ischemic injury"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23576609",
"endSection": "abstract",
"offsetInBeginSection": 1572,
"offsetInEndSection": 1838,
"text": "Overall, these experiments point to a neurodegenerative but antiapoptotic effect of endogenous ghrelin in this model of global ischemia, highlighting that further research is essential before we can apply ghrelin treatments to neurodegenerative insults in the clinic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19352052",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 367,
"text": "In the present study, we investigated the role of prostate apoptosis response-4 (Par-4), a proapoptotic gene the expression of which is increased after ischemic injury, in ghrelin-mediated neuroprotection during middle cerebral artery occlusion (MCAO)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1106,
"offsetInEndSection": 1250,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1106,
"offsetInEndSection": 1250,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1106,
"offsetInEndSection": 1250,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1106,
"offsetInEndSection": 1250,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22167137",
"endSection": "abstract",
"offsetInBeginSection": 1106,
"offsetInEndSection": 1250,
"text": "Adipokines and ghrelin play an important role in ischemic stroke, but their function in stroke subtypes seems to be different and sex influenced"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/GHRL_LITCT",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054439"
] |
[] |
551c2c276b348bb82c00000c
| 364 |
yesno
|
Can fetal aneuploidy be detected with non-invasive prenatal testing?
|
['yes']
|
[
"yes"
] |
['Yes, the non-invasive preanatal test of cell-free fetal DNA is being used for fetal aneuploidy screening.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23526649",
"http://www.ncbi.nlm.nih.gov/pubmed/25543032",
"http://www.ncbi.nlm.nih.gov/pubmed/21749752",
"http://www.ncbi.nlm.nih.gov/pubmed/25044397",
"http://www.ncbi.nlm.nih.gov/pubmed/25138112",
"http://www.ncbi.nlm.nih.gov/pubmed/26252102",
"http://www.ncbi.nlm.nih.gov/pubmed/23553438",
"http://www.ncbi.nlm.nih.gov/pubmed/22863603",
"http://www.ncbi.nlm.nih.gov/pubmed/24667696",
"http://www.ncbi.nlm.nih.gov/pubmed/24990604",
"http://www.ncbi.nlm.nih.gov/pubmed/23470070",
"http://www.ncbi.nlm.nih.gov/pubmed/10655451",
"http://www.ncbi.nlm.nih.gov/pubmed/24603453",
"http://www.ncbi.nlm.nih.gov/pubmed/23299662",
"http://www.ncbi.nlm.nih.gov/pubmed/23765643",
"http://www.ncbi.nlm.nih.gov/pubmed/21574485",
"http://www.ncbi.nlm.nih.gov/pubmed/23712453",
"http://www.ncbi.nlm.nih.gov/pubmed/25449088",
"http://www.ncbi.nlm.nih.gov/pubmed/26080919",
"http://www.ncbi.nlm.nih.gov/pubmed/24482806",
"http://www.ncbi.nlm.nih.gov/pubmed/24352524",
"http://www.ncbi.nlm.nih.gov/pubmed/25238658",
"http://www.ncbi.nlm.nih.gov/pubmed/17186566",
"http://www.ncbi.nlm.nih.gov/pubmed/24312358",
"http://www.ncbi.nlm.nih.gov/pubmed/22500971",
"http://www.ncbi.nlm.nih.gov/pubmed/26237478",
"http://www.ncbi.nlm.nih.gov/pubmed/21749753",
"http://www.ncbi.nlm.nih.gov/pubmed/25478006",
"http://www.ncbi.nlm.nih.gov/pubmed/23089167",
"http://www.ncbi.nlm.nih.gov/pubmed/21076134",
"http://www.ncbi.nlm.nih.gov/pubmed/24783433"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23526649",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Non-invasive prenatal testing with cell-free DNA: US physician attitudes toward implementation in clinical practice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23526649",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 200,
"text": "The aim of this study was to assess awareness, potential adoption, and current utilization of non-invasive prenatal testing (NIPT) analysis for common fetal aneuploidies among obstetricians"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25543032",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Cell-free DNA has been used for fetal rhesus factor and sex determination, fetal aneuploidy screening, cancer diagnostics and monitoring, and other applications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22863603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "The recent release of new, non-invasive prenatal tests for fetal aneuploidy using cell-free fetal DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23765643",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Non-invasive prenatal testing (NIPT) for aneuploidy using cell-free DNA in maternal plasma is revolutionizing prenatal screening and diagnosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23712453",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "SNP-based non-invasive prenatal testing detects sex chromosome aneuploidies with high accuracy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25138112",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Non-invasive prenatal testing (NIPT) of cell-free fetal DNA in maternal plasma is a novel approach, designed for detecting common aneuploidies in the fetus."
},
{
"beginSection": "abstract",
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"text": "This study aimed to develop a single-nucleotide polymorphism-based and informatics-based non-invasive prenatal test that detects sex chromosome aneuploidies early in pregnancy."
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"text": "RAPIDR: an analysis package for non-invasive prenatal testing of aneuploidy."
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"text": "Non-invasive prenatal testing for aneuploidy: current status and future prospects."
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"text": "Non-invasive prenatal testing of fetal whole chromosome aneuploidy by massively parallel sequencing."
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"text": "Attitudes towards non-invasive prenatal testing for aneuploidy among US adults of reproductive age."
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/21574485",
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"text": "[Non-invasive prenatal test in the diagnosis of aneuploidy 13, 18 and 21--theoretical and practical aspects]."
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"text": "Non-invasive prenatal testing (NIPT) for aneuploidy using cell-free DNA in maternal plasma is revolutionizing prenatal screening and diagnosis."
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22863603",
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"text": "The recent release of new, non-invasive prenatal tests for fetal aneuploidy using cell-free fetal DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field."
},
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"text": "RAPIDR: an analysis package for non-invasive prenatal testing of aneuploidy."
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"text": "Non-invasive prenatal testing for aneuploidy: current status and future prospects."
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"text": "Non-invasive prenatal testing of fetal whole chromosome aneuploidy by massively parallel sequencing."
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"text": "Attitudes towards non-invasive prenatal testing for aneuploidy among US adults of reproductive age."
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25449088",
"endSection": "abstract",
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"text": "To track and analyze two false positive cases from non-invasive prenatal testing for potential fetal aneuploidy."
},
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"endSection": "abstract",
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"text": "Non-invasive prenatal testing (NIPT) of fetal aneuploidy using cell-free fetal DNA is becoming part of routine clinical practice."
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"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23553438",
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"text": "To report secondary or additional findings arising from introduction of non-invasive prenatal testing (NIPT) for aneuploidy by whole genome sequencing as a clinical service."
},
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25138112",
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"text": "Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of fetal aneuploidy."
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24482806",
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"text": "In recent years, technical advances in the molecular analysis of fetal DNA (e.g., digital PCR and massively parallel sequencing (MPS)) has enabled the successful implementation of noninvasive testing into clinical practice, such as fetal sex assessment, RhD genotyping, and fetal chromosomal aneuploidy detection.With the ability to decipher the entire fetal genome from maternal plasma DNA, we foresee that an increased number of non-invasive prenatal tests will be available for detecting many single-gene disorders in the near future"
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"text": "First identified in 1997, cell-free fetal DNA (cffDNA) has just recently been used to detect fetal aneuploidy of chromosomes 13, 18, and 21, showing its potential to revolutionize prenatal genetic testing as a non-invasive screening tool"
},
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"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25238658",
"endSection": "abstract",
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"text": "Non-invasive prenatal testing (NIPT) using cell-free fetal DNA in maternal plasma has been developed for the detection of fetal aneuploidy"
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"text": "Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of fetal aneuploidy"
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"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25044397",
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"text": "Non-invasive prenatal testing for fetal aneuploidies in the first trimester of pregnancy"
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"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26252102",
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"text": "To explore the value of next-generation sequencing for the non-invasive prenatal testing of fetal chromosomal aneuploidies"
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"text": "Secondary findings from non-invasive prenatal testing for common fetal aneuploidies by whole genome sequencing as a clinical service"
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"text": "To report secondary or additional findings arising from introduction of non-invasive prenatal testing (NIPT) for aneuploidy by whole genome sequencing as a clinical service"
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"text": "Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of fetal aneuploidy."
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"text": "SNP-based non-invasive prenatal testing detects sex chromosome aneuploidies with high accuracy."
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"text": "Motivations for undertaking DNA sequencing-based non-invasive prenatal testing for fetal aneuploidy: a qualitative study with early adopter patients in Hong Kong."
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"text": "OBJECTIVE: To determine whether non-invasive prenatal testing by maternal plasma DNA sequencing can uncover all fetal chromosome aneuploidies in one simple sequencing event. "
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"text": "Non-invasive prenatal diagnosis of fetal aneuploidies using massively parallel sequencing-by-ligation and evidence that cell-free fetal DNA in the maternal plasma originates from cytotrophoblastic cells."
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"text": "Secondary findings from non-invasive prenatal testing for common fetal aneuploidies by whole genome sequencing as a clinical service."
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"text": "OBJECTIVE: To determine whether non-invasive prenatal testing by maternal plasma DNA sequencing can uncover all fetal chromosome aneuploidies in one simple sequencing event. "
},
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"text": "Non-invasive prenatal testing (NIPT) of fetal aneuploidy using cell-free fetal DNA is becoming part of routine clinical practice."
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"text": "Israeli Society of Medical Genetics NIPT Committee Opinion 072013: Non-invasive prenatal testing of cell-free DNA in maternal plasma for detection of fetal aneuploidy."
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"text": "Non-invasive prenatal testing (NIPT) using cell-free fetal DNA in maternal plasma has been developed for the detection of fetal aneuploidy."
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"text": "Non-invasive prenatal testing (NIPT) of cell-free fetal DNA in maternal plasma is a novel approach, designed for detecting common aneuploidies in the fetus."
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"text": "Non-invasive prenatal testing (NIPT) of cell-free fetal DNA in maternal plasma is a novel approach, designed for detecting common aneuploidies in the fetus."
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"endSection": "abstract",
"offsetInBeginSection": 28,
"offsetInEndSection": 227,
"text": "non-invasive prenatal tests for fetal aneuploidy using cell-free fetal DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field."
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"text": " Non-invasive prenatal testing (NIPT) of fetal aneuploidy using cell-free fetal DNA is becoming part of routine clinical practice. RAPIDR (Reliable Accurate Prenatal non-Invasive Diagnosis R package) is an easy-to-use open-source R package that implements several published NIPT analysis methods."
},
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"text": "The clinical data collected thus far indicate that NIPT is highly sensitive in detecting trisomies 21 and 18, and fairly sensitive in detecting trisomy 13 and sex chromosome aneuploidies. Because false-positive results may occur, an abnormal result must be validated by invasive prenatal testing."
},
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"text": "When non-invasive prenatal screening for aneuploidy is available, maternal age alone should not be an indication for invasive prenatal diagnosis in a twin pregnancy. (II-2A) If non-invasive prenatal screening is not available, invasive prenatal diagnosis in twins should be offered to women aged 35 and over."
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"text": "Therefore, methods with high sensitivity and precision are required to detect and differentiate fetal DNA from the large background of maternal DNA. In recent years, technical advances in the molecular analysis of fetal DNA (e.g., digital PCR and massively parallel sequencing (MPS)) has enabled the successful implementation of noninvasive testing into clinical practice, such as fetal sex assessment, RhD genotyping, and fetal chromosomal aneuploidy detection.With the ability to decipher the entire fetal genome from maternal plasma DNA, we foresee that an increased number of non-invasive prenatal tests will be available for detecting many single-gene disorders in the near future."
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"text": "Non-invasive prenatal testing (NIPT) of cell-free fetal DNA in maternal plasma is a novel approach, designed for detecting common aneuploidies in the fetus."
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"text": "To explore the value of next-generation sequencing for the non-invasive prenatal testing of fetal chromosomal aneuploidies."
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"text": "[Cell-free nucleic acid-based non-invasive prenatal diagnosis of fetal aneuploidies]."
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"text": "Maternal age alone is a poor minimum standard for prenatal screening for aneuploidy, and it should not be used a basis for recommending invasive testing when non-invasive prenatal screening for aneuploidy is available."
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"text": "Maternal age alone is a poor minimum standard for prenatal screening for aneuploidy, and it should not be used a basis for recommending invasive testing when non-invasive prenatal screening for aneuploidy is available."
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"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "The recent release of new, non-invasive prenatal tests for fetal aneuploidy using cell-free fetal DNA (cffDNA) has been hailed as a revolution in prenatal testing and has triggered significant commercial interest in the field."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24990604",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Non-invasive prenatal testing (NIPT) of fetal aneuploidy using cell-free fetal DNA is becoming part of routine clinical practice."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25044397",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Non-invasive prenatal testing for fetal aneuploidies in the first trimester of pregnancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24667696",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "Non-invasive prenatal testing (NIPT) by massively parallel sequencing is a useful clinical test for the detection of common fetal aneuploidies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25138112",
"endSection": "abstract",
"offsetInBeginSection": 268,
"offsetInEndSection": 455,
"text": "The clinical data collected thus far indicate that NIPT is highly sensitive in detecting trisomies 21 and 18, and fairly sensitive in detecting trisomy 13 and sex chromosome aneuploidies."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004247",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011296"
] |
[] |
57136cbf1174fb1755000007
| 365 |
yesno
|
Can capivasertib be used for breast cancer?
|
['yes']
|
[
"yes"
] |
['Yes. Capivasertib is effective and be used for treatment of breast cancer']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37046675",
"http://www.ncbi.nlm.nih.gov/pubmed/36901954",
"http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"http://www.ncbi.nlm.nih.gov/pubmed/35398754",
"http://www.ncbi.nlm.nih.gov/pubmed/36508589"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36508589",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Capivasertib Doubles PFS in Some Breast Cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36508589",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 311,
"text": "In the phase III CAPItello-291 study, the combination of fulvestrant and capivasertib more than doubled progression-free survival compared with fulvestrant alone in patients with hormone receptor-positive, HER2-negative breast cancer who have developed resistance to aromatase inhibitors and CDK4/6 inhibitors. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37046675",
"endSection": "abstract",
"offsetInBeginSection": 633,
"offsetInEndSection": 1189,
"text": "In this setting of high unmet need, several clinical trials of novel drugs have recently reported encouraging results: the addition of the AKT-inhibitor capivasertib to fulvestrant demonstrated a significant improvement in progression-free survival (PFS); the oral selective estrogen receptor degrader (SERD) elacestrant prolonged PFS compared to traditional ET in a phase 3 trial, particularly among patients with detectable ESR1 mutations; finally, PARP inhibitors are available treatment options for patients with pathogenic BRCA1/2 germline mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"endSection": "abstract",
"offsetInBeginSection": 2088,
"offsetInEndSection": 2418,
"text": "CONCLUSIONS: Capivasertib-fulvestrant therapy resulted in significantly longer progression-free survival than treatment with fulvestrant alone among patients with hormone receptor-positive advanced breast cancer whose disease had progressed during or after previous aromatase inhibitor therapy with or without a CDK4/6 inhibitor. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Capivasertib in Hormone Receptor-Positive Advanced Breast Cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35398754",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 53,
"text": "\"The emerging role of capivasertib in breast cancer\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"endSection": "abstract",
"offsetInBeginSection": 2094,
"offsetInEndSection": 2422,
"text": "SIONS: Capivasertib-fulvestrant therapy resulted in significantly longer progression-free survival than treatment with fulvestrant alone among patients with hormone receptor-positive advanced breast cancer whose disease had progressed during or after previous aromatase inhibitor therapy with or without a CDK4/6 inhibitor. (Fun"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37256976",
"endSection": "abstract",
"offsetInBeginSection": 255,
"offsetInEndSection": 1646,
"text": "re limited.METHODS: In a phase 3, randomized, double-blind trial, we enrolled eligible pre-, peri-, and postmenopausal women and men with hormone receptor-positive, human epidermal growth factor receptor 2-negative advanced breast cancer who had had a relapse or disease progression during or after treatment with an aromatase inhibitor, with or without previous cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor therapy. Patients were randomly assigned in a 1:1 ratio to receive capivasertib plus fulvestrant or placebo plus fulvestrant. The dual primary end point was investigator-assessed progression-free survival assessed both in the overall population and among patients with AKT pathway-altered (PIK3CA, AKT1, or PTEN) tumors. Safety was assessed.RESULTS: Overall, 708 patients underwent randomization; 289 patients (40.8%) had AKT pathway alterations, and 489 (69.1%) had received a CDK4/6 inhibitor previously for advanced breast cancer. In the overall population, the median progression-free survival was 7.2 months in the capivasertib-fulvestrant group, as compared with 3.6 months in the placebo-fulvestrant group (hazard ratio for progression or death, 0.60; 95% confidence interval [CI], 0.51 to 0.71; P<0.001). In the AKT pathway-altered population, the median progression-free survival was 7.3 months in the capivasertib-fulvestrant group, as compared with 3.1 months in the"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 257,
"text": "BACKGROUND: Capivasertib, an AKT inhibitor, added to fulvestrant, was previously reported to improve progression-free survival in women with aromatase inhibitor-resistant oestrogen receptor (ER)-positive, HER2-negative advanced breast cancer. The benefit ap"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "BACKGROUND: Capivasertib, an AKT inhibitor, added to fulvestrant, was previously reported to improve progression-free survival in women with aromatase inhibitor-resistant oestrogen receptor (ER)-positive, HER2-negative advanced breast cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 241,
"text": "Capivasertib, an AKT inhibitor, added to fulvestrant, was previously reported to improve progression-free survival in women with aromatase inhibitor-resistant oestrogen receptor (ER)-positive, HER2-negative advanced breast cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36901954",
"endSection": "abstract",
"offsetInBeginSection": 357,
"offsetInEndSection": 635,
"text": "Among these, the PIK3CA isoform-specific inhibitor alpelisib and the pan-AKT inhibitor capivasertib were recently approved in combination with the estrogen receptor degrader fulvestrant for the treatment of ER+ advanced breast cancer after progression on an aromatase inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35671774",
"endSection": "abstract",
"offsetInBeginSection": 4246,
"offsetInEndSection": 4453,
"text": "RETATION: Updated FAKTION data showed that capivasertib addition to fulvestrant extends the survival of participants with aromatase inhibitor-resistant ER-positive, HER2-negative advanced breast cancer. The "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36508589",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 310,
"text": "In the phase III CAPItello-291 study, the combination of fulvestrant and capivasertib more than doubled progression-free survival compared with fulvestrant alone in patients with hormone receptor-positive, HER2-negative breast cancer who have developed resistance to aromatase inhibitors and CDK4/6 inhibitors."
}
] | 13 |
BioASQ-training13b
| null | null |
65cfe1d21930410b1300002a
| 366 |
yesno
|
Are de novo mutations in regulatory elements responsible for neurodevelopmental disorders?
|
['yes']
|
[
"yes"
] |
['Yes. De novo mutations in highly evolutionarily conserved fetal brain-active elements are significantly and specifically enriched in neurodevelopmental disorders. It is estimated that, genome-wide, 1-3% of patients without a diagnostic coding variant carry pathogenic de novo mutations in fetal brain-active regulatory elements and that only 0.15% of all possible mutations within highly conserved fetal brain-active elements cause neurodevelopmental disorders with a dominant mechanism.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29562236"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29562236",
"endSection": "abstract",
"offsetInBeginSection": 137,
"offsetInEndSection": 1008,
"text": "The role of de novo mutations in regulatory elements affecting genes associated with developmental disorders, or other genes, has been essentially unexplored. We identified de novo mutations in three classes of putative regulatory elements in almost 8,000 patients with developmental disorders. Here we show that de novo mutations in highly evolutionarily conserved fetal brain-active elements are significantly and specifically enriched in neurodevelopmental disorders. We identified a significant twofold enrichment of recurrently mutated elements. We estimate that, genome-wide, 1-3% of patients without a diagnostic coding variant carry pathogenic de novo mutations in fetal brain-active regulatory elements and that only 0.15% of all possible mutations within highly conserved fetal brain-active elements cause neurodevelopmental disorders with a dominant mechanism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29562236",
"endSection": "abstract",
"offsetInBeginSection": 688,
"offsetInEndSection": 1008,
"text": "We estimate that, genome-wide, 1-3% of patients without a diagnostic coding variant carry pathogenic de novo mutations in fetal brain-active regulatory elements and that only 0.15% of all possible mutations within highly conserved fetal brain-active elements cause neurodevelopmental disorders with a dominant mechanism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29562236",
"endSection": "abstract",
"offsetInBeginSection": 432,
"offsetInEndSection": 607,
"text": "Here we show that de novo mutations in highly evolutionarily conserved fetal brain-active elements are significantly and specifically enriched in neurodevelopmental disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29562236",
"endSection": "abstract",
"offsetInBeginSection": 761,
"offsetInEndSection": 1081,
"text": "We estimate that, genome-wide, 1-3% of patients without a diagnostic coding variant carry pathogenic de novo mutations in fetal brain-active regulatory elements and that only 0.15% of all possible mutations within highly conserved fetal brain-active elements cause neurodevelopmental disorders with a dominant mechanism. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29562236",
"endSection": "abstract",
"offsetInBeginSection": 505,
"offsetInEndSection": 680,
"text": "Here we show that de novo mutations in highly evolutionarily conserved fetal brain-active elements are significantly and specifically enriched in neurodevelopmental disorders. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29562236",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 209,
"text": "De novo mutations in regulatory elements in neurodevelopmental disorders.We previously estimated that 42% of patients with severe developmental disorders carry pathogenic de novo mutations in coding sequences. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c643485e842deac67000015
| 367 |
yesno
|
Does ESN364 activate the hypothalamic-pituitary-gonadal axis?
|
['no']
|
[
"no"
] |
['No, the NK3R antagonist, ESN364, suppressed the hypothalamic-pituitary-gonadal axis in healthy volunteers by selective modulation of gonadotropin secretion']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26653113"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26653113",
"endSection": "abstract",
"offsetInBeginSection": 1798,
"offsetInEndSection": 2042,
"text": "Oral administration of the NK3R antagonist, ESN364, suppressed the hypothalamic-pituitary-gonadal axis in healthy volunteers by selective modulation of gonadotropin secretion, leading to a restrained decrease in ovarian hormone levels in women."
}
] | 11 |
BioASQ-training11b
| null | null |
5e5508e2b761aafe09000006
| 368 |
yesno
|
Is UGT1A1 implicated in Crigler–Najjar syndrome?
|
['yes']
|
[
"yes"
] |
['Yes. Crigler-Najjar syndrome is a rare disorder of bilirubin metabolism caused by uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) mutations characterized by hyperbilirubinemia and jaundice.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33102778",
"http://www.ncbi.nlm.nih.gov/pubmed/19830808",
"http://www.ncbi.nlm.nih.gov/pubmed/37602038",
"http://www.ncbi.nlm.nih.gov/pubmed/30544479",
"http://www.ncbi.nlm.nih.gov/pubmed/25319636",
"http://www.ncbi.nlm.nih.gov/pubmed/22340355",
"http://www.ncbi.nlm.nih.gov/pubmed/37759499",
"http://www.ncbi.nlm.nih.gov/pubmed/23992562",
"http://www.ncbi.nlm.nih.gov/pubmed/23403257",
"http://www.ncbi.nlm.nih.gov/pubmed/24401909",
"http://www.ncbi.nlm.nih.gov/pubmed/37137832",
"http://www.ncbi.nlm.nih.gov/pubmed/21319362",
"http://www.ncbi.nlm.nih.gov/pubmed/14550264",
"http://www.ncbi.nlm.nih.gov/pubmed/14616765",
"http://www.ncbi.nlm.nih.gov/pubmed/11868392",
"http://www.ncbi.nlm.nih.gov/pubmed/26220753",
"http://www.ncbi.nlm.nih.gov/pubmed/37585628",
"http://www.ncbi.nlm.nih.gov/pubmed/27722180",
"http://www.ncbi.nlm.nih.gov/pubmed/31553814",
"http://www.ncbi.nlm.nih.gov/pubmed/25966095",
"http://www.ncbi.nlm.nih.gov/pubmed/23461146",
"http://www.ncbi.nlm.nih.gov/pubmed/10412811",
"http://www.ncbi.nlm.nih.gov/pubmed/23162302",
"http://www.ncbi.nlm.nih.gov/pubmed/28280378",
"http://www.ncbi.nlm.nih.gov/pubmed/11013440",
"http://www.ncbi.nlm.nih.gov/pubmed/20973621",
"http://www.ncbi.nlm.nih.gov/pubmed/34807779",
"http://www.ncbi.nlm.nih.gov/pubmed/23875061",
"http://www.ncbi.nlm.nih.gov/pubmed/32536060",
"http://www.ncbi.nlm.nih.gov/pubmed/16386929",
"http://www.ncbi.nlm.nih.gov/pubmed/36936447",
"http://www.ncbi.nlm.nih.gov/pubmed/29176474",
"http://www.ncbi.nlm.nih.gov/pubmed/9497253",
"http://www.ncbi.nlm.nih.gov/pubmed/19953640",
"http://www.ncbi.nlm.nih.gov/pubmed/25315738",
"http://www.ncbi.nlm.nih.gov/pubmed/22765254",
"http://www.ncbi.nlm.nih.gov/pubmed/24793765",
"http://www.ncbi.nlm.nih.gov/pubmed/25729974",
"http://www.ncbi.nlm.nih.gov/pubmed/33604208",
"http://www.ncbi.nlm.nih.gov/pubmed/15712364",
"http://www.ncbi.nlm.nih.gov/pubmed/23290513",
"http://www.ncbi.nlm.nih.gov/pubmed/24065680",
"http://www.ncbi.nlm.nih.gov/pubmed/23430851",
"http://www.ncbi.nlm.nih.gov/pubmed/11855932",
"http://www.ncbi.nlm.nih.gov/pubmed/26250421"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36936447",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "Crigler-Najjar syndrome is a rare disorder of bilirubin metabolism caused by uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) mutations characterized by hyperbilirubinemia and jaundice. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37137832",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 829,
"text": "Conclusion: The compound heterozygous pathogenic mutations (c.-3279T > G, c.211G > A, and c.1456T > G) at three loci of the UGT1A1 gene may be the feature of the newly discovered CNS-II family genes based on the CNS-II family study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37602038",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Crigler-Najjar syndrome (CNS) type I is a rare genetic disease caused by mutations in the UGT1A1 gene, resulting in a lack of Uridine 5'-diphospho-glucuronosyltransferase (UDPGT) enzyme. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37585628",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 263,
"text": "BACKGROUND: Patients with the Crigler-Najjar syndrome lack the enzyme uridine diphosphoglucuronate glucuronosyltransferase 1A1 (UGT1A1), the absence of which leads to severe unconjugated hyperbilirubinemia that can cause irreversible neurologic injury and death. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37759499",
"endSection": "abstract",
"offsetInBeginSection": 264,
"offsetInEndSection": 430,
"text": "A defect in the UGT1A1 enzyme-encoding gene, which is directly responsible for bilirubin conjugation, can cause Crigler-Najjar syndrome (CNS) and Gilbert's syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37759499",
"endSection": "abstract",
"offsetInBeginSection": 264,
"offsetInEndSection": 428,
"text": "A defect in the UGT1A1 enzyme-encoding gene, which is directly responsible for bilirubin conjugation, can cause Crigler-Najjar syndrome (CNS) and Gilbert's syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37602038",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "Crigler-Najjar syndrome (CNS) type I is a rare genetic disease caused by mutations in the UGT1A1 gene, resulting in a lack of Uridine 5'-diphospho-glucuronosyltransferase (UDPGT) enzyme"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37585628",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 261,
"text": "Patients with the Crigler-Najjar syndrome lack the enzyme uridine diphosphoglucuronate glucuronosyltransferase 1A1 (UGT1A1), the absence of which leads to severe unconjugated hyperbilirubinemia that can cause irreversible neurologic injury and death"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32536060",
"endSection": "abstract",
"offsetInBeginSection": 107,
"offsetInEndSection": 207,
"text": "Crigler-Najjar syndrome (CNS) in relation to uridine diphosphate glucuronosyltransferase A1 (UGT1A1)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19953640",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 322,
"text": "Crigler-Najjar syndrome is another rare disorder of bilirubin metabolism caused by mutation in the gene coding the enzyme UGT1A1. We report a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16386929",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 201,
"text": "Crigler-Najjar syndromes are familial unconjugated hyperbilirubinemias caused by genetic lesions involving a single complex locus encoding for bilirubin UDP-glucuronosyltransferase (UGT1A1)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14616765",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Crigler-Najjar syndrome type I is a severe form of hereditary unconjugated hyperbilirubinemia and is caused by homozygous or compound heterozygous mutations of the bilirubin UDP-glucuronosyltransferase gene (UGT1A1). We analyzed"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33102778",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 237,
"text": "Crigler-Najjar syndrome (CNs) is a rare hereditary unconjugated hyperbilirubinemia caused by mutations in the bilirubin Uridine (UDP) glucuronosyltransferase family 1 member A1 (UGT1A1, ENSG00000241635) gene. Two patients were clinically"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9497253",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 412,
"text": "Crigler-Najjar syndrome type 1 (CN-1) is a recessively inherited, potentially lethal disorder characterized by severe unconjugated hyperbilirubinemia resulting from deficiency of the hepatic enzyme bilirubin-UDP-glucuronosyltransferase. In all CN-1 patients studied, structural mutations in one of the five exons of the gene (UGT1A1) encoding the uridinediphosphoglucuronate glucuronosyltransferase (UGT) isoform"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25729974",
"endSection": "abstract",
"offsetInBeginSection": 227,
"offsetInEndSection": 973,
"text": "Crigler-Najjar syndrome type I (CN1), Crigler-Najjar syndrome type II, and Gilbert's syndrome. CN1 is a severe form of unconjugated hyperbilirubinemia caused by homozygous or compound heterozygous mutations in the gene for uridine 5'-diphosphate glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1), resulting in complete loss of enzyme function. Here, we report a novel homozygous mutation of UGT1A1 in a female Thai infant who was diagnosed with CN1, and her parents were found to be heterozygous carriers. The patient was homozygous for the c.558C>A mutation, which resulted in a premature stop codon in exon 1. Her asymptomatic parents were carriers of the nonsense c.558C>A mutation. Our result suggests an important role for homozygous"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26220753",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "Crigler-Najjar syndrome presents as severe unconjugated hyperbilirubinemia and is characteristically caused by a mutation in the UGT1A1 gene, encoding the enzyme responsible for bilirubin glucuronidation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11855932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "Crigler-Najjar syndrome type 1 (CN-1) is characterized by severe unconjugated hyperbilirubinemia due to an inherited deficiency of hepatic bilirubin uridinediphosphoglucuronate glucuronosyltransferase (UGT1A1), inherited as an autosomal recessive characteristic."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19830808",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Crigler-Najjar syndrome (CN), caused by deficiency of UGT isoform 1A1 (UGT1A1), is characterized by severe unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24065680",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Crigler-Najjar syndrome is a rare autosomal recessive disease caused by mutations in the UGT1A1 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24401909",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Mutations in the gene encoding bilirubin UDP-glucuronosyltransferase (UGT1A1) are known to cause Crigler-Najjar syndrome type II (CN-II)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11013440",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "Genetic lesions of bilirubin uridine-diphosphoglucuronate glucuronosyltransferase (UGT1A1) causing Crigler-Najjar and Gilbert syndromes: correlation of genotype to phenotype."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27722180",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Crigler-Najjar syndrome is a severe metabolic disease of the liver due to a reduced activity of the UDP Glucuronosyltransferase 1A1 (UGT1A1) enzyme."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23403257",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "UGT1A1 enzyme defects are responsible of both Gilbert syndrome (GS) and Crigler-Najjar syndrome (CNS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16386929",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Gilbert and Crigler-Najjar syndromes are familial unconjugated hyperbilirubinemias caused by genetic lesions involving a single complex locus encoding for bilirubin UDP-glucuronosyltransferase (UGT1A1) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22765254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "Crigler-Najjar syndrome is an autosomal recessive disorder with severe unconjugated hyperbilirubinemia due to deficiency of bilirubin UDP-glucuronosyltransferase isozyme 1A1 (UGT1A1) encoded by the UGT1A1 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25315738",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1353,
"text": "Crigler-Najjar syndrome is the severe inherited form of unconjugated hyperbilirubinaemia due to mutations in the UGT1A1 gene, which can cause kernicterus early in life and can be even lethal when left untreated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21319362",
"endSection": "abstract",
"offsetInBeginSection": 490,
"offsetInEndSection": 677,
"text": "Sequence analysis of the UGT1A1 gene revealed that she was a compound heterozygote with p.[G71R; Y486D] + [Y486D] mutations, which suggests Crigler-Najjar syndrome type II rather than GS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34807779",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 301,
"text": "Inactivation and very low activity of UGT1A1 in the liver can be fatal or lead to lifelong Gilbert's syndrome (GS) and Crigler-Najjar syndrome (CN)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23461146",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 334,
"text": "The UDP-glucuronosyltransferase 1A1 gene that encode the enzyme UGT1A1 responsible for glucuronidation undergoes several variations that may affect the enzymatic activity or expression and which are the cause of metabolic disorders related to the glucuronidation of bilirubin, such as Gilbert's syndrome and Crigler Najjar's syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28280378",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Mutations in the UGT1A1 gene have been implicated in Gilbert syndrome, which shows mild hyperbilirubinemia, and a more aggressive childhood subtype, Crigler-Najjar syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24065680",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Crigler-Najjar syndrome is a rare autosomal recessive disease caused by mutations in the UGT1A1 gene. These mutations result in the deficiency of UGT1A1, a hepatic enzyme essential for bilirubin conjugation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25966095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 580,
"text": "Mutations in the UGT1A1 gene cause Crigler-Najjar syndrome (CN), which causes non-hemolytic unconjugated hyperbilirubinemia, and is categorized as CN1 and CN2 according to the severity of bilirubin levels. The UGT1A1 gene is responsible for encoding the liver enzyme uridine diphosphate-glucuronosyltransferase, UGT1A1. This protein adds glucuronic acid to unconjugated bilirubin in bilirubin metabolism to form conjugated bilirubin. CN2 occurs when UGT1A1 activity is low, while CN1 is the absence of UGT1A1 activity; therefore, the CN2 phenotype is not as severe as that of CN1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15712364",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 454,
"text": "Crigler-Najjar syndrome types I and II (CN1 and CN2) are usually inherited as autosomal recessive conditions and are characterized by non-hemolytic unconjugated hyperbilirubinaemia. CN1 is the most severe form, associated with the absence of hepatic bilirubin-uridinediphosphoglucuronate glucuronosyltransferase (UGT1A1) activity. CN2 presents intermediate levels of hyperbilirubinaemia as a result of an incomplete deficiency of hepatic UGT1A1 activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23875061",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Crigler-Najjar syndrome (CNS) type I and type II are usually inherited as autosomal recessive conditions that result from mutations in the UGT1A1 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20973621",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "Crigler-Najjar syndrome type I is a severe inborn error of bilirubin metabolism caused by a complete deficiency of uridine diphospho-glucuronosyl transferase 1A1 (UGT1A1) and results in life-threatening unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10412811",
"endSection": "abstract",
"offsetInBeginSection": 507,
"offsetInEndSection": 761,
"text": " Homozygous missense mutations of the gene have been generally recognized as responsible for Crigler-Najjar syndrome type II; the results obtained here, however, confirm that Gilbert syndrome may also be caused by a homozygous missense mutation of UGT1A1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36936447",
"endSection": "abstract",
"offsetInBeginSection": 1366,
"offsetInEndSection": 1486,
"text": "Therefore, lipid nanoparticle-encapsulated hUGT1A1 mRNA may represent a potential treatment for Crigler-Najjar syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14550264",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 246,
"text": "UDP-glucuronosyltransferase form 1A1 (UGT1A1) is the only bilirubin-glucuronidating isoform of this protein, and genetic deficiencies of UGT1A1 cause Crigler-Najjar syndrome, a disorder resulting from nonhemolytic unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24065680",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Crigler-Najjar syndrome is a rare autosomal recessive disease caused by mutations in the UGT1A1 gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31553814",
"endSection": "abstract",
"offsetInBeginSection": 21,
"offsetInEndSection": 192,
"text": "We describe the pathophysiology, treatment, and outcome of Crigler-Najjar type 1 syndrome (CN1) in 28 UGT1A1 c.222C>A homozygotes followed for 520 aggregate patient-years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23875061",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Crigler-Najjar syndrome (CNS) type I and type II are usually inherited as autosomal recessive conditions that result from mutations in the UGT1A1 gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23290513",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 305,
"text": "To assess the clinical utility of UGT1A1 genetic testing and describe the spectrum and prevalence of UGT1A1 variations identified in pediatric unconjugated hyperbilirubinemia (UCH), and to characterize specific genotype-phenotype relationships in suspected Gilbert and Crigler-Najjar syndromes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30544479",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 728,
"text": "Pfam database, SWISS-model, and Pymol were used for UGT1A1 protein domain analysis and protein modeling for assessing the effect of novel missense variants on protein structure.Seventy four cases, including 21 prolonged unconjugated hyperbilirubinemia (PUCH), 30 Gilbert syndrome (GS), 22 Crigler-Najjar syndrome type II (CNS-II), and 1 Crigler-Najjar syndrome type I (CNS-I) phenotypes were analyzed"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25966095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "Mutations in the UGT1A1 gene cause Crigler-Najjar syndrome (CN), which causes non-hemolytic unconjugated hyperbilirubinemia, and is categorized as CN1 and CN2 according to the severity of bilirubin levels"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29176474",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 210,
"text": "Crigler-Najjar syndrome type I (CNI) arises from biallelic variants of UGT1A1 that abrogate uridine diphosphate glucuronosyltransferase (UGT1A1) activity resulting in unconjugated hyperbilirubinemia"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25729974",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "A novel stop codon mutation in exon 1 (558C>A) of the UGT1A1 gene in a Thai neonate with Crigler-Najjar syndrome type I."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25319636",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 713,
"text": "Many mutations have already been identified in patients with inherited disorders with unconjugated hyperbilirubinemia, such as Crigler-Najjar syndromes and Gilbert's syndrome.CASE PRESENTATION: In this report, we presented a boy with intermittent unconjugated hyperbilirubinemia, whose genetic analysis showed a new compound heterozygote determined by three mutations, c.211G > A (p.G71R), c.508_510delTTC (p.F170-) and c.1456 T > G (p.Y486D) in the hotspot regions of the UGT1A1 gene (exons 1 and 5) in Asian populations, presenting a genotype compatible with clinical picture of CNS-II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33604208",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Crigler-Najjar syndrome is an inborn error of metabolism caused by a point mutation in one of the five exons of UGT1A1 gene, the product of which is responsible for elimination of bilirubin via bile."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15712364",
"endSection": "abstract",
"offsetInBeginSection": 455,
"offsetInEndSection": 926,
"text": "Here, we present the analysis of UGT1A1 gene in 31 unrelated Crigler-Najjar (CN) syndrome patients. This analysis allowed us to identify 22 mutations, 12 of which were not previously described, expanding the spectrum of known UGT1 mutations to 77. Novel mutations, considered pathogenic, including one nonsense mutation, two altered splice sites, one single base deletion and nine missense mutations were identified in coding exons of the UGT1A1gene and flanking introns."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22340355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 460,
"text": "We present a case of severe persisting unconjugated hyperbilirubinemia in a Uigur infant boy, eventually diagnosed as Crigler-Najjar syndrome type I. DNA analysis of his blood of the UGT1A1 gene sequence demonstrated that he was homozygous for an insertion mutation causing a change of the coding exons with a frame-shift, resulting in the substitution of 27 abnormal amino acid residues in his hepatic bilirubin uridine diphosphoglucuronyl transferase enzyme."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22340355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 521,
"text": "We present a case of severe persisting unconjugated hyperbilirubinemia in a Uigur infant boy, eventually diagnosed as Crigler-Najjar syndrome type I. DNA analysis of his blood of the UGT1A1 gene sequence demonstrated that he was homozygous for an insertion mutation causing a change of the coding exons with a frame-shift, resulting in the substitution of 27 abnormal amino acid residues in his hepatic bilirubin uridine diphosphoglucuronyl transferase enzyme. Both of his parents were heterozygous for the same mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15712364",
"endSection": "abstract",
"offsetInBeginSection": 1006,
"offsetInEndSection": 1123,
"text": "In addition, the evaluation of Gilbert-type promoter of UGT1A1in Crigler-Najjar (CN) syndrome patients was performed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33604208",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 498,
"text": "Crigler-Najjar syndrome is an inborn error of metabolism caused by a point mutation in one of the five exons of UGT1A1 gene, the product of which is responsible for elimination of bilirubin via bile. A number of hyperbilirubinemia disorders similar to Crigler-Najjar syndrome are reported, but they differ in their level of unconjugated bilirubin and responses to the treatment. Here we report a 14-year-old male patient admitted to hospital with the complaint of vomiting and frequent tonsillitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33102778",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 463,
"text": "Crigler-Najjar syndrome (CNs) is a rare hereditary unconjugated hyperbilirubinemia caused by mutations in the bilirubin Uridine (UDP) glucuronosyltransferase family 1 member A1 (UGT1A1, ENSG00000241635) gene. Two patients were clinically diagnosed with Crigler-Najjar Syndrome types II (CNs-II) can be clinically diagnosed which were based on the level of total bilirubin, efficacy of phenobarbital treatment, normal liver architecture and exclusion of hemolysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23162302",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 407,
"text": "Crigler-Najjar syndrome type 2 is a rare cause for persistent unconjugated hyperbilirubinemia, inherited in an autosomal recessive manner. Even though it is compatible with normal life span, in the absence of prompt suspicion and intensive management it can prove fatal not only in the neonatal period but also during adult life. Here, we describe a case with a novel homozygous UGT1A1 p.Pro176Leu mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23992562",
"endSection": "abstract",
"offsetInBeginSection": 48,
"offsetInEndSection": 148,
"text": "Crigler-Najjar syndrome and Gilbert syndrome, arise due to deficiency of UGT1A1 enzyme activity. Cri"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15712364",
"endSection": "abstract",
"offsetInBeginSection": 392,
"offsetInEndSection": 533,
"text": "result of an incomplete deficiency of hepatic UGT1A1 activity. Here, we present the analysis of UGT1A1 gene in 31 unrelated Crigler-Najjar (C"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26250421",
"endSection": "abstract",
"offsetInBeginSection": 45,
"offsetInEndSection": 457,
"text": "hyperbilirubinemias, Crigler-Najjar syndrome type I, Crigler-Najjar syndrome type II (CN-2), and Gilbert syndrome (GS) all result from mutations of the bilirubin uridine 5'-diphosphate (UDP)-glucuronosyltransferase gene (UGT1A1). Often, to distinguish between CN-2 and GS is difficult because the borderline of the two syndromes is unclear. We analyzed the genotypes and phenotypes of 163 Japanese patients with "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11013440",
"endSection": "abstract",
"offsetInBeginSection": 382,
"offsetInEndSection": 1128,
"text": "or partial inactivation of the enzyme causing the rare autosomal recessively inherited conditions, Crigler-Najjar syndrome type-1 (CN-1) and type 2 (CN-2), respectively. Inactivation of the enzyme leads to accumulation of unconjugated bilirubin in the serum. Severe hyperbilirubinemia seen in CN-1 can cause bilirubin encephalopathy (kernicterus). Kernicterus can be fatal or may leave behind permanent neurological sequelae. Here, we have compiled more than 50 genetic lesions of UGT1A1 that cause CN-1 (including 9 novel mutations) or CN-2 (including 3 novel mutations) and have presented a correlation of structure to function of UGT1A1. In contrast to Crigler-Najjar syndromes, Gilbert syndrome is a common inherited condition characterized b"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33102778",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Crigler-Najjar syndrome (CNs) is a rare hereditary unconjugated hyperbilirubinemia caused by mutations in the bilirubin Uridine (UDP) glucuronosyltransferase family 1 member A1 (UGT1A1, ENSG00000241635) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14616765",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "Crigler-Najjar syndrome type I is a severe form of hereditary unconjugated hyperbilirubinemia and is caused by homozygous or compound heterozygous mutations of the bilirubin UDP-glucuronosyltransferase gene (UGT1A1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23430851",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 252,
"text": "Crigler-Najjar syndrome type I (CN-I, MIM #218800) is a rare and severe autosomal disorder. It is caused by deficiency of the liver enzyme responsible for bilirubin elimination, the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1; EC 2.4.1.17)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23992562",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "Two inherited unconjugated hyperbilirubinemias, Crigler-Najjar syndrome and Gilbert syndrome, arise due to deficiency of UGT1A1 enzyme activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793765",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 239,
"text": "Crigler-Najjar syndrome type I (CN-I) is the most severe type of hereditary unconjugated hyperbilirubinemia. It is caused by homozygous or compound heterozygous mutations of the UDP-glycuronosyltransferase gene (UGT1A1) on chromosome 2q37."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11868392",
"endSection": "abstract",
"offsetInBeginSection": 473,
"offsetInEndSection": 627,
"text": "UGT1A1 conjugates bilirubin, and mutations of the gene cause hereditary unconjugated hyperbilirubinemias (Crigler-Najjar syndrome and Gilbert's syndrome)."
}
] | 13 |
BioASQ-training13b
| null | null |
65cfcc8f1930410b13000018
| 369 |
yesno
|
Are mutations in the nf1 gene associated with memory?
|
['yes']
|
[
"yes"
] |
['Yes, distinct functional domains of neurofibromatosis type 1 regulate immediate versus long-term memory formation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19475561",
"http://www.ncbi.nlm.nih.gov/pubmed/17581973"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19475561",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 423,
"text": "We hypothesized that NF1 mutations disturb the expression of genes important for memory formation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17581973",
"endSection": "abstract",
"offsetInBeginSection": 489,
"offsetInEndSection": 734,
"text": "Our previous work has shown that defective cAMP signaling leads to the learning phenotype in Drosophila Nf1 mutants. In the present report, our experiments showed that in addition to learning, long-term memory was also abolished in Nf1 mutants. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17581973",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Distinct functional domains of neurofibromatosis type 1 regulate immediate versus long-term memory formation."
}
] | 11 |
BioASQ-training11b
| null | null |
5a87efa961bb38fb2400000e
| 370 |
yesno
|
Optogenetics refers to the study of gene expression optimization
|
['no']
|
[
"no"
] |
['Optogenetics allows the experimental manipulation of excitable cells by a light stimulus without the need for technically challenging and invasive procedures.', 'No, optogenetics refers to the use of light to control cells in living tissue, typically neurons, that have been genetically modified to express light-sensitive ion channels.', 'No, optogenetics is a technique that uses light to control genetically modified cells or neurons in living organisms.', 'No, optogenetics refers to a technique that uses light to control the activity of genetically modified neurons, allowing precise manipulation of neural circuits in living organisms.', 'Optogenetics is a field of neuroscience that uses light to control and study the activity of neurons in living tissue. It combines the use of genetic engineering to introduce light-sensitive proteins into cells, with the use of light to control the activity of those cells. This technique has been used to study the function of neurons in the brain, as well as to develop treatments for neurological disorders.', 'False. Optogenetics does not refer to the study of gene expression optimization. It refers to the experimental manipulation of excitable cells by a light stimulus in order to study complex neural circuits.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35273478",
"http://www.ncbi.nlm.nih.gov/pubmed/34429103",
"http://www.ncbi.nlm.nih.gov/pubmed/35718324",
"http://www.ncbi.nlm.nih.gov/pubmed/33119964",
"http://www.ncbi.nlm.nih.gov/pubmed/27069384",
"http://www.ncbi.nlm.nih.gov/pubmed/20971436",
"http://www.ncbi.nlm.nih.gov/pubmed/26412943",
"http://www.ncbi.nlm.nih.gov/pubmed/28726577",
"http://www.ncbi.nlm.nih.gov/pubmed/34487118",
"http://www.ncbi.nlm.nih.gov/pubmed/22245580",
"http://www.ncbi.nlm.nih.gov/pubmed/33543619",
"http://www.ncbi.nlm.nih.gov/pubmed/34423469",
"http://www.ncbi.nlm.nih.gov/pubmed/32543249",
"http://www.ncbi.nlm.nih.gov/pubmed/29118219",
"http://www.ncbi.nlm.nih.gov/pubmed/28255969",
"http://www.ncbi.nlm.nih.gov/pubmed/32601426",
"http://www.ncbi.nlm.nih.gov/pubmed/32795553",
"http://www.ncbi.nlm.nih.gov/pubmed/35998606",
"http://www.ncbi.nlm.nih.gov/pubmed/35204770",
"http://www.ncbi.nlm.nih.gov/pubmed/26310015"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34429103",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 170,
"text": "Optogenetics allows the experimental manipulation of excitable cells by a light stimulus without the need for technically challenging and invasive procedures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35718324",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 349,
"text": "Optogenetics has revolutionized the capability of controlling genetically modified neurons in vitro and in vivo and has become an indispensable neuroscience tool. Using light as a probe for selective neuronal activation or inhibition and as a means to read out neural activity has dramatically enhanced our understanding of complex neural circuits. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32543249",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Optogenetics controls neural activity and behavior in living organisms through genetically targetable actuators and light. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26310015",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 409,
"text": "This is a review of the current state of optogenetics-based research in the field of ophthalmology and physiology of vision. Optogenetics employs an interdisciplinary approach that amalgamates gene engineering, optics, and physiology. It involves exogenous expression of a light-activated protein in a very particular retinal cell enabling regulation (stimulation vs. inhibition) of its physiological activity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35273478",
"endSection": "abstract",
"offsetInBeginSection": 583,
"offsetInEndSection": 901,
"text": "In contrast, optogenetics leverages light-sensitive proteins to control cellular signaling dynamics and target gene expression and, by virtue of precise hardware control over illumination, offers the capacity to interrogate how spatiotemporally varying signals modulate gene regulatory networks and cellular behaviors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22245580",
"endSection": "abstract",
"offsetInBeginSection": 86,
"offsetInEndSection": 261,
"text": "As light-gated protein switches, signaling photoreceptors provide the basis for optogenetics, a term that refers to the control of organismal physiology and behavior by light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33119964",
"endSection": "abstract",
"offsetInBeginSection": 546,
"offsetInEndSection": 840,
"text": "In this review, we summarize the main optogenetic systems implemented in the budding yeast Saccharomyces cerevisiae, which allow orthogonal control (by light) of gene expression, protein subcellular localization, reconstitution of protein activity, and protein sequestration by oligomerization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32601426",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Optogenetics is the genetic approach for controlling cellular processes with light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20971436",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "The recently introduced term 'optogenetics' describes a variety of techniques for expressing genes in nerve cells that render them responsive to light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34487118",
"endSection": "abstract",
"offsetInBeginSection": 92,
"offsetInEndSection": 238,
"text": "Optogenetic expression systems can provide precise control over gene expression timing, location, and amplitude using light as the inducing agent."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33119964",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Optogenetics refers to the control of biological processes with light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34423469",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Optogenetics refers to a technique that uses light to modulate neuronal activity with a high spatiotemporal resolution, which enables the manipulation of learning and memory functions in the human brain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35998606",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "In optogenetics, as in nature, sensory photoreceptors serve to control cellular processes by light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28255969",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Optogenetics refers to the genetic modification of cells to express light-sensitive proteins, which mediate ion flow or secondary signalling cascades upon light exposure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28726577",
"endSection": "abstract",
"offsetInBeginSection": 231,
"offsetInEndSection": 360,
"text": " Optogenetics involves the use of genetically encoded and optically active proteins, namely opsins, to control neuronal circuits."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32795553",
"endSection": "abstract",
"offsetInBeginSection": 659,
"offsetInEndSection": 794,
"text": " (3) A completely different interpretation of optogenetics refers to the light activated expression of a genetically induced construct."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26412943",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 69,
"text": "Optogenetics is an innovative technique for optical control of cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35204770",
"endSection": "abstract",
"offsetInBeginSection": 97,
"offsetInEndSection": 198,
"text": " Optogenetics refers to techniques that use light to control the cellular activity of targeted cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22245580",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 306,
"text": "basis for optogenetics, a term that refers to the control of organismal physiology and behavior by light. We establish as novel optogenetic tools the "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27069384",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Optogenetics refers to the ability to control cells that have been genetically modified to express light-sensitive ion channels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33119964",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Optogenetics refers to the control of biological processes with light. The activation of cellular phenomena by defined wavelengths has several advanta"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29118219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Optogenetics is the use of genetically coded, light-gated ion channels or pumps (opsins) for millisecond resolution control of neural activity."
}
] | 12 |
BioASQ-training12b
| null | null |
6415b7b8690f196b5100000c
| 371 |
yesno
|
Does prudent diet reduce cardiovascular risk?
|
['yes']
|
[
"yes"
] |
a high adherence to prudent diet is associated with reduced risk of CVD. The adherence to prudent diet was associated to a 28% lower risk of cardiovascular mortality and a 17% lower risk of all-cause mortality in a large cohort of healthy women
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23953031",
"http://www.ncbi.nlm.nih.gov/pubmed/22739999",
"http://www.ncbi.nlm.nih.gov/pubmed/19656644",
"http://www.ncbi.nlm.nih.gov/pubmed/19303267",
"http://www.ncbi.nlm.nih.gov/pubmed/18936332",
"http://www.ncbi.nlm.nih.gov/pubmed/18574045",
"http://www.ncbi.nlm.nih.gov/pubmed/14972059",
"http://www.ncbi.nlm.nih.gov/pubmed/10597981",
"http://www.ncbi.nlm.nih.gov/pubmed/16401383",
"http://www.ncbi.nlm.nih.gov/pubmed/9430390",
"http://www.ncbi.nlm.nih.gov/pubmed/22012753",
"http://www.ncbi.nlm.nih.gov/pubmed/11493127"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23953031",
"endSection": "abstract",
"offsetInBeginSection": 685,
"offsetInEndSection": 902,
"text": "Using this approach, large prospective studies have reported reductions in CVD risk ranging from 10 to 60% in groups whose diets can be variously classified as ‘Healthy’, ‘Prudent’, Mediterranean’ or ‘DASH compliant’."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22739999",
"endSection": "abstract",
"offsetInBeginSection": 1456,
"offsetInEndSection": 1595,
"text": "Our findings suggest that a heart healthy dietary pattern is associated with moderately reduced risk of MI, but not related to risk of VTE."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19656644",
"endSection": "abstract",
"offsetInBeginSection": 965,
"offsetInEndSection": 1165,
"text": "The systematically reviewed studies reveal that a high adherence to a Mediterranean type of diet or \"prudent diet\" is associated with reduced risk of CVD and some types of cancer, even in the elderly."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19303267",
"endSection": "abstract",
"offsetInBeginSection": 1399,
"offsetInEndSection": 1693,
"text": "In a large healthy Italian population, non-predefined dietary patterns including foods considered to be rather unhealthy, were associated with higher levels of cardiovascular risk factors, CRP and individual global CVD risk, whereas a \"prudent-healthy\" pattern was associated with lower levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18936332",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 790,
"text": "We observed an inverse association between the prudent pattern and AMI, with higher levels being protective."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18574045",
"endSection": "abstract",
"offsetInBeginSection": 1031,
"offsetInEndSection": 1314,
"text": "After multivariable adjustment, the prudent diet was associated with a 28% lower risk of cardiovascular mortality (95% confidence interval [CI], 13 to 40) and a 17% lower risk of all-cause mortality (95% CI, 10 to 24) when the highest quintile was compared with the lowest quintile. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18574045",
"endSection": "abstract",
"offsetInBeginSection": 1530,
"offsetInEndSection": 1731,
"text": "Greater adherence to the prudent pattern may reduce the risk of cardiovascular and total mortality, whereas greater adherence to the Western pattern may increase the risk among initially healthy women."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14972059",
"endSection": "abstract",
"offsetInBeginSection": 1317,
"offsetInEndSection": 1456,
"text": "Composite diets (such as DASH diets, Mediterranean diet, 'prudent' diet) have been demonstrated to reduce the risk of hypertension and CHD."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012307",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002318",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004032",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012306",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005526",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006331",
"http://www.disease-ontology.org/api/metadata/DOID:114"
] |
[] |
53319653d6d3ac6a3400003e
| 372 |
yesno
|
Is Mical an oxidoreductase?
|
['yes']
|
[
"yes"
] |
['Yes,\nMICAL is an oxidoreductase']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31949908",
"http://www.ncbi.nlm.nih.gov/pubmed/12700098",
"http://www.ncbi.nlm.nih.gov/pubmed/27223600",
"http://www.ncbi.nlm.nih.gov/pubmed/33671465"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33671465",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 497,
"text": "the MICALs, which are flavoprotein monooxygenase/hydroxylase enzymes that associate with flavin adenine dinucleotide (FAD) and use the co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH) in Redox reactions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31949908",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 26,
"text": "MICAL is an oxidoreductase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27223600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "We have recently identified a new family of multidomain oxidoreductase (redox) enzymes, the MICALs,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12700098",
"endSection": "abstract",
"offsetInBeginSection": 1552,
"offsetInEndSection": 1576,
"text": "the oxidoreductase MICAL"
}
] | 11 |
BioASQ-training11b
| null | null |
62515021e764a53204000018
| 373 |
yesno
|
Are ultraconserved enhancers important for normal development?
|
['yes']
|
[
"yes"
] |
['Yes, ultraconserved enhancers are required for normal development.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29358049"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29358049",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "Ultraconserved Enhancers Are Required for Normal Development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29358049",
"endSection": "abstract",
"offsetInBeginSection": 177,
"offsetInEndSection": 403,
"text": "However, initial deletion studies in mice revealed that loss of such extraordinarily constrained sequences had no immediate impact on viability. Here, we show that ultraconserved enhancers are required for normal development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29358049",
"endSection": "abstract",
"offsetInBeginSection": 322,
"offsetInEndSection": 402,
"text": "Here, we show that ultraconserved enhancers are required for normal development."
}
] | 11 |
BioASQ-training11b
| null | null |
5c531e887e3cb0e231000018
| 374 |
yesno
|
Does SATB1 regulate the RAG1 and RAG2 genes?
|
['yes']
|
[
"yes"
] |
['SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters.', 'An anti-silencer- and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expression', 'High level expression of the Xlr nuclear protein in immature thymocytes and colocalization with the matrix-associated region-binding SATB1 protein Its onset preceded the rearrangement of TCR genes, as Xlr expression was conserved in thymus cells from RAG1(0/0) mice. An anti-silencer- and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expression during thymocyte development. SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters.', ' SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters. Our results provide a novel framework for understanding ASE function and demonstrate a novel role for SATB1 as a regulator of Rag locus organization and gene expression in DP thymocytes.', 'An anti-silencer- and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expression during thymocyte development.', ' Its onset preceded the rearrangement of TCR genes, as Xlr expression was conserved in thymus cells from RAG1(0/0) mice. SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters.', 'An anti-silencer- and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expression during thymocyte development. SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25847946",
"http://www.ncbi.nlm.nih.gov/pubmed/9886398"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9886398",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "High level expression of the Xlr nuclear protein in immature thymocytes and colocalization with the matrix-associated region-binding SATB1 protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9886398",
"endSection": "abstract",
"offsetInBeginSection": 527,
"offsetInEndSection": 648,
"text": " Its onset preceded the rearrangement of TCR genes, as Xlr expression was conserved in thymus cells from RAG1(0/0) mice. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25847946",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "An anti-silencer- and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expression during thymocyte development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25847946",
"endSection": "abstract",
"offsetInBeginSection": 793,
"offsetInEndSection": 961,
"text": " SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25847946",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1148,
"text": "Our results provide a novel framework for understanding ASE function and demonstrate a novel role for SATB1 as a regulator of Rag locus organization and gene expression in DP thymocytes."
}
] | 11 |
BioASQ-training11b
| null | null |
5d36bb777bc3fee31f00000a
| 375 |
yesno
|
Can Preimplantation Genetic Diagnosis (PGD) be used for gender selection?
|
['yes']
|
[
"yes"
] |
Preimplantation Genetic Diagnosis can be used for gender selection.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20638568",
"http://www.ncbi.nlm.nih.gov/pubmed/20102489",
"http://www.ncbi.nlm.nih.gov/pubmed/19891844",
"http://www.ncbi.nlm.nih.gov/pubmed/19294755",
"http://www.ncbi.nlm.nih.gov/pubmed/19251775",
"http://www.ncbi.nlm.nih.gov/pubmed/18829009",
"http://www.ncbi.nlm.nih.gov/pubmed/18667646",
"http://www.ncbi.nlm.nih.gov/pubmed/18222917",
"http://www.ncbi.nlm.nih.gov/pubmed/12615807",
"http://www.ncbi.nlm.nih.gov/pubmed/12470342",
"http://www.ncbi.nlm.nih.gov/pubmed/9329835"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20638568",
"endSection": "abstract",
"offsetInBeginSection": 96,
"offsetInEndSection": 390,
"text": "This testing is used for identifying singlegene disorders, chromosomal abnormalities, mitochondrial disorders, gender selection in non-mendelian disorders with unequal gender distribution, aneuploidy screening, and other preconceptually identified genetic abnormalities in prospective parents. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20102489",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 289,
"text": " Although many clinics offer PGD for HA by gender selection, an approach that detects the presence of the underlying F8 mutation has several advantages. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19891844",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 719,
"text": "Preimplantation genetic diagnosis (PGD) for gender selection for non-medical reasons has been considered an unethical procedure by several authors and agencies in the Western society on the basis that it could disrupt the sex ratio, that it discriminates against women and that it leads to disposal of normal embryos of the non-desired gender. In this study, the analysis of a large series of PGD procedures for gender selection from a wide geographical area in the USA shows that, in general, there is no deviation in preference towards any specific gender except for a preference of males in some ethnic populations of Chinese, Indian and Middle Eastern origin that represent a small percentage of the US population. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19294755",
"endSection": "abstract",
"offsetInBeginSection": 928,
"offsetInEndSection": 1111,
"text": " In response to one specific question, one-third of the couples agreed to use the donor child as a lifetime organ donor and supported the use of PGD for non-medical gender selection. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19251775",
"endSection": "abstract",
"offsetInBeginSection": 245,
"offsetInEndSection": 455,
"text": "More specifically, I illustrate how the prescriptions of deliberative democracy can be applied to the issue of regulating non-medical uses of pre-implantation genetic diagnosis (PGD), such as gender selection. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18829009",
"endSection": "abstract",
"offsetInBeginSection": 805,
"offsetInEndSection": 1124,
"text": "Private clinics were more likely than other programs to be on either the East or West Coast, list certain PGD risks (e.g., diagnostic error), note that PGD was new or controversial, reference source of PGD information, provide accuracy rates of genetic testing of embryos, and offer gender selection for social reasons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18667646",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 552,
"text": "The purpose of this article is to ascertain and appraise the ethical issues inherent to the utilisation of preimplantation genetic diagnosis for gender selection in infertile patients anticipating undergoing a medically indicated assisted reproductive technique procedure. Performance of preimplantation genetic diagnosis per request specifically for gender selection by an infertile couple undergoing medically indicated assisted reproductive technique may not breach the principles of ethics, and is unlikely to alter the population balance of sexes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18222917",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 653,
"text": "One possible use of PGD is to perform gender selection for couples whose offspring are at increased risk of disorders that do not follow Mendelian inheritance, but which are substantially more common in one sex than another (unequal sex incidence). Here, we examine the clinical and ethical issues to be considered prior to offering PGD gender selection to reduce the risk of a child being affected by a non-Mendelian condition with unequal sex incidence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12615807",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 301,
"text": "New uses of PGD have been reported in the past year for screening embryos for susceptibility to cancer, for late-onset diseases, for HLA-matching for existing children, and for gender. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12615807",
"endSection": "abstract",
"offsetInBeginSection": 436,
"offsetInEndSection": 708,
"text": "This article describes current and likely future uses of PGD, and then analyses the ethical issues posed by new uses of PGD to screen embryos for susceptibility and late-onset conditions, for HLA-matching for tissue donation to an existing child, and for gender selection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12470342",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 312,
"text": "The use of PGD for sex selection arouses considerable debate, especially in countries like India that have a marked cultural preference for boys. It is argued that using PGD for sex selection is a treatment option that can be ethically offered to couples who desire to use this technology to plan their families."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9329835",
"endSection": "abstract",
"offsetInBeginSection": 688,
"offsetInEndSection": 785,
"text": "Another concern is the use of this technology for nongenetic disorders such as gender selection. "
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005783",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012743",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019836"
] |
[] |
52b2ed144003448f55000004
| 377 |
yesno
|
Has small pox been eradicated from the world?
|
['yes']
|
[
"yes"
] |
['smallpox is now eradicated.', 'Yes, small pox has been eradicated.', 'smallpox is now eradicated', 'small pox has been eradicated.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22566811",
"http://www.ncbi.nlm.nih.gov/pubmed/11808015",
"http://www.ncbi.nlm.nih.gov/pubmed/10742580",
"http://www.ncbi.nlm.nih.gov/pubmed/14969309",
"http://www.ncbi.nlm.nih.gov/pubmed/23436190",
"http://www.ncbi.nlm.nih.gov/pubmed/7013291",
"http://www.ncbi.nlm.nih.gov/pubmed/11503361",
"http://www.ncbi.nlm.nih.gov/pubmed/22185830"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10742580",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 183,
"text": "small pox has been eradicated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11808015",
"endSection": "abstract",
"offsetInBeginSection": 837,
"offsetInEndSection": 863,
"text": "smallpox is now eradicated"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7013291",
"endSection": "abstract",
"offsetInBeginSection": 819,
"offsetInEndSection": 1144,
"text": "In May 1980 the World Health Assembly in Geneva announced in solemn form the world-wide eradication of the small-pox and gave recommendations to the member countries for concluding measures concerning the small-pox vaccination, the foundation of vaccine reserves and the control of the epidemiological situation in the world."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10742580",
"endSection": "abstract",
"offsetInBeginSection": 65,
"offsetInEndSection": 182,
"text": "As a result of vaccination, diseases such as polio and measles have been controlled and small pox has been eradicated"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23436190",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 277,
"text": "Small pox eradication from the world is the perfect example of the role of mass vaccination of the entire community of the universe. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11503361",
"endSection": "abstract",
"offsetInBeginSection": 914,
"offsetInEndSection": 1057,
"text": "The French owe a lot to this Central Committee of Vaccine, which greatly contributed to fighting small pox and eradicating the disease finally."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23436190",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 276,
"text": "Small pox eradication from the world is the perfect example of the role of mass vaccination of the entire community of the universe."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22566811",
"endSection": "abstract",
"offsetInBeginSection": 669,
"offsetInEndSection": 868,
"text": "Also, the vaccine that Jenner used, which decreased the prevalence of Small Pox worldwide in his own time, and later was used to eradicate Small Pox altogether, is discussed in light of recent data.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12822115",
"endSection": "abstract",
"offsetInBeginSection": 516,
"offsetInEndSection": 760,
"text": "the only known cases of smallpox happened from an outbreak in Birmingham, England caused by a laboratory accident in the year of 1979. On May the 8 th 1980 the disease was declared as eliminated from the world by the WHO (WHO-Resolution 33.33)."
}
] | 6 |
BioASQ-training6b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:8736",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012899",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012900"
] | null |
58a1da4e78275d0c4a000059
| 378 |
yesno
|
Is there any role of interleukin-11 in cardiovascular fibrosis?
|
['yes']
|
[
"yes"
] |
['Yes. Interleukin 11 (IL11) upregulation is the dominant transcriptional response to TGFB1 exposure and required for its profibrotic effect. IL11 and its receptor (IL11RA) are expressed specifically in fibroblasts where they drive non-canonical, ERK-dependent autocrine signalling that is required for fibrogenic protein synthesis. In mice, fibroblast-specific Il11 transgene expression or Il11 injection causes heart and kidney fibrosis and organ failure whereas genetic deletion of Il11ra1 is protective against disease. Thus, inhibition of IL11 prevents fibroblast activation across organs and species in response to a range of important pro-fibrotic stimuli.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29160304"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29160304",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 57,
"text": "IL11 is a crucial determinant of cardiovascular fibrosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29160304",
"endSection": "abstract",
"offsetInBeginSection": 492,
"offsetInEndSection": 1380,
"text": "Using integrated imaging-genomics analyses of primary human fibroblasts, we found that Interleukin 11 (IL11) upregulation is the dominant transcriptional response to TGFB1 exposure and required for its profibrotic effect. IL11 and its receptor (IL11RA) are expressed specifically in fibroblasts where they drive non-canonical, ERK-dependent autocrine signalling that is required for fibrogenic protein synthesis. In mice, fibroblast-specific Il11 transgene expression or Il11 injection causes heart and kidney fibrosis and organ failure whereas genetic deletion of Il11ra1 is protective against disease. Thus, inhibition of IL11 prevents fibroblast activation across organs and species in response to a range of important pro-fibrotic stimuli. These data reveal a central role of IL11 in fibrosis and we propose inhibition of IL11 as a new therapeutic strategy to treat fibrotic diseases."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29160304",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 58,
"text": "IL11 is a crucial determinant of cardiovascular fibrosis."
}
] | 11 |
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D005355",
"https://meshb.nlm.nih.gov/record/ui?ui=D017370"
] | null |
5a8b292afcd1d6a10c00001f
| 379 |
yesno
|
Is thyroid hormone therapy indicated in patients with heart failure?
|
['no']
|
[
"no"
] |
There are several experimental and clinical evidences of the potential benefits of Thyroid hormone replacement therapy in heart failure. Initial clinical data showed also a good safety profile and tolerance of TH replacement therapy in patients withheart failure.
However currently there is no indication to treat patients with heart failure withTHreplacementtherapy.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23660007",
"http://www.ncbi.nlm.nih.gov/pubmed/20100314",
"http://www.ncbi.nlm.nih.gov/pubmed/19808346",
"http://www.ncbi.nlm.nih.gov/pubmed/18221125",
"http://www.ncbi.nlm.nih.gov/pubmed/18171701",
"http://www.ncbi.nlm.nih.gov/pubmed/9485134",
"http://www.ncbi.nlm.nih.gov/pubmed/23837113",
"http://www.ncbi.nlm.nih.gov/pubmed/23369135",
"http://www.ncbi.nlm.nih.gov/pubmed/19778808",
"http://www.ncbi.nlm.nih.gov/pubmed/19506112",
"http://www.ncbi.nlm.nih.gov/pubmed/17893267",
"http://www.ncbi.nlm.nih.gov/pubmed/19125327",
"http://www.ncbi.nlm.nih.gov/pubmed/8333798",
"http://www.ncbi.nlm.nih.gov/pubmed/7954115",
"http://www.ncbi.nlm.nih.gov/pubmed/15572044",
"http://www.ncbi.nlm.nih.gov/pubmed/17710084",
"http://www.ncbi.nlm.nih.gov/pubmed/8936682",
"http://www.ncbi.nlm.nih.gov/pubmed/19917524",
"http://www.ncbi.nlm.nih.gov/pubmed/10194658",
"http://www.ncbi.nlm.nih.gov/pubmed/2189307",
"http://www.ncbi.nlm.nih.gov/pubmed/8936683",
"http://www.ncbi.nlm.nih.gov/pubmed/12165115",
"http://www.ncbi.nlm.nih.gov/pubmed/12165118",
"http://www.ncbi.nlm.nih.gov/pubmed/8353891",
"http://www.ncbi.nlm.nih.gov/pubmed/9312172",
"http://www.ncbi.nlm.nih.gov/pubmed/10474790",
"http://www.ncbi.nlm.nih.gov/pubmed/15604125",
"http://www.ncbi.nlm.nih.gov/pubmed/12145478",
"http://www.ncbi.nlm.nih.gov/pubmed/22009366"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23660007",
"endSection": "abstract",
"offsetInBeginSection": 1252,
"offsetInEndSection": 1405,
"text": "Patients with chronic heart failure and subclinical hypothyroidism significantly improved their physical performance when normal TSH levels were reached."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20100314",
"endSection": "abstract",
"offsetInBeginSection": 1613,
"offsetInEndSection": 1870,
"text": "Early and sustained physiological restoration of circulating L-T3 levels after MI halves infarct scar size and prevents the progression towards heart failure. This beneficial effect is likely due to enhanced capillary formation and mitochondrial protection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19808346",
"endSection": "abstract",
"offsetInBeginSection": 1818,
"offsetInEndSection": 2006,
"text": "These data indicate that T(3) replacement to euthyroid levels improves systolic function and tends to improve diastolic function, potentially through changes in myocardial gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18221125",
"endSection": "abstract",
"offsetInBeginSection": 751,
"offsetInEndSection": 951,
"text": "In these patients, the administration of synthetic triiodothyronine (T(3)) was well tolerated and induced significant improvement in cardiac function without increased heart rate and metabolic demand."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18171701",
"endSection": "abstract",
"offsetInBeginSection": 1939,
"offsetInEndSection": 2077,
"text": "In DC patients, short-term synthetic L-T(3) replacement therapy significantly improved neuroendocrine profile and ventricular performance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9485134",
"endSection": "abstract",
"offsetInBeginSection": 909,
"offsetInEndSection": 1277,
"text": "Triiodothyronine was well tolerated without episodes of ischemia or clinical arrhythmia. There was no significant change in heart rate or metabolic rate and there was minimal increase in core temperature. Cardiac output increased with a reduction in systemic vascular resistance in patients receiving the largest dose, consistent with a peripheral vasodilatory effect."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020249",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006333",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013963",
"http://www.disease-ontology.org/api/metadata/DOID:6000",
"http://www.disease-ontology.org/api/metadata/DOID:9651",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054143",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006321"
] |
[] |
531b4269b166e2b80600003e
| 380 |
yesno
|
Does an interferon (IFN) signature exist for SLE patients?
|
['yes']
|
[
"yes"
] |
['Interferon type I (IFN-I) plays a pivotal role in the pathogenesis of SLE. An IFN-I score (positive or negative), as a measure of IFN-I activation, is assessed using the expression values of IFN-I signature genes (IFI44, IFI44L, IFIT1, Ly6e, MxA, IFITM1) in CD14+ monocytes of cSLE patients and healthy controls (HCs).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29850618",
"http://www.ncbi.nlm.nih.gov/pubmed/21576205",
"http://www.ncbi.nlm.nih.gov/pubmed/29321042",
"http://www.ncbi.nlm.nih.gov/pubmed/28830352"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21576205",
"endSection": "title",
"offsetInBeginSection": 69,
"offsetInEndSection": 167,
"text": "Interferon regulatory factor 7 activation correlates with the IFN signature and recurrent disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21576205",
"endSection": "abstract",
"offsetInBeginSection": 801,
"offsetInEndSection": 941,
"text": "In SLE post-transplant, recurrent disease activity and induction of IRF7 protein expression correlated with activation of the IFN signature."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28830352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28830352",
"endSection": "abstract",
"offsetInBeginSection": 1068,
"offsetInEndSection": 1329,
"text": "We also detected decreased expression of several IFN-signature genes Ifit3 and Isg15 in CD4+ from SLE-prone mice following TOFA and DEXA treatment, and IFIT3 in CD3+ T cells from human patients following immunosuppressant therapy including steroid, respectively"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29850618",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 992,
"text": "We found that cDCs from prediseased TCSle male mice express the IFN signature as female TCSle cDCs do. Estrogens are necessary but not sufficient to express this IFN signature, but high doses of E2 can compensate for other steroidal components."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29850618",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Conventional DCs from Male and Female Lupus-Prone B6.NZM Sle1/Sle2/Sle3 Mice Express an IFN Signature and Have a Higher Immunometabolism That Are Enhanced by Estrogen."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29321042",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "Type I IFN signature in childhood-onset systemic lupus erythematosus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29321042",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 190,
"text": " Interferon type I (IFN-I) plays a pivotal role in the pathogenesis of SLE. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29321042",
"endSection": "abstract",
"offsetInBeginSection": 401,
"offsetInEndSection": 677,
"text": "The IFN-I score (positive or negative), as a measure of IFN-I activation, was assessed using real-time quantitative PCR (RT-PCR) expression values of IFN-I signature genes (IFI44, IFI44L, IFIT1, Ly6e, MxA, IFITM1) in CD14+ monocytes of cSLE patients and healthy controls (HCs)"
}
] | 11 |
BioASQ-training11b
| null | null |
5c7019557c78d6947100005f
| 381 |
yesno
|
Can calcium dietary supplementation reduce the risk of colorectal cancer?
|
['yes']
|
[
"yes"
] |
['Calcium dietary supplementation may potentially reduce the risk of colorectal cancer, as suggested by a study that found an inverse association between postdiagnostic total calcium intake and colorectal cancer-specific mortality. The study compared the highest with the lowest quartile intake of postdiagnostic total calcium and found that the multivariable hazard ratio for colorectal cancer-specific mortality was 0.56 (95% CI, 0.32-0.96; P trend = 0.04). Additionally, postdiagnostic supplemental calcium intake was also inversely associated with colorectal cancer-specific mortality, with a multivariable hazard ratio of 0.67 (95% CI, 0.42-1.06; P trend = 0.047). However, these inverse associations were primarily observed in women, and calcium from diet or dairy sources was associated with lower risk in men. Another study found that higher dietary calcium intake was significantly associated with a lower risk of colorectal cancer in women, but not in men. Therefore, calcium dietary supplementation may potentially reduce the risk of colorectal cancer, particularly in women, but more research is needed to confirm these findings.', 'Daily supplementation of calcium with vitamin D for seven years did not affect the overall incidence of colorectal cancer among postmenopausal women. However, high calcium intake was found to have a greater protective effect against tumors of the distal colon and rectal cancer compared to proximal colon cancer. The risk reduction associated with calcium was similar for both dietary and supplemental sources. Additionally, calcium consumption was inversely related to colorectal cancer risk in a Korean population, where the national average calcium intake level is lower than in Western countries. Therefore, while calcium dietary supplementation may not reduce the overall risk of colorectal cancer, it could potentially have a protective effect against certain sub-sites of the colon and rectal cancer, and its risk reduction effects may be more pronounced in populations with lower calcium intake levels.', "The evidence on whether calcium supplementation can reduce the risk of colorectal cancer is mixed and inconclusive. Some observational studies suggest that higher calcium intake may be associated with a reduced colorectal cancer risk, especially for distal colon and rectal tumors. However, a large clinical trial found that daily supplementation of calcium with vitamin D for seven years had no effect on colorectal cancer incidence among postmenopausal women. The long latency period for colorectal cancer development and the trial's duration may have contributed to this null finding. While calcium consumption was inversely related to colorectal cancer risk in a Korean population study, more research is needed to clarify calcium supplementation's role in colorectal cancer prevention.", 'The evidence on the effect of calcium dietary supplementation on colorectal cancer risk is mixed. Some studies suggest that high calcium intake, from both dietary and supplemental sources, may have a protective effect against colorectal cancer, particularly in the distal colon and rectum. However, other studies have found no effect of calcium supplementation on colorectal cancer risk. The inconsistency in findings may be due to differences in study design, population characteristics, and the duration and dose of calcium supplementation. More research is needed to determine the role of calcium supplementation in colorectal cancer prevention.', 'Based on the provided abstracts, it appears that calcium dietary supplementation may have a moderate degree of prevention against colorectal adenomatous polyps. A systematic review of two randomized controlled trials found that calcium supplementation reduced the development of recurrent colorectal adenoma (OR 0.74, CI 0.58,0.95). Additionally, a study in mice showed that increased dietary calcium was associated with induced apoptosis in normal distal colonic epithelium, which might contribute to its potential chemopreventive role in colorectal carcinogenesis. However, the evidence is not yet sufficient to recommend the general use of calcium supplements for preventing colorectal cancer. Further studies are needed to fully understand the relationship between calcium supplementation and colorectal cancer risk reduction.', 'Based on the evidence from multiple studies, calcium dietary supplementation may reduce the risk of colorectal cancer, but the effect appears to be modest. Several studies found an inverse association between higher calcium intake and colorectal cancer incidence. Calcium, along with vitamin D, may play a protective role through a joint action in colorectal carcinogenesis.\n\nHowever, while the evidence suggests calcium supplementation could be beneficial, the magnitude of risk reduction is not definitive. More research is needed to establish clear recommendations on dosage and to determine the extent of protection provided by calcium supplements alone versus in combination with vitamin D.\n\nIn summary, calcium supplementation shows promise as part of a preventive strategy against colorectal cancer, but should be considered alongside other important lifestyle factors like a balanced diet, regular exercise, and avoiding smoking and excessive alcohol consumption. The benefits of supplementation must be weighed against potential risks on an individual basis. Current evidence supports a modest protective effect, but is not conclusive enough to universally recommend calcium supplements solely for colorectal cancer prevention.', 'Based on the information provided, it is not possible to conclude that calcium dietary supplementation can reduce the risk of colorectal cancer. The first abstract describes a case-control study showing an inverse relationship between dietary calcium intake and colorectal cancer risk in a Korean population with relatively low calcium intake. However, a randomized controlled trial described in the second abstract found no significant difference in colorectal cancer incidence between women who received calcium plus vitamin D supplementation and those who received placebo. A meta-analysis of observational studies in the third abstract suggests that higher consumption of milk/dairy products reduces the risk of colon cancer, and high calcium intake reduces the risk of colorectal cancer (CRC), but it does not specifically evaluate calcium supplementation. Therefore, more research is needed to determine whether calcium dietary supplementation can reduce the risk of colorectal cancer.', 'Yes, calcium dietary supplementation can reduce the risk of colorectal cancer. Studies have shown that higher intake of calcium is associated with a lower risk of colorectal cancer. The protective effect of calcium is thought to be due to its ability to bind to bile acids and fatty acids in the colon, reducing their ability to damage the colon lining and promote cancer development. Additionally, calcium may also have a direct effect on colon cells, promoting their normal growth and differentiation. However, it is important to note that the evidence for the protective effect of calcium is not conclusive and more research is needed to confirm these findings.', 'The mixed data on the impact of calcium supplementation for reducing colorectal cancer risk shows no significant effect from a study involving postmenopausal women over seven years, though this could be due to trial length and latency. However, high calcium intake is linked with greater protective effects against distal colon and rectal cancers, and the inverse relationship between calcium consumption and colorectal cancer risk has been observed in a Korean population with lower national average calcium intake levels. A decreased colorectal cancer risk associated with calcium was also seen across all subgroups studied.', 'Yes, calcium dietary supplementation has been shown to reduce the risk of colorectal cancer in several studies. The evidence suggests that calcium intake is inversely associated with colorectal cancer risk, with a significant reduction in risk observed for high levels of dietary calcium consumption. The mechanism by which calcium may reduce colorectal cancer risk is not fully understood, but it is thought to involve the inhibition of cell proliferation and the promotion of apoptosis in colonic epithelial cells. Further research is needed to confirm these findings and to determine the optimal level of calcium intake for colorectal cancer prevention.', 'No, daily supplementation of calcium with vitamin D for seven years had no effect on the incidence of colorectal cancer among postmenopausal women. The long latency associated with the development of colorectal cancer, along with the seven-year duration of the trial, may have contributed to this null finding. Ongoing follow-up will assess the longer-term effect of this intervention.', 'Yes, calcium dietary supplementation can reduce the risk of colorectal cancer. A study found that calcium intake was significantly, inversely associated with colorectal cancer risk. Another study reported that individuals with >or=1000IU/day oral Vitamin D or >or=33ng/ml (82nmol/l) serum 25-hydroxyvitamin D had 50% lower incidence of colorectal cancer compared to reference values. The findings support the hypothesis of protective roles for calcium, vitamin D, and dairy products in the risk of colorectal cancer.', 'Calcium dietary supplementation might reduce the risk of colorectal adenomatous polyps, but not enough evidence exists yet for recommending general use of calcium supplements to prevent colorectal cancer. High dietary calcium intake could be associated with lower risks; however, more research is necessary to understand this relationship fully.', '500 mg/d of calcium can decrease the risk of colorectal cancer in people with a history of adenoma, but further studies are needed to confirm the results and to evaluate the effect on the general population', 'Yes, calcium intake from dietary or supplemental sources appears to reduce the risk of colorectal cancer, especially for tumors in the distal colon and rectum. However, one study found that daily supplementation of calcium with vitamin D for seven years did not affect colorectal cancer incidence in postmenopausal women, possibly due to the long latency period for colorectal cancer development. The protective effect of calcium was observed in a Korean population with relatively low average calcium intake compared to Western countries.', 'Based on the provided snippets, the data regarding calcium dietary supplementation reducing the risk of colorectal cancer is mixed. One study found that daily supplementation of calcium with vitamin D for seven years had no effect on the incidence of colorectal cancer among postmenopausal women. However, this null finding may be due to the long latency associated with colorectal cancer development and the relatively short duration of the trial. , On a positive note, high calcium intake was found to have a greater protective effect against tumors of the distal colon and rectal cancer versus proximal colon. The risk reduction associated with calcium was similar for dietary and supplemental sources. Furthermore, calcium consumption was inversely related to colorectal cancer risk in a Korean population where national average calcium intake level is relatively lower than Western countries. A decreased risk of colorectal cancer by calcium intake was also observed in all sub', 'Yes, calcium dietary supplementation can reduce the risk of colorectal cancer. Several studies have found that higher calcium intake is associated with a lower incidence of colorectal cancer:\n\n- Calcium intake was significantly, inversely associated with colorectal cancer risk in a dose-response manner. The highest vs lowest quintile of calcium intake had a 36% lower risk.\n\n- Administration of supplemental calcium may have a significant effect on reducing colonic polyp and colon cancer incidence. \n\n- Results from a large study support the hypothesis that calcium modestly reduces risk of colorectal cancer.\n\n- Calcium intake, along with vitamin D, appears to play a protective role in reducing the risk of colorectal cancer.\n\nThe evidence suggests calcium supplementation, especially in combination with vitamin D, can help prevent colorectal cancer. A dose-response relationship has been observed, with higher calcium intake providing greater risk reduction.', 'Yes, calcium dietary supplementation has been shown to reduce the risk of colorectal cancer in several studies. A meta-analysis of 14 prospective cohort studies found that high calcium intake was associated with a 25% reduction in colorectal cancer risk. Additionally, a randomized controlled trial found that 9 months of high-dose wheat bran fiber and calcium carbonate supplementation in participants with a history of recently resected colorectal cancer was associated with a 25% reduction in risk of colorectal cancer. The mechanisms by which calcium may reduce colorectal cancer risk are not fully understood, but may involve the inhibition of colonic hyperproliferation and the promotion of apoptosis in colonic epithelial cells. Further studies are needed to confirm these findings and to determine the optimal dosage and duration of calcium supplementation for colorectal cancer prevention.', 'No, calcium dietary supplementation has not been proven to reduce the risk of colorectal cancer. While some studies suggest that calcium may have a role in colorectal cancer prevention, the evidence is not conclusive. A meta-analysis of 10 randomized controlled trials found no significant reduction in colorectal cancer risk with calcium supplementation. Additionally, a randomized controlled trial of calcium supplementation in individuals with a history of colorectal adenomas found no significant reduction in the risk of recurrent adenomas. Therefore, it is not recommended to take calcium supplements specifically for the purpose of reducing colorectal cancer risk.', 'The evidence suggests that calcium dietary supplementation might contribute to a moderate degree to the prevention of colorectal adenomatous polyps, but it is not sufficient to recommend the general use of calcium supplements to prevent colorectal cancer. Two well-designed trials with 13,446 subjects found a reduction in recurrent colorectal adenoma with calcium supplementation (OR 0.74, CI 0.58-0.95). However, other studies have inconsistent results, and it is unclear whether the decrease in labeling index correlates with a decrease in occurrence or recurrence of colonic tumors. Additionally, a recent study found that only high dietary calcium intake (>1485 mg/day) was associated with a reduced risk of colorectal cancer, but supplementation had no significant effect. Further replication in other studies is needed to confirm these findings.', 'Calcium intake had protective effect against tumor of the colon. A decreased risk of colorectal cancer by calcium intake is observed in all sub-sites in men and women.', 'Calcium dietary supplementation has been shown to reduce the risk of colorectal cancer, particularly in the distal colon and rectal cancer. However, the effect of calcium supplementation on colorectal cancer risk is not consistent across all studies and may depend on the source of calcium (dietary vs. supplemental) and the duration of supplementation. While some studies have found no effect of calcium supplementation on colorectal cancer risk, others have reported a reduced risk associated with higher calcium intake. The long latency associated with the development of colorectal cancer and the duration of supplementation may contribute to the inconsistent findings. Further research is needed to determine the optimal dosage and duration of calcium supplementation for colorectal cancer prevention.', 'The evidence on the association between calcium dietary supplementation and the risk of colorectal cancer is not conclusive. Some studies suggest that calcium may help reduce the risk by binding to bile and fatty acids in the gut, but other studies have not found a significant association. High calcium intake may have a greater protective effect against tumors of the distal colon and rectal cancer compared to proximal colon. However, excessive calcium intake can lead to hypercalcemia, which may cause symptoms such as anorexia, nausea, vomiting, memory loss, confusion, muscle weakness, increased urination, dehydration, and metabolic bone disease. Therefore, it is recommended to maintain appropriate calcium levels through a balanced diet and, if necessary, supplementation under the guidance of a healthcare professional.', 'Calcium dietary supplementation has been shown to reduce the risk of colorectal cancer, particularly in the distal colon and rectal cancer. However, the null finding in a recent trial among postmenopausal women may be due to the long latency associated with colorectal cancer development and the duration of the trial. Further follow-up is needed to assess the longer-term effect of calcium supplementation on colorectal cancer risk. Additionally, the inverse association between calcium consumption and colorectal cancer risk has been observed in various populations, including Korean men and women. While procalcitonin can guide the identification of children at higher risk of morbidity and mortality, the optimal monitoring and treatment strategies for these individuals are not yet clear. Finally, while CT colonography may be more costly and result in more deaths than colonoscopy, the latter remains the dominant strategy for colorectal cancer screening in Canada.', "Yes, several studies suggest that calcium intake, either through diet or supplements, can potentially reduce the risk of colorectal cancer. However, the protective effect seems to be more significant for tumors of the distal colon and rectal cancer compared to the proximal colon. It's also worth noting that a seven-year trial found no effect of daily supplementation of calcium with vitamin D on the incidence of colorectal cancer among postmenopausal women, suggesting that the impact of calcium may vary depending on other factors such as age, gender, and the specific location of the cancer within the colon", 'While randomized clinical trials have not found a significant reduction in the risk of colorectal cancer, a meta-analysis of prospective studies suggested a modest reduction of 15% in colorectal cancer risk in people with the highest intakes of calcium.', "Yes, calcium dietary supplementation may reduce the risk of colorectal cancer, especially in postmenopausal women. However, the effectiveness of calcium supplementation may depend on the individual's calcium intake level and the duration of supplementation", 'Yes, calcium dietary supplementation can reduce the risk of colorectal cancer by providing a protective effect against tumors in the distal colon and rectal cancer. This inverse relationship between calcium consumption and colorectal cancer risk has been observed across various populations regardless of gender or source (dietary or supplemental). While initial trials showed no effect on incidence, ongoing follow-ups may provide further evidence for long-term benefits.', 'According to the provided abstracts, the evidence suggests that calcium dietary supplementation may contribute to a moderate degree to the prevention of colorectal adenomatous polyps. However, this does not constitute sufficient evidence to recommend the general use of calcium supplements to prevent colorectal cancer. The systematic review found a reduction in the development of recurrent colorectal adenoma (OR 0.74, CI 0.58,0.95) when combining the results from two well-designed trials. Another study found that high dietary calcium intake (>1485mg/day) was associated with a reduced risk of colorectal cancer, but this association may be modified by genetic variation associated with serum calcium concentrations. Overall, while there is some evidence suggesting a potential benefit, more research is needed to fully understand the relationship between calcium supplementation and colorectal cancer prevention.', "Based on available studies and a meta-analysis, there isn't sufficient evidence that calcium dietary supplementation reduces the risk of colorectal cancer. Some observational studies suggest an inverse relationship between calcium intake from dairy products and CRC risk, but this association is not definitive in randomized controlled trials or when specifically assessing calcium supplementation. More research is needed to confirm a direct protective effect of calcium dietary supplements against colorectal cancer."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/8515888",
"http://www.ncbi.nlm.nih.gov/pubmed/10668490",
"http://www.ncbi.nlm.nih.gov/pubmed/31826765",
"http://www.ncbi.nlm.nih.gov/pubmed/30545821",
"http://www.ncbi.nlm.nih.gov/pubmed/15570055",
"http://www.ncbi.nlm.nih.gov/pubmed/10511318",
"http://www.ncbi.nlm.nih.gov/pubmed/18254022",
"http://www.ncbi.nlm.nih.gov/pubmed/24623471",
"http://www.ncbi.nlm.nih.gov/pubmed/9839734",
"http://www.ncbi.nlm.nih.gov/pubmed/21866684",
"http://www.ncbi.nlm.nih.gov/pubmed/32854492",
"http://www.ncbi.nlm.nih.gov/pubmed/1544142",
"http://www.ncbi.nlm.nih.gov/pubmed/7752258",
"http://www.ncbi.nlm.nih.gov/pubmed/26675033",
"http://www.ncbi.nlm.nih.gov/pubmed/37621239",
"http://www.ncbi.nlm.nih.gov/pubmed/15240785",
"http://www.ncbi.nlm.nih.gov/pubmed/36650676",
"http://www.ncbi.nlm.nih.gov/pubmed/19116875",
"http://www.ncbi.nlm.nih.gov/pubmed/8653938",
"http://www.ncbi.nlm.nih.gov/pubmed/8045031",
"http://www.ncbi.nlm.nih.gov/pubmed/16034903",
"http://www.ncbi.nlm.nih.gov/pubmed/15668485",
"http://www.ncbi.nlm.nih.gov/pubmed/33951958",
"http://www.ncbi.nlm.nih.gov/pubmed/34708323",
"http://www.ncbi.nlm.nih.gov/pubmed/36566517",
"http://www.ncbi.nlm.nih.gov/pubmed/14974021",
"http://www.ncbi.nlm.nih.gov/pubmed/27466215",
"http://www.ncbi.nlm.nih.gov/pubmed/36701139",
"http://www.ncbi.nlm.nih.gov/pubmed/15098858",
"http://www.ncbi.nlm.nih.gov/pubmed/36432621",
"http://www.ncbi.nlm.nih.gov/pubmed/15531687",
"http://www.ncbi.nlm.nih.gov/pubmed/36315018",
"http://www.ncbi.nlm.nih.gov/pubmed/33369946",
"http://www.ncbi.nlm.nih.gov/pubmed/1775941",
"http://www.ncbi.nlm.nih.gov/pubmed/16481636",
"http://www.ncbi.nlm.nih.gov/pubmed/12708719",
"http://www.ncbi.nlm.nih.gov/pubmed/12467133",
"http://www.ncbi.nlm.nih.gov/pubmed/18843026",
"http://www.ncbi.nlm.nih.gov/pubmed/28677025",
"http://www.ncbi.nlm.nih.gov/pubmed/31784301",
"http://www.ncbi.nlm.nih.gov/pubmed/12917206"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16481636",
"endSection": "abstract",
"offsetInBeginSection": 1450,
"offsetInEndSection": 1832,
"text": " Daily supplementation of calcium with vitamin D for seven years had no effect on the incidence of colorectal cancer among postmenopausal women. The long latency associated with the development of colorectal cancer, along with the seven-year duration of the trial, may have contributed to this null finding. Ongoing follow-up will assess the longer-term effect of this intervention."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19116875",
"endSection": "abstract",
"offsetInBeginSection": 805,
"offsetInEndSection": 1023,
"text": " High calcium intake had a greater protective effect against tumors of the distal colon and rectal cancer vs. proximal colon. The risk reduction associated with calcium was similar for dietary and supplemental sources."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26675033",
"endSection": "abstract",
"offsetInBeginSection": 1421,
"offsetInEndSection": 1701,
"text": "calcium consumption was inversely related to colorectal cancer risk in Korean population where national average calcium intake level is relatively lower than Western countries. A decreased risk of colorectal cancer by calcium intake was observed in all sub-sites in men and women."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37621239",
"endSection": "abstract",
"offsetInBeginSection": 545,
"offsetInEndSection": 714,
"text": "Calcium intake has also been found to have a beneficial role in reducing the incidence and improving survival rates of colorectal cancer in several observational studies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36701139",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 267,
"text": "However, whether these isoforms modify the effects of vitamin D3 and/or calcium supplementation on colorectal adenoma recurrence is unclear"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36566517",
"endSection": "abstract",
"offsetInBeginSection": 2481,
"offsetInEndSection": 2649,
"text": "Concerning cancer, vitamin D deficiency is associated with increased incidence of and mortality from several types of cancer, such as colorectal, lung and breast cancer"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36432621",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Vitamin D and Calcium as Key Potential Factors Related to Colorectal Cancer Prevention and Treatment: A Systematic Review."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31784301",
"endSection": "abstract",
"offsetInBeginSection": 1016,
"offsetInEndSection": 2006,
"text": ": 0.86, 95% CI: 0.81-0.91). The CRC incidence was decreased by circulating 25(OH)D (RR: 0.67, 95% CI: 0.59-0.77), vitamin D intake (RR: 0.85, 95% CI: 0.78-0.93) and calcium intake (RR: 0.75, 95% CI: 0.70-0.79). High-level circulating 25(OH)D triggered better overall survival (HR: 0.67, 95% CI: 0.57-0.79) and CRC-specific survival (HR: 0.63, 95% CI: 0.53-0.74). Stratified analyses showed that vitamin D and calcium significantly suppressed colorectal tumour incidence among women. Left-sided CRC risk was reversely related to circulating 25(OH)D (RR: 0.60, 95% CI: 0.41-0.88) and vitamin D intake (RR: 0.73, 95% CI: 0.57-0.93). Circulating 25(OH)D decreased colorectal adenoma (RR: 0.63, 95% CI: 0.48-0.82) and CRC (RR: 0.69, 95% CI: 0.56-0.86) risk in populations with higher calcium intake. European and American populations benefited more from vitamin D intake against colorectal tumour. A significant dose-response relationship was observed between intake of vitamin D or calcium and "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30545821",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1398,
"text": "PURPOSE: Although evidence suggests an inverse association between calcium intake and colorectal cancer incidence, the influence of calcium on survival after colorectal cancer diagnosis remains unclear.Experimental Design: We prospectively assessed the association of postdiagnostic calcium intake with colorectal cancer-specific and overall mortality among 1,660 nonmetastatic colorectal cancer patients within the Nurses' Health Study and the Health Professionals Follow-up Study. Patients completed a validated food frequency questionnaire between 6 months and 4 years after diagnosis and were followed up for death. Multivariable hazard ratios (HRs) and 95% confidence intervals (95% CI) were calculated using Cox proportional hazards regression.RESULTS: Comparing the highest with the lowest quartile intake of postdiagnostic total calcium, the multivariable HRs were 0.56 (95% CI, 0.32-0.96; P trend = 0.04) for colorectal cancer-specific mortality and 0.80 (95% CI, 0.59-1.09; P trend = 0.11) for all-cause mortality. Postdiagnostic supplemental calcium intake was also inversely associated with colorectal cancer-specific mortality (HR, 0.67; 95% CI, 0.42-1.06; P trend = 0.047) and all-cause mortality (HR, 0.71; 95% CI, 0.54-0.94; P trend = 0.008), although these inverse associations were primarily observed in women. In addition, calcium from diet or dairy sources was associated with l"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36432621",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1204,
"text": "Colorectal cancer (CRC) is currently considered one of the most common and lethal types of tumors. Nutrition is of notorious relevance, given its influence in CRC prevention and treatment. This systematic review aimed to revise and update the state of knowledge regarding the potential role of vitamin D and calcium as key factors involved in the prevention and treatment of CRC. A literature search was performed in PubMed and Web of Science. A total of eight studies were finally included in the present review. Vitamin D showed a protective role by promoting transcriptomic changes associated with antitumor effects. However, no significant effects of vitamin D were noted in the relapse-free survival of patients at 5 years. On the other hand, previous scientific evidence demonstrated that calcium regulates the expression of colonic proteins that decrease cell proliferation and increase cell differentiation. Nevertheless, an increased risk of associated serrated adenomas was found in response to calcium and calcium + vitamin D supplementation. Moreover, supplementation with both nutrients showed positive changes on relevant CRC biomarkers including TGFα, TGFβ1, APC, β-catenin and E-cadherin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32854492",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1483,
"text": "PURPOSE: Dietary calcium intake has been suggested to be protective against the development of colorectal cancer. The mean dietary calcium intake of Koreans is 490 mg/day, which is far below the recommended calcium intake of 700-800 mg/day. In this study, we explored the relationship between dietary calcium intake and colorectal cancer development in Koreans with relatively low calcium intake compared with individuals in Western countries.MATERIALS AND METHODS: The Health Examinees Study, a large-scale genomic community-based prospective cohort study, was designed to identify the general characteristics of major chronic diseases in Koreans. A total of 119,501 participants aged 40-69 years recruited between 2004 and 2013 were included in this analysis. The calcium intake level was categorized using the Dietary Reference Intakes for Koreans (KDRIs). The Cox proportional hazards regression model was used to estimate the hazard ratio (HR) and the corresponding 95% confidence intervals (CIs) for colorectal cancer risk, adjusting for potential confounders.RESULTS: In the multivariable-adjusted model, compared with the group that consumed less than the recommended amount of calcium, the group that consumed more than the recommended intake of calcium showed a significant reduction in the risk of colorectal cancer in women. (HR, 0.54; 95% CI, 0.31 to 0.95). Among men, however, no significant association was observed between dietary calcium intake and colorectal cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33369946",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1106,
"text": "OBJECTIVES: Previous studies showed that high calcium intake may be associated with the reduced colorectal cancer (CRC) risk, but results were inconclusive. In this study, we evaluated whether calcium intake from diet and supplements, as well as the calcium levels itself, were associated with the CRC risk in middle-aged and older individuals. Also, we evaluated whether these associations were modified by genetic variation of calcium homeostasis.DESIGN: This study was embedded in the Rotterdam study, a prospective cohort study among adults aged 55 years and older without CRC at baseline, from the Ommoord district of Rotterdam, The Netherlands (N = 10 941). Effect modification by a predefined polygenetic risk score (PRS) from seven loci known to be associated with calcium concentrations, was evaluated.RESULTS: The incidence rate of CRC in the study population was 2.9 per 1000 person-years. Relative to the recommended dietary calcium intake, only higher than the recommended dietary calcium intake (≥1485 mg/day) was associated with a reduced risk of CRC [hazard ratio (HR), 0.66; 95% confidence"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31826765",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1346,
"text": "The effects of dietary vitamin D, Ca and dairy products intakes on colorectal cancer risk remain controversial. The present study investigated the association between these dietary intakes and the risk of colorectal cancer in Guangdong, China. From July 2010 to December 2018, 2380 patients with colorectal cancer and 2389 sex- and age-matched controls were recruited. Dietary intake data were collected through face-to-face interviews using a validated FFQ. Unconditional multivariable logistic regression models were used to calculate the OR and 95 % CI after adjusting for various confounders. Higher dietary vitamin D and Ca intakes were associated with 43 and 52 % reductions in colorectal cancer risk, with OR of 0·57 (95 % CI 0·46, 0·70) and 0·48 (95 % CI 0·39, 0·61), respectively, for the highest quartile (v. the lowest quartile) intakes. A statistically significant inverse association was observed between total dairy product intake and colorectal cancer risk, with an adjusted OR of 0·32 (95 % CI 0·27, 0·39) for the highest v. the lowest tertile. Subjects who drank milk had a 48 % lower risk of colorectal cancer than those who did not (OR 0·52, 95 % CI 0·45, 0·59). The inverse associations of dietary vitamin D, Ca, total dairy products and milk intakes with the risk of colorectal cancer were independent of sex and cancer site."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36315018",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 812,
"text": "BACKGROUND: Although colorectal cancer (CRC) incidence is declining among adults aged ≥65 years, CRC incidence in younger adults has been rising. The protective role of calcium in colorectal carcinogenesis has been well established, but evidence is lacking on whether the association varies by age at diagnosis. We investigated the association between total calcium intake and risk of overall CRC and CRC before age 55 years.METHODS: In the Nurses' Health Study II (1991-2015), 94 205 women aged 25-42 years at baseline were included in the analysis. Diet was assessed every 4 years through validated food frequency questionnaires. Multivariable-adjusted hazard ratios (HRs) and 95% CIs for CRC were estimated using the Cox proportional hazards model.RESULTS: We documented 349 incident CRC cases during 2 202 60"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34708323",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1005,
"text": "PURPOSE: The aim of this study is to analyze the current evidence about the relationships between calcium/vitamin D and CRC based on case-control studies according to sex, tumor location and continental region to complement the information obtained in meta-analyses of other designs.METHODS: The articles were located in three databases (PUBMED, EMBASE and SCOPUS), they should be written in English language, with a case and control design and published between 1 January 1970 and 31 October 2019.RESULTS: There were 37 selected studies, 32 for intake of calcium, that involved 24,353 CRC cases and 30,650 controls, and 23 for that of VIT D, with a total of 19,076 cases and 36.746 controls included. For dietary calcium intake, the overall OR was 0.94 (95% CI 0.92-0.97), suggesting a reducing effect with a 6% decrease in CRC risk for every 300 mg of calcium ingested daily. Regarding vitamin D intake a global OR of 0.96 (95% CI 0.93-0.98) was observed, what means a 4% decrease in the risk of CRC per"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28677025",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 725,
"text": "BACKGROUND: Concerning the chemopreventive potential of calcium against colorectal neoplasms, strong evidence from initial randomized controlled trials (RCTs) of colorectal adenoma has not been confirmed from the most recent large RCT. To explain the conflicting results, a new hypothesis was proposed that the benefit of calcium may be confined to lean individuals.METHODS: To test this hypothesis, we examined heterogeneity of the associations of calcium intake with adenoma and CRC, using data from the most recent meta-analyses of observational studies and conducting subgroup analysis by average body mass index (BMI) of study population.RESULTS: An inverse association of calcium intake with adenoma and CRC did not var"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14974021",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "Dietary calcium supplementation for preventing colorectal cancer and adenomatous polyps."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7752258",
"endSection": "abstract",
"offsetInBeginSection": 2144,
"offsetInEndSection": 2929,
"text": "A statistically significant reduction in cytolytic activity was determined during calcium supplementation (from 57% +/- 41% to 32% +/- 30%; P < .05), whereas in the placebo group, it did not change (from 42% +/- 41% to 36% +/- 27%; P > .10).CONCLUSIONS: Oral calcium supplementation was shown to cause only a minor nonstatistically significant reduction of epithelial cell proliferation in the rectum, compared with placebo, and to have no effect on the same parameter in the sigmoid and descending colon in first-degree relatives of hereditary nonpolyposis colorectal cancer patients.IMPLICATION: These results cast doubt on the value of calcium supplementation in the prevention of colorectal cancer, especially in individuals already consuming an adequate amount of dietary calcium."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14974021",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 948,
"text": "Intervention studies with colorectal cancer as an endpoint are difficult to perform owing to the large number of patients and the long follow-up required; studies using the appearance of colorectal adenomatous polyps as a surrogate endpoint are therefore considered in reviewing the existing evidence.OBJECTIVES: This systematic review aims to assess the effect of supplementary dietary calcium on the incidence of colorectal cancer and the incidence or recurrence of adenomatous polyps.SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register, the Cochrane Colorectal Cancer Group specialised register, MEDLINE, Cancerlit, and Embase, to April 2002."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12467133",
"endSection": "abstract",
"offsetInBeginSection": 1388,
"offsetInEndSection": 1471,
"text": "In sum, our data suggest that high calcium intake may lower colorectal cancer risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15668485",
"endSection": "abstract",
"offsetInBeginSection": 1383,
"offsetInEndSection": 1646,
"text": "These data indicate that a difference of < 400 to > 800 mg of calcium per day was associated with an approximately 25% reduction in risk of colorectal cancer, and this reduction in risk occurred regardless of the source of the calcium (i.e., diet or supplements)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37621239",
"endSection": "abstract",
"offsetInBeginSection": 545,
"offsetInEndSection": 715,
"text": "Calcium intake has also been found to have a beneficial role in reducing the incidence and improving survival rates of colorectal cancer in several observational studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19116875",
"endSection": "abstract",
"offsetInBeginSection": 1097,
"offsetInEndSection": 1334,
"text": "Higher consumption of milk/dairy products reduces the risk of colon cancer, and high calcium intake reduces the risk of CRC. Low vitamin D intake in the study populations may limit the ability to detect a protective effect if one exists."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21866684",
"endSection": "abstract",
"offsetInBeginSection": 1498,
"offsetInEndSection": 1720,
"text": "In conclusion, a high calcium intake and the use of calcium supplements may be protective against colorectal neoplasia, although a greater sample may be required to observe significant associations in a multivariate model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10668490",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Experimental and observational findings suggest that calcium intake may protect against colorectal neoplasia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1775941",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 798,
"text": "Diet is a major determinant of colon cancer risk. Calcium may protect against colon cancer, presumably by binding cytotoxic bile acids and fatty acids. Numerous studies support this proposition. In subjects at risk for colon cancer oral calcium supplementation has been shown to reduce rectal epithelial proliferation rate, thereby supposedly decreasing cancer risk. In contrast to the original hypothesis that phosphate counteracts the effect of calcium, evidence has now been provided that phosphate is crucial for the intraluminal binding of bile acids in complexes of calcium, phosphate, and bile acids. Supplemental calcium has been shown to reduce the cytotoxic potential of fecal water, which is probably attributable to the profound effect of calcium on bile acid and fatty acid metabolism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15098858",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 564,
"text": "There is convincing laboratory evidence that calcium reduces the risk of colorectal cancer, but previous epidemiologic studies have reported somewhat inconsistent results. A recent large prospective study confirms that higher calcium intake is associated with a modestly reduced risk of distal colorectal cancer. There was little additional risk reduction associated with consumers of more than 700 mg calcium/day. This study also suggests that certain subgroups, such as males, smokers, and people who consume low levels of vitamin D, may be at differential risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12467133",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "Although laboratory data and a few adenoma prevention trials suggest that calcium supplementation may reduce the risk of colorectal neoplasia, the results of observational studies of calcium intake and colorectal cancer risk are contradictory."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16481636",
"endSection": "abstract",
"offsetInBeginSection": 1359,
"offsetInEndSection": 1594,
"text": "There were no significant treatment interactions with baseline characteristics.CONCLUSIONS: Daily supplementation of calcium with vitamin D for seven years had no effect on the incidence of colorectal cancer among postmenopausal women."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12467133",
"endSection": "abstract",
"offsetInBeginSection": 822,
"offsetInEndSection": 1061,
"text": "Women with the highest calcium intake (median 914 mg/day) had a reduced risk of colorectal cancer (rate ratio = 0.72, 95% confidence interval = 0.056-0.93, P for trend = 0.02) compared with women with the lowest intake (median 486 mg/day)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33951958",
"endSection": "abstract",
"offsetInBeginSection": 1018,
"offsetInEndSection": 1262,
"text": "Our results suggest that natural sources of calcium such as dairy products and foods may have more effective role than supplementary calcium in terms of reducing the risk of incidence and recurrence of colorectal adenomas and advanced adenomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15531687",
"endSection": "abstract",
"offsetInBeginSection": 1162,
"offsetInEndSection": 1441,
"text": "CI: 0.76, 1.02; P for trend = 0.04). The protective association between total calcium and colorectal adenoma was largely due to calcium supplement use, with a 27% decrease in adenoma risk for participants taking >1200 mg/d than for nonusers of supplements (odds ratio: 0.73; 95% "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14974021",
"endSection": "abstract",
"offsetInBeginSection": 2439,
"offsetInEndSection": 2729,
"text": "oma, a reduction was found (OR 0.74, CI 0.58,0.95) when the results from both trials were combined.REVIEWER'S CONCLUSIONS: Although the evidence from two RCTs suggests that calcium supplementation might contribute to a moderate degree to the prevention of colorectal adenomatous polyps, thi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16034903",
"endSection": "abstract",
"offsetInBeginSection": 2439,
"offsetInEndSection": 2729,
"text": "oma, a reduction was found (OR 0.74, CI 0.58,0.95) when the results from both trials were combined.AUTHORS' CONCLUSIONS: Although the evidence from two RCTs suggests that calcium supplementation might contribute to a moderate degree to the prevention of colorectal adenomatous polyps, this "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18254022",
"endSection": "abstract",
"offsetInBeginSection": 2439,
"offsetInEndSection": 2729,
"text": "oma, a reduction was found (OR 0.74, CI 0.58,0.95) when the results from both trials were combined.AUTHORS' CONCLUSIONS: Although the evidence from two RCTs suggests that calcium supplementation might contribute to a moderate degree to the prevention of colorectal adenomatous polyps, this "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33369946",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "OBJECTIVES: Previous studies showed that high calcium intake may be associated with the reduced colorectal cancer (CRC) risk, but results were i"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10668490",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 822,
"text": "There was a lower risk of recurrent adenomas in subjects assigned calcium."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9839734",
"endSection": "abstract",
"offsetInBeginSection": 523,
"offsetInEndSection": 872,
"text": "e odds ratios (OR).RESULTS: Higher levels of calcium intake were associated with reduced colon and rectal cancer risk. The following adjusted OR and 95% confidence intervals (CI) were observed, comparing the fifth quintile (based on control intake) with the first: colon cancer: OR = 0.6, 95% CI: 0.4-1.0, P-trend: 0.03; rectal cancer: OR = 0.6, 95%"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1544142",
"endSection": "abstract",
"offsetInBeginSection": 1474,
"offsetInEndSection": 1742,
"text": "In epidemiological studies, several investigators reported inverse correlations between levels of dietary calcium intake and the incidence of colon cancer. Extrapolation of the data have suggested a protective effect of total calcium intakes above 1500 to 1800 mg/day."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8653938",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 382,
"text": "Dietary supplements of calcium, vitamins A, C, and E, carotenoids, and omega-3 fatty acids can reduce the yield of experimental cancers in animals and reverse the pattern of abnormal epithelial proliferation in animals and humans. Epidemiological studies indicate that diets containing high amounts of these agents convey a protective effect against the development of colon cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19116875",
"endSection": "abstract",
"offsetInBeginSection": 806,
"offsetInEndSection": 930,
"text": "High calcium intake had a greater protective effect against tumors of the distal colon and rectal cancer vs. proximal colon."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19116875",
"endSection": "abstract",
"offsetInBeginSection": 931,
"offsetInEndSection": 1023,
"text": "The risk reduction associated with calcium was similar for dietary and supplemental sources."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19116875",
"endSection": "abstract",
"offsetInBeginSection": 1097,
"offsetInEndSection": 1221,
"text": "Higher consumption of milk/dairy products reduces the risk of colon cancer, and high calcium intake reduces the risk of CRC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12917206",
"endSection": "abstract",
"offsetInBeginSection": 1150,
"offsetInEndSection": 1488,
"text": "In whites, high beta-carotene, vitamin C, and calcium intakes were associated with 40-60% reductions in colon cancer risk when contrasting highest to lowest quartiles in both energy-adjusted and non-energy-adjusted models, e.g., OR = 0.4 (95% confidence interval, 0.3-0.6) for the highest quartile of calcium in the energy-adjusted model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16034903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 273,
"text": "BACKGROUND: Several dietary factors have been considered to be involved in the increasing incidence of colorectal cancer in industrialised countries. Experimental and epidemiological evidence has been suggestive but not conclusive for a protective role for high dietary cal"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8045031",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 289,
"text": "Dietary factors are major determinants of colorectal cancer risk. Especially a diet high in fat and low in fiber is recognized to be a risk factor. Dietary calcium has been suggested to be protective against colorectal cancer through the binding of intraluminal fatty acids and bile acids."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15570055",
"endSection": "abstract",
"offsetInBeginSection": 1518,
"offsetInEndSection": 1668,
"text": "Because of the apparent synergistic effect of vitamin D and calcium, cosupplementation of both nutrients in cancer prevention programs may be advised."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12467133",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1387,
"text": "Although laboratory data and a few adenoma prevention trials suggest that calcium supplementation may reduce the risk of colorectal neoplasia, the results of observational studies of calcium intake and colorectal cancer risk are contradictory. However, few studies have examined the association among women or effects in specific colon subsites. Women with colorectal cancer diagnosed through 31 December 2000 were identified by linkage to regional cancer registries. During an average 11.3 yr of follow-up of 61,463 women, we observed 572 incident cases of colorectal cancer. Using data obtained from a 67-item food frequency questionnaire and Cox proportional hazards models to estimate rate ratios and 95% confidence intervals, we found an inverse association between dietary calcium intake and colorectal cancer risk. Women with the highest calcium intake (median 914 mg/day) had a reduced risk of colorectal cancer (rate ratio = 0.72, 95% confidence interval = 0.056-0.93, P for trend = 0.02) compared with women with the lowest intake (median 486 mg/day). Furthermore, our results suggest that the inverse association may be strongest in relation to distal cancers and among older women. The association with dairy products was less clear, suggesting that calcium intake per se is more important than specific calcium sources. Vitamin D intake was not clearly associated with risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15531687",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1161,
"text": "BACKGROUND: Calcium can reduce the risk of colorectal tumors by binding secondary bile and fatty acids, which leads to antiproliferative effects in the bowel, or by acting directly on the colonic epithelium, which affects differentiation and apoptosis.OBJECTIVE: We investigated calcium intake and risk of colon adenoma to evaluate the association of calcium intake with early stages of colorectal tumor development.DESIGN: We compared the supplemental and dietary calcium intakes of 3696 participants with histologically verified adenoma of the distal colon (ie, descending colon, sigmoid colon, or rectum) with the calcium intakes of 34 817 sigmoidoscopy-negative control participants in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Calcium intake was assessed at study entry with a 137-item food-frequency questionnaire and additional questions on the amount and duration of calcium supplement use.RESULTS: After adjustment for known risk factors, adenoma risk was lower by 12% for participants in the highest quintile of total calcium intake (>1767 mg/d) than for participants in the lowest quintile (<731 mg/d) (odds ratio: 0.88; 95%"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15668485",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1382,
"text": "We investigated the association between calcium intake and colorectal cancer in a prospective cohort of 45,354 women without a history of colorectal cancer who successfully completed a 62-item National Cancer Institute/Block food-frequency questionnaire. Women were followed for an average of 8.5 years, during which time 482 subjects developed colorectal cancer. We used Cox proportional hazards models, with age as the underlying time metric, to estimate risk of colorectal cancer. Cut points between quintiles of energy-adjusted dietary calcium were 412, 529, 656, and 831 mg/day. We created categories for calcium from supplements as follows: 0 mg/day (n = 25,441), 0 to 400 mg/day (n = 9,452), 401 to 800 mg/day (n = 4,176), and >800 mg/day (n =6,285). Risk ratios and confidence intervals (95% CI) for increasing quintiles of dietary calcium relative to the lowest quintile were 0.79 (0.60-1.04), 0.77 (0.59-1.02), 0.78 (0.60-1.03), and 0.74 (0.56-0.98), P(trend) = 0.05. For increasing categories of calcium from supplements, the risk ratios (and 95% CI) relative to no supplement use were 1.08 (0.87-1.34), 0.96 (0.70-1.32), and 0.76 (0.56-1.02), P(trend) = 0.09. Simultaneously high consumption of calcium from diet and calcium from supplements resulted in even further risk reduction, RR = 0.54 (95% CI, 0.37-0.79) compared with low consumption of both sources of calcium."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18254022",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 2438,
"text": "g evidence.OBJECTIVES: This systematic review aims to assess the effect of supplementary dietary calcium on the incidence of colorectal cancer and the incidence or recurrence of adenomatous polyps.SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register, the Cochrane Colorectal Cancer Group specialised register, MEDLINE, Cancerlit , and Embase, to July 2007. The reference lists of identified studies were inspected for further studies, and the review literature was scrutinized.SELECTION CRITERIA: Randomised controlled trials of the effects of dietary calcium on the development of colonic cancer and adenomatous polyps in humans are reviewed. Studies of healthy adults and studies of adults at higher risk of colon cancer due to family history, previous adenomatous polyps, or inflammatory bowel disease were considered; data from subjects with familial polyposis coli are excluded. The primary outcomes were the occurrence of colon cancer, and occurrence or recurrence of any new adenomas of the colon. Secondary outcomes were any adverse event that required discontinuation of calcium supplementation, and drop-outs before the end of the study.DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted data, assessed trial quality and resolved discrepancies by consensus. The outcomes were reported as odds ratios (OR) with 95% confidence intervals (CI). The data were combined with the fixed effects model.MAIN RESULTS: Two studies with 1346 subjects met the inclusion criteria. Both trials were well designed, double - blind, placebo controlled trials, included participants with previous adenomas. The doses of supplementary elemental calcium used were 1200 mg daily for a mean duration of 4 years, and 2000 mg/day for three years. The rates of loss to follow -up were 14 % and 11%. For the development of recurrent colorectal ade"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14974021",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 2438,
"text": "g evidence.OBJECTIVES: This systematic review aims to assess the effect of supplementary dietary calcium on the incidence of colorectal cancer and the incidence or recurrence of adenomatous polyps.SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register, the Cochrane Colorectal Cancer Group specialised register, MEDLINE, Cancerlit, and Embase, to April 2002. The reference lists of identified studies were inspected for further studies, and the review literature was scrutinized.SELECTION CRITERIA: Randomised controlled trials of the effects of dietary calcium on the development of colonic cancer and adenomatous polyps in humans are reviewed. Studies of healthy adults and studies of adults at higher risk of colon cancer due to family history, previous adenomatous polyps, or inflammatory bowel disease were considered; data from subjects with familial polyposis coli are excluded. The primary outcomes were the occurrence of colon cancer, and occurrence or recurrence of any new adenomas of the colon. Secondary outcomes were any adverse event that required discontinuation of calcium supplementation, and drop-outs before the end of the study.DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted data, assessed trial quality and resolved discrepancies by consensus. The outcomes were reported as odds ratios (OR) with 95% confidence intervals (CI). The data were combined with the fixed effects model.MAIN RESULTS: Two studies with 1346 subjects met the inclusion criteria. Both trials were well designed, double - blind, placebo controlled trials, included participants with previous adenomas. The doses of supplementary elemental calcium used were 1200 mg daily for a mean duration of 4 years, and 2000 mg/day for three years. The rates of loss to follow -up were 14 % and 11%. For the development of recurrent colorectal ade"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16034903",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 2438,
"text": "g evidence.OBJECTIVES: This systematic review aims to assess the effect of supplementary dietary calcium on the incidence of colorectal cancer and the incidence or recurrence of adenomatous polyps.SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register, the Cochrane Colorectal Cancer Group specialised register, MEDLINE, Cancerlit, and Embase, to April 2002. The reference lists of identified studies were inspected for further studies, and the review literature was scrutinized.SELECTION CRITERIA: Randomised controlled trials of the effects of dietary calcium on the development of colonic cancer and adenomatous polyps in humans are reviewed. Studies of healthy adults and studies of adults at higher risk of colon cancer due to family history, previous adenomatous polyps, or inflammatory bowel disease were considered; data from subjects with familial polyposis coli are excluded. The primary outcomes were the occurrence of colon cancer, and occurrence or recurrence of any new adenomas of the colon. Secondary outcomes were any adverse event that required discontinuation of calcium supplementation, and drop-outs before the end of the study.DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted data, assessed trial quality and resolved discrepancies by consensus. The outcomes were reported as odds ratios (OR) with 95% confidence intervals (CI). The data were combined with the fixed effects model.MAIN RESULTS: Two studies with 1346 subjects met the inclusion criteria. Both trials were well designed, double - blind, placebo controlled trials, included participants with previous adenomas. The doses of supplementary elemental calcium used were 1200 mg daily for a mean duration of 4 years, and 2000 mg/day for three years. The rates of loss to follow -up were 14 % and 11%. For the development of recurrent colorectal ade"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7752258",
"endSection": "abstract",
"offsetInBeginSection": 375,
"offsetInEndSection": 2681,
"text": "ion occurs. Oral calcium supplementation has been proposed as a dietary intervention for individuals at high risk of colorectal cancer because of its ability to reduce rectal epithelial cell proliferation through the binding of fatty and bile acids. Placebo-controlled studies, however, have yielded varying results.PURPOSE: We conducted a randomized, double-blinded, placebo-controlled trial to test oral calcium supplementation in patients at high risk of developing hereditary nonpolyposis colorectal cancer.METHODS: Thirty subjects at risk for this cancer, with an increased epithelial cell proliferation along the colon and rectum, were randomly assigned to either a placebo group (n = 15) or a treatment group (n = 15). They received either oral calcium carbonate (CaCO3) supplements (1.5 g) or placebo (cellulose and starch) three times a day during a 12-week period. Colonic biopsy specimens (rectal, sigmoidal, and descending) were obtained prior to and after the intervention trial, during endoscopy, for determination of labeling index (LI) of whole crypts and crypt compartments by 5-bromo-2'-deoxyuridine incorporation and immunohistochemistry. Proportional bile acid compositions in duodenal bile and cytolytic activity of fecal water were also determined. All P values represent two-tailed tests of statistical significance.RESULTS: Statistically significant reductions, comparing before with after intervention, in rectal whole-crypt LI after receiving either calcium supplements (from 10.9% +/- 5.2% [mean +/- SD] to 6.2% +/- 1.5%; P < .02) or placebo (from 11.7% +/- 4.7% to 8.2% +/- 3.1%; P < .05) were observed. In the three bowel segments, no statistically significant differences were observed between the supplemental calcium and placebo groups. A statistically significant reduction in cytolytic activity was determined during calcium supplementation (from 57% +/- 41% to 32% +/- 30%; P < .05), whereas in the placebo group, it did not change (from 42% +/- 41% to 36% +/- 27%; P > .10).CONCLUSIONS: Oral calcium supplementation was shown to cause only a minor nonstatistically significant reduction of epithelial cell proliferation in the rectum, compared with placebo, and to have no effect on the same parameter in the sigmoid and descending colon in first-degree relatives of her"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8045031",
"endSection": "abstract",
"offsetInBeginSection": 66,
"offsetInEndSection": 672,
"text": "Especially a diet high in fat and low in fiber is recognized to be a risk factor. Dietary calcium has been suggested to be protective against colorectal cancer through the binding of intraluminal fatty acids and bile acids. Because of their cell-damaging properties these substances may stimulate colorectal epithelial cell proliferation and so promote colorectal cancer development. In this article data from in vitro, animal and human studies on the intraluminal effects of calcium, on its effects on colorectal epithelium and on the association between calcium intake and colorectal cancer are reviewed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15240785",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1167,
"text": "BACKGROUND: Studies in animals have suggested that calcium may reduce the risk of colorectal cancer. However, results from epidemiologic studies of intake of calcium or dairy foods and colorectal cancer risk have been inconclusive.METHODS: We pooled the primary data from 10 cohort studies in five countries that assessed usual dietary intake by using a validated food frequency questionnaire at baseline. For most studies, follow-up was extended beyond that in the original publication. The studies included 534 536 individuals, among whom 4992 incident cases of colorectal cancer were diagnosed between 6 and 16 years of follow-up. Pooled multivariable relative risks for categories of milk intake and quintiles of calcium intake and 95% confidence intervals (CIs) were calculated. All statistical tests were two-sided.RESULTS: Milk intake was related to a reduced risk of colorectal cancer. Compared with the lowest category of intake (<70 g/day), relative risks of colorectal cancer for increasing categories (70-174, 175-249, and > or =250 g/day) of milk intake were 0.94 (95% CI = 0.86 to 1.02), 0.88 (95% CI = 0.81 to 0.96), and 0.85 (95% CI = 0.78 to 0.94), r"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32854492",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "PURPOSE: Dietary calcium intake has been suggested to be protective against the development of colorecta"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31784301",
"endSection": "abstract",
"offsetInBeginSection": 2007,
"offsetInEndSection": 2191,
"text": "olorectal tumour incidence.CONCLUSIONS: Vitamin D and calcium play additively chemopreventive roles in colorectal adenoma incidence, malignant transformation and progression, especiall"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31826765",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "The effects of dietary vitamin D, Ca and dairy products intakes on colorectal cancer risk remain controversial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36315018",
"endSection": "abstract",
"offsetInBeginSection": 813,
"offsetInEndSection": 883,
"text": " person-years of follow-up. Higher total calcium intake was associated"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34708323",
"endSection": "abstract",
"offsetInBeginSection": 1006,
"offsetInEndSection": 1096,
"text": "100 IU/day of vitamin D.CONCLUSION: Higher dietary intakes of calcium and vitamin D are as"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36432621",
"endSection": "abstract",
"offsetInBeginSection": 1205,
"offsetInEndSection": 1500,
"text": "In conclusion, vitamin D supplementation seems to have a protective effect in the prevention and treatment of CRC, while calcium intake showed contradictory effects as a prevention or treatment tool; therefore, further studies are necessary to well understand its relevance in patients with CRC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28677025",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "BACKGROUND: Concerning the chemopreventive potential of calcium against colorectal neoplasms, strong evidence from initial randomized controlled trials (RCTs) of colorectal adenoma has not been confirmed from the most recen"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14974021",
"endSection": "abstract",
"offsetInBeginSection": 149,
"offsetInEndSection": 772,
"text": " Experimental and epidemiological evidence has been suggestive but not conclusive for a protective role for high dietary calcium intake. Intervention studies with colorectal cancer as an endpoint are difficult to perform owing to the large number of patients and the long follow-up required; studies using the appearance of colorectal adenomatous polyps as a surrogate endpoint are therefore considered in reviewing the existing evidence.OBJECTIVES: This systematic review aims to assess the effect of supplementary dietary calcium on the incidence of colorectal cancer and the incidence or recurrence of adenomatous polyps"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16034903",
"endSection": "abstract",
"offsetInBeginSection": 149,
"offsetInEndSection": 772,
"text": " Experimental and epidemiological evidence has been suggestive but not conclusive for a protective role for high dietary calcium intake. Intervention studies with colorectal cancer as an endpoint are difficult to perform owing to the large number of patients and the long follow-up required; studies using the appearance of colorectal adenomatous polyps as a surrogate endpoint are therefore considered in reviewing the existing evidence.OBJECTIVES: This systematic review aims to assess the effect of supplementary dietary calcium on the incidence of colorectal cancer and the incidence or recurrence of adenomatous polyps"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26675033",
"endSection": "abstract",
"offsetInBeginSection": 1367,
"offsetInEndSection": 1558,
"text": "ctum in both men and women.CONCLUSION: In conclusion, calcium consumption was inversely related to colorectal cancer risk in Korean population where national average calcium intake level is r"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14974021",
"endSection": "abstract",
"offsetInBeginSection": 2291,
"offsetInEndSection": 2438,
"text": "ion of 4 years, and 2000 mg/day for three years. The rates of loss to follow -up were 14 % and 11%. For the development of recurrent colorectal ade"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24623471",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Mechanistic and epidemiologic studies provide considerable evidence for a protective association between calcium intake and incident colorectal cancer (CRC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24623471",
"endSection": "abstract",
"offsetInBeginSection": 1460,
"offsetInEndSection": 1575,
"text": "In conclusion, both dietary and supplementary calcium intake may continue to decrease CRC risk beyond 1,000 mg/day."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27466215",
"endSection": "abstract",
"offsetInBeginSection": 571,
"offsetInEndSection": 743,
"text": "Total calcium intake (≥1,400 vs. <600 mg/d) was associated with a statistically significant lower risk of colon cancer (multivariable relative risk: 0.78, 95%CI: 0.65-0.95)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27466215",
"endSection": "abstract",
"offsetInBeginSection": 1388,
"offsetInEndSection": 1506,
"text": ". Higher calcium intake was associated with a lower risk of developing colon cancer, especially for distal colon cance"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8515888",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 532,
"text": "It is also unclear whether the decrease in the index correlates with a decrease in occurrence or recurrence of colonic tumors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8515888",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Several recent studies have examined the hypothesis that calcium supplementation (1.2-2.0 g/day) protects against colon cancer in persons at high risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8515888",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 405,
"text": "Although in most studies the labeling index tended to decrease during supplementation, the results were inconsistent."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8515888",
"endSection": "abstract",
"offsetInBeginSection": 533,
"offsetInEndSection": 647,
"text": "Use of calcium prophylaxis for persons at risk for colon cancer should be reserved for controlled clinical trials."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8515888",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 69,
"text": "Does dietary calcium supplementation reduce the risk of colon cancer?"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31784301",
"endSection": "abstract",
"offsetInBeginSection": 1016,
"offsetInEndSection": 1198,
"text": ": 0.86, 95% CI: 0.81-0.91). The CRC incidence was decreased by circulating 25(OH)D (RR: 0.67, 95% CI: 0.59-0.77), vitamin D intake (RR: 0.85, 95% CI: 0.78-0.93) and calcium intake (R"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31784301",
"endSection": "abstract",
"offsetInBeginSection": 1881,
"offsetInEndSection": 2006,
"text": " against colorectal tumour. A significant dose-response relationship was observed between intake of vitamin D or calcium and "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18843026",
"endSection": "abstract",
"offsetInBeginSection": 564,
"offsetInEndSection": 859,
"text": "In a multivariate analysis adjusting for potential confounding variables, calcium intake was significantly, inversely associated with colorectal cancer risk (P for trend=0.01); the odds ratio for the highest versus lowest quintile of calcium intake was 0.64 (95% confidence interval, 0.45-0.93)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18843026",
"endSection": "abstract",
"offsetInBeginSection": 1394,
"offsetInEndSection": 1514,
"text": "These results add to support for a joint action of calcium and vitamin D in the prevention of colorectal carcinogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10511318",
"endSection": "abstract",
"offsetInBeginSection": 1637,
"offsetInEndSection": 1816,
"text": "These combined data suggest that administration of supplemental calcium or low-fat dairy foods may have a significant effect upon colonic polyp and perhaps colon cancer incidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12708719",
"endSection": "abstract",
"offsetInBeginSection": 1323,
"offsetInEndSection": 1414,
"text": "t related to overall risk.CONCLUSIONS: Our results support the hypothesis that calcium mode"
}
] | 13 |
BioASQ-training13b
| null | null |
662fc0bc187cba990d000011
| 382 |
yesno
|
Can the neonatal Pediatric Sepsis Biomarker Risk Model (nPERSEVERE) accurately predict mortality in neonatal sepsis?
|
['yes']
|
[
"yes"
] |
['Yes, nPERSEVERE can accurately predict mortality in neonatal sepsis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36513805"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36513805",
"endSection": "abstract",
"offsetInBeginSection": 1043,
"offsetInEndSection": 1147,
"text": "IL-8 and nPERSEVERE demonstrated good prognostic performance in a small cohort of neonates with sepsis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36513805",
"endSection": "abstract",
"offsetInBeginSection": 614,
"offsetInEndSection": 826,
"text": "Amongst PERSEVERE II biomarkers, IL-8 showed good prognostic performance for mortality prediction with a cutoff of 300 pg/mL (sensitivity 100%, specificity 65%, negative predictive value 100%, AUC 0.87, p 0.0003)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36513805",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 1029,
"text": "We derived a new decision tree that is neonate specific (nPERSEVERE) with improved performance compared to IL-8 (sensitivity 100%, specificity 86%, negative predictive value 100%, AUC 0.95, p < 0.0001)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36513805",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1366,
"text": "BACKGROUND: Prognostic biomarker research neonatal sepsis is lacking. We assessed the utility of a validated pediatric prognostic tool called PERSEVERE II that uses decision tree methodology to predict mortality at discharge in neonates who experienced sepsis.METHODS: Prospective study in a dual-center cohort of neonates with sepsis admitted between June 2020 and December 2021. Biomarker analysis was done on serum samples obtained at the time of evaluation for the event.RESULTS: In a cohort of 59 neonates with a mortality rate of 15.3%, PERSEVERE II was 67% sensitive and 59% specific for mortality, p 0.27. Amongst PERSEVERE II biomarkers, IL-8 showed good prognostic performance for mortality prediction with a cutoff of 300 pg/mL (sensitivity 100%, specificity 65%, negative predictive value 100%, AUC 0.87, p 0.0003). We derived a new decision tree that is neonate specific (nPERSEVERE) with improved performance compared to IL-8 (sensitivity 100%, specificity 86%, negative predictive value 100%, AUC 0.95, p < 0.0001).CONCLUSIONS: IL-8 and nPERSEVERE demonstrated good prognostic performance in a small cohort of neonates with sepsis. Moving toward precision medicine in sepsis, our study proposes an important tool for clinical trial prognostic enrichment that needs to be validated in larger studies.IMPACT: Prognostic and predictive biomarker research"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36513805",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 1146,
"text": "We derived a new decision tree that is neonate specific (nPERSEVERE) with improved performance compared to IL-8 (sensitivity 100%, specificity 86%, negative predictive value 100%, AUC 0.95, p < 0.0001).CONCLUSIONS: IL-8 and nPERSEVERE demonstrated good prognostic performance in a small cohort of neonates with sepsis."
}
] | 13 |
BioASQ-training13b
| null | null |
661d19d5eac11fad33000007
| 383 |
yesno
|
Are there randomised controlled trials on sevoflurane?
|
['yes']
|
[
"yes"
] |
['Yes. There are < 10 studies reported, answering questions like : how to improve speed of recovery, relationship to dreaming and anesthetic experience, effect on cardiac troponin release, effect on myocardial injury, postoperative delirium, haemodynamics & emergence and recovery characteristics of total intravenous anaesthesia, costs of postoperative nausea and vomiting, pediatric conscious sedation for dental procedures']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23452265",
"http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"http://www.ncbi.nlm.nih.gov/pubmed/22103571",
"http://www.ncbi.nlm.nih.gov/pubmed/21733178",
"http://www.ncbi.nlm.nih.gov/pubmed/21675061",
"http://www.ncbi.nlm.nih.gov/pubmed/20683334",
"http://www.ncbi.nlm.nih.gov/pubmed/16867087",
"http://www.ncbi.nlm.nih.gov/pubmed/15310345",
"http://www.ncbi.nlm.nih.gov/pubmed/12693995",
"http://www.ncbi.nlm.nih.gov/pubmed/11966554"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23452265",
"endSection": "sections.0",
"offsetInBeginSection": 459,
"offsetInEndSection": 641,
"text": "After Ethics Review Board approval, 44 ASA I-III patients undergoing elective gynaecological surgery were randomised after surgery to either hypercapnic hyperpnoea or control groups."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23452265",
"endSection": "sections.0",
"offsetInBeginSection": 1471,
"offsetInEndSection": 1617,
"text": "Hypercapnic hyperpnoea in spontaneously breathing patients halves the time of recovery from sevoflurane-induced anaesthesia in the operating room."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"endSection": "sections.0",
"offsetInBeginSection": 329,
"offsetInEndSection": 569,
"text": "A total of 200 women undergoing first trimester abortion (American Society of Anesthesiologists physical status I) participated in the study. Patients were randomly assigned to receive either sevoflurane or propofol for short-term sedation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"endSection": "sections.0",
"offsetInBeginSection": 650,
"offsetInEndSection": 841,
"text": "The results showed the incidence of dreaming was significantly different between anaesthesia groups with 60% (60/100) of the sevoflurane group and 33% (33/100) of the propofol group (P=0.000)"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"endSection": "sections.0",
"offsetInBeginSection": 1269,
"offsetInEndSection": 1569,
"text": "Anaesthesia administered had no effect on patient satisfaction. The results suggest that the incidence of dreaming was not affected by recovery time. Patient satisfaction was not influenced by choice of sedative and/or by the occurrence of dreaming during sevoflurane or propofol short-term sedation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22577917",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Prior reports suggest that dreaming during anaesthesia is dependent on recovery time. Dreaming during sedation may impact patient satisfaction"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22103571",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Sevoflurane vs. propofol in patients with coronary disease undergoing mitral surgery: a randomised study."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22103571",
"endSection": "sections.0",
"offsetInBeginSection": 197,
"offsetInEndSection": 373,
"text": "We therefore performed a randomised controlled trial (sevoflurane vs. propofol) to compare cardiac troponin release in patients with coronary disease undergoing mitral surgery."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21675061",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Myocardial injury in remifentanil-based anaesthesia for off-pump coronary artery bypass surgery: an equipotent dose of sevoflurane versus propofol"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21675061",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 340,
"text": "This randomised controlled trial compared the effect of equipotent anaesthetic doses of sevoflurane (S group) versus propofol (P group), during remifentanil-based anaesthesia for off-pump coronary artery bypass surgery, on myocardial injury. Either sevoflurane or propofol was titrated to maintain bispectral index values between 40 and 50."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20683334",
"endSection": "sections.0",
"offsetInBeginSection": 365,
"offsetInEndSection": 545,
"text": "This randomised, multicentre, parallel-group trial included 98 adult patients. Patients received intravenous propofol for induction followed by sevoflurane maintenance anaesthesia."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20683334",
"endSection": "sections.0",
"offsetInBeginSection": 654,
"offsetInEndSection": 747,
"text": "Patients were randomly allocated to receive sugammadex 2.0 mg kg(-1) or neostigmine 50 microg"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16867087",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "We compared the haemodynamics, emergence and recovery characteristics of total intravenous anaesthesia using propofol/remifentanil with sevoflurane/remifentanil anaesthesia, under bispectral index guidance, in 103 patients undergoing surgical procedures lasting > 3.5 h"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15310345",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "A randomised controlled trial of paediatric conscious sedation for dental treatment using intravenous midazolam combined with inhaled nitrous oxide or nitrous oxide/sevoflurane"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15310345",
"endSection": "sections.0",
"offsetInBeginSection": 1403,
"offsetInEndSection": 1643,
"text": "Intravenous midazolam, especially in combination with inhaled nitrous oxide or sevoflurane and nitrous oxide, are effective techniques, with the combination of midazolam and sevoflurane the one most likely to result in successful treatment."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12693995",
"endSection": "sections.0",
"offsetInBeginSection": 114,
"offsetInEndSection": 244,
"text": "We randomly assigned 1063 adult and 322 paediatric elective patients to one of four (adult) or two (paediatric) anaesthesia groups"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12693995",
"endSection": "sections.0",
"offsetInBeginSection": 842,
"offsetInEndSection": 1174,
"text": "In both studies, there was no difference in postdischarge outcomes at Day 7. Sevoflurane/sevoflurane was more costly with higher PONV rates in both studies. In adults, the cost per extra episode of PONV avoided was pound 296 (propofol/propofol vs. propofol/ sevoflurane) and pound 333 (propofol/sevoflurane vs. propofol/isoflurane)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11966554",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "Comparison of sevoflurane and nitrous oxide mixture with nitrous oxide alone for inhalation conscious sedation in children having dental treatment: a randomised controlled trial."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11966554",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "We studied 411 children aged 3-10 years who were referred for dental treatment. They were randomly allocated to have inhalation conscious sedation with either sevoflurane/nitrous oxide mixture or nitrous oxide alone"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4252326"
] | null |
515d9e5c298dcd4e5100000e
| 384 |
yesno
|
Can bioprinting use human cells?
|
['yes']
|
[
"yes"
] |
['Yes, human cells can be used for bioprinting']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21358040",
"http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"http://www.ncbi.nlm.nih.gov/pubmed/24188635",
"http://www.ncbi.nlm.nih.gov/pubmed/20811115",
"http://www.ncbi.nlm.nih.gov/pubmed/24334142",
"http://www.ncbi.nlm.nih.gov/pubmed/22394017",
"http://www.ncbi.nlm.nih.gov/pubmed/22508498",
"http://www.ncbi.nlm.nih.gov/pubmed/25384685",
"http://www.ncbi.nlm.nih.gov/pubmed/24998183",
"http://www.ncbi.nlm.nih.gov/pubmed/24157694",
"http://www.ncbi.nlm.nih.gov/pubmed/21504055",
"http://www.ncbi.nlm.nih.gov/pubmed/24695367",
"http://www.ncbi.nlm.nih.gov/pubmed/24887553",
"http://www.ncbi.nlm.nih.gov/pubmed/25093879",
"http://www.ncbi.nlm.nih.gov/pubmed/20546891",
"http://www.ncbi.nlm.nih.gov/pubmed/24961492",
"http://www.ncbi.nlm.nih.gov/pubmed/25047630",
"http://www.ncbi.nlm.nih.gov/pubmed/23184715",
"http://www.ncbi.nlm.nih.gov/pubmed/23380571",
"http://www.ncbi.nlm.nih.gov/pubmed/25242654",
"http://www.ncbi.nlm.nih.gov/pubmed/21527813",
"http://www.ncbi.nlm.nih.gov/pubmed/24439284",
"http://www.ncbi.nlm.nih.gov/pubmed/23562089",
"http://www.ncbi.nlm.nih.gov/pubmed/22767299",
"http://www.ncbi.nlm.nih.gov/pubmed/25130390",
"http://www.ncbi.nlm.nih.gov/pubmed/25048797",
"http://www.ncbi.nlm.nih.gov/pubmed/23015540",
"http://www.ncbi.nlm.nih.gov/pubmed/24758832",
"http://www.ncbi.nlm.nih.gov/pubmed/24903714",
"http://www.ncbi.nlm.nih.gov/pubmed/23197691",
"http://www.ncbi.nlm.nih.gov/pubmed/23719889",
"http://www.ncbi.nlm.nih.gov/pubmed/22436025",
"http://www.ncbi.nlm.nih.gov/pubmed/20353253",
"http://www.ncbi.nlm.nih.gov/pubmed/25457969",
"http://www.ncbi.nlm.nih.gov/pubmed/23260439",
"http://www.ncbi.nlm.nih.gov/pubmed/23575660"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21358040",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 273,
"text": "In this study, human adipose-derived stem cells (hASCs) were printed in a free-scalable 3D grid pattern by means of LaBP."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21358040",
"endSection": "abstract",
"offsetInBeginSection": 648,
"offsetInEndSection": 777,
"text": " Additionally, we provide the proof that even pre-differentiated hASCs could be utilized for the generation of 3D tissue grafts. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24334142",
"endSection": "abstract",
"offsetInBeginSection": 856,
"offsetInEndSection": 1131,
"text": "In this study, 3-D printable formulations of hybrid hydrogels are developed, based on methacrylated hyaluronic acid (Me-HA) and methacrylated gelatin (Me-Gel), and used to bioprint heart valve conduits containing encapsulated human aortic valvular interstitial cells (HAVIC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24695367",
"endSection": "abstract",
"offsetInBeginSection": 250,
"offsetInEndSection": 370,
"text": "Bioprinting can be used to precisely position cells and cell-laden materials to generate controlled tissue architecture."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20811115",
"endSection": "abstract",
"offsetInBeginSection": 692,
"offsetInEndSection": 996,
"text": "Bioprinting can be defined as the use of computer-aided transfer processes for patterning and assembling living and non-living materials with a prescribed 2D or 3D organization in order to produce bio-engineered structures serving in regenerative medicine, pharmacokinetic and basic cell biology studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25093879",
"endSection": "abstract",
"offsetInBeginSection": 1095,
"offsetInEndSection": 1303,
"text": "3D bioprinting has already been used for the generation and transplantation of several tissues, including multilayered skin, bone, vascular grafts, tracheal splints, heart tissue and cartilaginous structures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20811115",
"endSection": "abstract",
"offsetInBeginSection": 692,
"offsetInEndSection": 996,
"text": "Bioprinting can be defined as the use of computer-aided transfer processes for patterning and assembling living and non-living materials with a prescribed 2D or 3D organization in order to produce bio-engineered structures serving in regenerative medicine, pharmacokinetic and basic cell biology studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25242654",
"endSection": "abstract",
"offsetInBeginSection": 308,
"offsetInEndSection": 539,
"text": "Here we report the development of clinically relevant sized tissue analogs by 3-D bioprinting, delivering human nasal inferior turbinate tissue-derived mesenchymal progenitor cells encapsulated in silk fibroin-gelatin (SF-G) bioink"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25047630",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Sodium alginate hydrogel, stabilized with gelatin, is a suitable, biologically inert matrix that can be used for encapsulating and 3D bioprinting of bone-related SaOS-2 cells. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25047630",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Sodium alginate hydrogel, stabilized with gelatin, is a suitable, biologically inert matrix that can be used for encapsulating and 3D bioprinting of bone-related SaOS-2 cells. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25130390",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Bioactive nanoparticles stimulate bone tissue formation in bioprinted three-dimensional scaffold and human mesenchymal stem cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25047630",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Sodium alginate hydrogel, stabilized with gelatin, is a suitable, biologically inert matrix that can be used for encapsulating and 3D bioprinting of bone-related SaOS-2 cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "OBJECTIVE: To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23562089",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Cellular behavior in micropatterned hydrogels by bioprinting system depended on the cell types and cellular interaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25047630",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Sodium alginate hydrogel, stabilized with gelatin, is a suitable, biologically inert matrix that can be used for encapsulating and 3D bioprinting of bone-related SaOS-2 cells. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25047630",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Engineering a morphogenetically active hydrogel for bioprinting of bioartificial tissue derived from human osteoblast-like SaOS-2 cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25130390",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Bioactive nanoparticles stimulate bone tissue formation in bioprinted three-dimensional scaffold and human mesenchymal stem cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20811115",
"endSection": "abstract",
"offsetInBeginSection": 823,
"offsetInEndSection": 961,
"text": "At the same time, the principal feasibility of bioprinting vascularized human organs as well as in vivo bioprinting has been demonstrated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20811115",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1095,
"text": "The bioprinting of complex 3D human tissues and constructs in vitro and especially in vivo are exciting, but long-term, applications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20811115",
"endSection": "abstract",
"offsetInBeginSection": 390,
"offsetInEndSection": 694,
"text": "Bioprinting can be defined as the use of computer-aided transfer processes for patterning and assembling living and non-living materials with a prescribed 2D or 3D organization in order to produce bio-engineered structures serving in regenerative medicine, pharmacokinetic and basic cell biology studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 1407,
"offsetInEndSection": 1581,
"text": "In this study, the 3D bioprinting of hDPCs mixtures was realized, thus laying initial foundations for the application of the 3D bioprinting technology in tooth regeneration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20811115",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1095,
"text": "The bioprinting of complex 3D human tissues and constructs in vitro and especially in vivo are exciting, but long-term, applications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24334142",
"endSection": "abstract",
"offsetInBeginSection": 496,
"offsetInEndSection": 861,
"text": "Furthermore, it is not known how human valve cells respond to these printed environments. In this study, 3-D printable formulations of hybrid hydrogels are developed, based on methacrylated hyaluronic acid (Me-HA) and methacrylated gelatin (Me-Gel), and used to bioprint heart valve conduits containing encapsulated human aortic valvular interstitial cells (HAVIC)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25047630",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Engineering a morphogenetically active hydrogel for bioprinting of bioartificial tissue derived from human osteoblast-like SaOS-2 cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20811115",
"endSection": "abstract",
"offsetInBeginSection": 963,
"offsetInEndSection": 1096,
"text": "The bioprinting of complex 3D human tissues and constructs in vitro and especially in vivo are exciting, but long-term, applications."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24334142",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Three-dimensional printed trileaflet valve conduits using biological hydrogels and human valve interstitial cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24334142",
"endSection": "abstract",
"offsetInBeginSection": 496,
"offsetInEndSection": 585,
"text": "Furthermore, it is not known how human valve cells respond to these printed environments."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "[Three dimensional bioprinting technology of human dental pulp cells mixtures]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25047630",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Engineering a morphogenetically active hydrogel for bioprinting of bioartificial tissue derived from human osteoblast-like SaOS-2 cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23411530",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "To explore the three dimensional(3D)bioprinting technology, using human dental pulp cells (hDPCs) mixture as bioink and to lay initial foundations for the application of the 3D bioprinting technology in tooth regeneration."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D062028",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002477",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006801"
] |
[] |
571394141174fb175500000b
| 385 |
yesno
|
Has RTA 408 received FDA approval?
|
['yes']
|
[
"yes"
] |
['Yes, RTA 408 is FDA approved.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33971103"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33971103",
"endSection": "abstract",
"offsetInBeginSection": 727,
"offsetInEndSection": 959,
"text": "Forced overexpression of HO-1, pharmacological activation of HO-1 with the agonists RTA-408 (omaveloxolone, an FDA-approved drug) and RTA-402 repressed cell death, and treatment with HO-1 antagonist SnPP exacerbated the cell death. "
}
] | 12 |
BioASQ-training12b
| null | null |
6440092d57b1c7a315000040
| 386 |
yesno
|
Should all babies diagnosed with spina bifida be operated within the first week of life?
|
['no']
|
[
"no"
] |
['No, not all babies diagnosed with spina bifida should be operated on within the first week of life. The recommendation for treatment depends on the type and severity of spina bifida. Myelomeningocele, the most severe form, may benefit from prenatal surgery, which involves operating on the fetus while it is still in the uterus, before the 26th week of gestation. This approach can decrease the need for ventriculoperitoneal shunt placement and improve motor function compared to standard postnatal surgery. , On the other hand, spina bifida occulta, a milder form, usually does not require any surgical intervention, as many people with this condition do not experience symptoms. For some forms of spina bifida, such as meningocele, surgery may be recommended after birth to prevent infection and aid in protecting the spinal cord. , In summary, the decision for spina bifida treatment, including the timing and type of surgery, should be made on a case-by-case basis, taking into account various factors such as gestational age, lesion level, associated defects, and family considerations. Therefore, it is essential to consult with medical professionals specializing in fetal and pediatric care for personalized recommendations and guidance.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36964773",
"http://www.ncbi.nlm.nih.gov/pubmed/37975651",
"http://www.ncbi.nlm.nih.gov/pubmed/37970655",
"http://www.ncbi.nlm.nih.gov/pubmed/27179533",
"http://www.ncbi.nlm.nih.gov/pubmed/35735913",
"http://www.ncbi.nlm.nih.gov/pubmed/30486637",
"http://www.ncbi.nlm.nih.gov/pubmed/2012704"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35735913",
"endSection": "abstract",
"offsetInBeginSection": 324,
"offsetInEndSection": 475,
"text": "treatment for spina bifida has made great advancements, from surgical closure of the defect after birth to the now state-of-the-art intrauterine repair"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30486637",
"endSection": "abstract",
"offsetInBeginSection": 363,
"offsetInEndSection": 479,
"text": "Advances in fetal treatment have made minimally invasive prenatal surgery a realistic consideration for spina bifida"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30486637",
"endSection": "abstract",
"offsetInBeginSection": 571,
"offsetInEndSection": 770,
"text": "Prenatal surgery for spina bifida via open fetal surgery with hysterotomy decreases the rate of ventriculoperitoneal shunt placement and improves motor function compared to standard postnatal surgery"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30486637",
"endSection": "abstract",
"offsetInBeginSection": 1643,
"offsetInEndSection": 1673,
"text": "fetoscopic spina bifida repair"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30486637",
"endSection": "abstract",
"offsetInBeginSection": 2124,
"offsetInEndSection": 2158,
"text": "prenatal treatment of spina bifida"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2012704",
"endSection": "abstract",
"offsetInBeginSection": 323,
"offsetInEndSection": 401,
"text": "Spina bifida should be found in utero for the immediate operation after birth."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36964773",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 334,
"text": "Babies born with spina bifida require early closure surgery, done within the first 2-3 days after birth."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37970655",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 555,
"text": "OBJECTIVES: To determine if the lower extremity motor function of a fetus with open spina bifida deteriorates within a four-week interval between their first prenatal motor assessment at 22 weeks of gestation and second presurgical evaluation in cases operated at later gestational age (26-27 weeks of gestation), and to compare prenatal and postnatal motor function to the anatomical level of the lesion.METHODS: Multicenter cohort study involving cases from two centers that perform percutaneous fetoscopic repair of open spina bifida (SAFER technique)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27179533",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "PURPOSE: Clinical guidelines recommend repair of open spina bifida (SB) prenatally or within the first days of an infant's life."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27179533",
"endSection": "abstract",
"offsetInBeginSection": 1257,
"offsetInEndSection": 1522,
"text": "Infants born in lower level nursery care hospitals with were less likely to have timely repairs (aPR = 0.71, 95 % CI 0.52-0.98) than those born in higher level nursery care hospitals.CONCLUSIONS: Most infants with SB had surgical repair in the first 2 days of life."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37975651",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 219,
"text": "To determine simple prenatal imaging parameters that can easily be acquired to predict the need for postnatal CSF diversion (PCD) surgery in fetuses undergoing open fetal surgery for open spina bifida (OSB)."
}
] | 13 |
BioASQ-training13b
| null | null |
65f859b2c4010b4d78000050
| 387 |
yesno
|
Is fish intake a protective factor against colorectal cancer?
|
['yes']
|
[
"yes"
] |
['Yes, fish intake is indeed a protective factor against colorectal cancer. Studies have shown that individuals who consume more fish have a significantly reduced risk of developing this type of cancer. Specifically, a 50-gram increase in daily fish consumption is associated with a 4% reduction in colorectal cancer risk', 'Yes, fish intake is a protective factor against colorectal cancer. A 50-g increment in daily fish consumption is associated with a 4% reduction in colorectal cancer risk.', 'Yes, fish intake appears to be a protective factor against colorectal cancer (CRC). Individuals in the highest category of fish consumption had a significantly reduced risk of CRC compared to those in the lowest category (SRR 0.94, 95%CI 0.89-0.99). Additionally, a dose-response meta-analysis found that a 50-gram increment in daily fish consumption was associated with a statistically significant 4% reduction in CRC risk (SRR 0.96, 95%CI 0.92-0.99).', 'Yes, fish intake has been shown to be a protective factor against colorectal cancer. In a meta-analysis of 17 cohort studies, individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category. Specifically, a 50-g increment in daily fish consumption was associated with a 4% reduction in colorectal cancer risk. The protective effect of fish intake was observed in both men and women and across all sub-sites of the colon and rectum. The mechanism by which fish intake reduces colorectal cancer risk is not fully understood, but may involve the omega-3 fatty acids and other nutrients found in fish.', 'According to the meta-analysis, yes, fish intake is a protective factor against colorectal cancer (CRC). The study found that individuals who consumed more fish had a significantly reduced risk of CRC. Specifically, those in the highest category of fish consumption had a 6% lower risk of CRC compared to those in the lowest category. Additionally, for every 50g increase in daily fish consumption, there was a 4% reduction in CRC risk. The study suggests that dietary recommendations for cancer prevention should take into account the evidence from epidemiological and preclinical studies that increasing fish consumption may be effective in preventing CRC.', 'Yes, fish intake is a protective factor against colorectal cancer, as indicated by multiple observational studies and meta-analyses showing an inverse association between fish consumption and colorectal cancer risk.', 'Yes, fish intake is a protective factor against colorectal cancer. This is based on a long-term prospective study that found intakes of fish and long-chain n-3 fatty acids from fish may decrease the risk for colorectal cancer. Additionally, a case-control study found that higher freshwater fish and sea fish intake is inversely associated with colorectal cancer risk among Chinese population.', 'Based on the provided snippets, the answer is yes, fish intake appears to be a protective factor against colorectal cancer (CRC). The data suggests that individuals who consume higher amounts of fish have a significantly reduced risk of CRC. Specifically, a daily increment of 50g in fish consumption is associated with a 4% reduction in CRC risk. This finding is supported by the statistically significant dose-response relationship observed in the meta-analysis. These results suggest that moderate fish consumption may be a useful strategy for reducing the risk of colorectal cancer.', 'Yes, fish intake appears to be a protective factor against colorectal cancer (CRC). According to a study, individuals who consumed fish at higher levels had a significantly reduced risk of CRC compared to those who consumed less fish. In a dose-response meta-analysis, a 50-g increase in daily fish consumption was associated with a statistically significant 4% reduction in CRC risk. Therefore, increasing fish intake may help lower the risk of developing colorectal cancer.', 'Yes, fish intake is a protective factor against colorectal cancer. Multiple studies have found that increased fish consumption is inversely associated with colorectal cancer risk. A meta-analysis found that fish consumption decreased the risk of colorectal cancer by 12%. Other studies have also found that high fish intake is associated with a decreased risk of colorectal cancer, which has been linked to the high content of n-3 polyunsaturated fatty acids (PUFAs) in some fish.', 'Fish intake is a protective factor against colorectal cancer (CRC). A meta-analysis found that individuals with higher fish consumption had a 6% lower risk of CRC, and for every 50g increase in daily fish consumption, there was a 4% reduction in CRC risk. The study suggests incorporating this information into dietary recommendations for cancer prevention.', 'The evidence is not conclusive to establish a causal relationship between fish intake and a reduced risk of colorectal cancer. While some studies suggest a protective effect, others show no association or even a positive correlation. The potential benefits of fish consumption should be weighed against the risks associated with contaminants such as mercury and polychlorinated biphenyls (PCBs). More research is needed to better understand the relationship between fish consumption and colorectal cancer risk, and to determine the optimal amount and type of fish intake for cancer prevention.', 'Yes, fish intake appears to be a protective factor against colorectal cancer. A meta-analysis found that individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category (SRR 0.94, 95% CI 0.89-0.99). The dose-response analysis showed that each 50g increment in daily fish consumption was associated with a statistically significant 4% reduction in colorectal cancer risk (SRR 0.96, 95% CI 0.92-0.99).', 'Yes, fish intake is considered to be a protective factor against colorectal cancer. A study found that individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category. Additionally, a dose-response meta-analysis found that a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in colorectal cancer risk.', 'Yes, fish intake appears to be a protective factor against colorectal cancer. Several epidemiological studies and meta-analyses have found an inverse association between fish consumption and colorectal cancer risk. The protective effect may be attributed to the high content of n-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in some fish. These PUFAs are thought to suppress the proliferation of colorectal mucosa and inhibit the development of colorectal cancer. Overall, the evidence suggests that increasing fish intake may have a preventive effect on colorectal cancer risk.', 'Yes, fish intake is a protective factor against colorectal cancer. Higher fish consumption significantly reduces the risk of colorectal cancer, and a 50-g daily increase in fish consumption is associated with a 4% reduction in colorectal cancer risk.', 'Fish intake has been inversely associated with colorectal cancer risk in several studies. A case-control study in Sweden found that canned fish consumption was lower among cases than among controls, and an inverse association was found between canned fish consumption and CRC risk. A cohort study in Sweden found that higher intake of long-chain omega-3 polyunsaturated fatty acids, which are abundant in fish, was associated with a lower risk of colorectal cancer in women. A meta-analysis of 41 studies found that fish consumption was associated with a lower risk of colorectal cancer. However, a cohort study in the United States found no association between fish intake and colorectal cancer risk. Overall, the evidence suggests that fish intake may be a protective factor against colorectal cancer, but more research is needed to confirm this association.', 'Yes, fish intake has been shown to be a protective factor against colorectal cancer. In a meta-analysis of 17 cohort studies, individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category. Additionally, a 50-g increment in daily fish consumption was associated with a 4% reduction in colorectal cancer risk. The protective effect of fish intake was observed in both men and women, and across all sub-sites of the colon and rectum. The mechanism by which fish intake reduces colorectal cancer risk is not fully understood, but may involve the omega-3 fatty acids and other nutrients found in fish.', 'Yes, fish intake is a protective factor against colorectal cancer. Individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer (CRC) compared to those in the lowest category. A 50-g increment in daily fish consumption was associated with a 4% reduction in CRC risk.', 'Yes, fish intake is a protective factor against colorectal cancer. Individuals in the highest category of fish consumption had a significantly reduced risk of CRC, and a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk', "Yes, according to the study, individuals with higher fish consumption had a significantly reduced risk of colorectal cancer (CRC). A 50-g increment in daily fish consumption was associated with a 4% reduction in CRC risk. \n\nPlease go ahead and ask your question. I'll respond accordingly. \n\n(Note: You can ask a question, and I'll provide an answer based on the given context. You can also ask follow-up questions based on my previous response.)", 'Based on the abstracts provided, it appears that fish intake is indeed a protective factor against colorectal cancer. The first study found an inverse association between fish intake and colorectal cancer risk, with a multivariate relative risk of 0.63 for the highest versus lowest category of fish intake. Similarly, the second study found a significant reduction in colorectal cancer risk at moderate fish intake (one or two servings per week), with an odds ratio of 0.70. The third study also suggested a protective effect of fish consumption against colorectal cancer, although the association was not statistically significant. Overall, the evidence suggests that consuming fish may decrease the risk of developing colorectal cancer.', 'Yes, fish intake is inversely associated with colorectal cancer risk, with a 12% decrease in risk found in a meta-analysis. This association is supported by multiple observational and clinical studies, which suggest that fish consumption may have a protective effect against colorectal cancer. The protective effect is thought to be due to the high content of n-3 polyunsaturated fatty acids, such as eicosapentaenoic acid and docosahexaenoic acid, in some fish.', 'Yes, fish intake is a protective factor against colorectal cancer. A number of studies have found an inverse relationship between fish consumption and the risk of developing colorectal cancer. For example, a case-control study in Eastern Europe found that increased fish intake was associated with a lower risk of colorectal cancer, even after adjusting for potential confounders such as demographic characteristics, body mass index, smoking status, and physical activity. Similarly, a prospective cohort study in the United States found that men who consumed fish at least once a week had a lower risk of colorectal cancer than those who rarely or never consumed fish. The protective effect of fish consumption on colorectal cancer risk may be due to the presence of long-chain n-3 fatty acids, which have been shown to have anti-inflammatory and antiproliferative effects in laboratory and animal studies. However, more research is needed to confirm these findings and to understand the underlying mechanisms', 'Fish intake is linked to reduced colorectal cancer (CRC) risk according to multiple studies. Moderate fish consumption and n-3 fatty acids from fish show inverse associations with CRC incidence, suggesting fish consumption provides protection against the disease.', 'Fish intake is linked to reduced colorectal cancer (CRC) risk, according to various studies. Moderate fish consumption and n-3 fatty acid intake from fish are associated with lower CRC incidence. Fish consumption of once a week or more might protect against CRC. Overall, these findings suggest that eating fish may have protective effects against the development of colorectal cancer.', 'Individuals in the highest (vs. lowest) category of fish consumption had a significantly reduced risk of CRC (SRR 0.94, 95%CI 0.89-0.99). In dose-response meta-analysis, a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk (SRR 0.96, 95%CI 0.92-0.99)', 'In summary, based on a meta-analysis, increased fish intake is associated with reduced colorectal cancer risk by 6% for those consuming more fish compared to the lowest category of consumers. For every 50g increase in daily consumption, there was an observed 4% decrease in CRC risk, suggesting that dietary recommendations may benefit from considering higher fish consumption as a potential preventative measure against colorectal cancer.', 'Yes, fish intake has been shown to be a protective factor against colorectal cancer. Studies have consistently found that higher consumption of fish, particularly fatty fish, is associated with a lower risk of colorectal cancer. The mechanisms by which fish consumption protects against colorectal cancer are thought to involve the n-3 polyunsaturated fatty acids found in fish, which have anti-inflammatory and antioxidant effects in the colon. Additionally, adherence to a Mediterranean-style diet, which includes high levels of fish consumption, has been shown to be protective against colorectal and breast cancer.', 'In summary, consuming more fish has been shown to lower the risk of colorectal cancer (CRC), with each 50g increase in daily intake associated with a 4% reduction in CRC risk according to the meta-analysis data and observed dose-response relationship.', 'Yes, fish intake is a protective factor against colorectal cancer. A study found that individuals in the highest category of fish consumption had a significantly reduced risk of colorectal cancer compared to those in the lowest category. Additionally, a dose-response meta-analysis found that a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in colorectal cancer risk.', 'Yes, fish intake is a protective factor against colorectal cancer. Individuals in the highest category of fish consumption had a significantly reduced risk of CRC. Also, a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17419892",
"http://www.ncbi.nlm.nih.gov/pubmed/12671534",
"http://www.ncbi.nlm.nih.gov/pubmed/29399003",
"http://www.ncbi.nlm.nih.gov/pubmed/35458225",
"http://www.ncbi.nlm.nih.gov/pubmed/26264963",
"http://www.ncbi.nlm.nih.gov/pubmed/37572059",
"http://www.ncbi.nlm.nih.gov/pubmed/17425596",
"http://www.ncbi.nlm.nih.gov/pubmed/16201848",
"http://www.ncbi.nlm.nih.gov/pubmed/19553301",
"http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"http://www.ncbi.nlm.nih.gov/pubmed/36092326",
"http://www.ncbi.nlm.nih.gov/pubmed/7549825",
"http://www.ncbi.nlm.nih.gov/pubmed/28804436",
"http://www.ncbi.nlm.nih.gov/pubmed/24706410",
"http://www.ncbi.nlm.nih.gov/pubmed/15456633",
"http://www.ncbi.nlm.nih.gov/pubmed/33998355",
"http://www.ncbi.nlm.nih.gov/pubmed/36014940",
"http://www.ncbi.nlm.nih.gov/pubmed/15956652",
"http://www.ncbi.nlm.nih.gov/pubmed/25619144",
"http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"http://www.ncbi.nlm.nih.gov/pubmed/32537063",
"http://www.ncbi.nlm.nih.gov/pubmed/21888535",
"https://pubmed.ncbi.nlm.nih.gov/7549825/",
"http://www.ncbi.nlm.nih.gov/pubmed/24615521",
"http://www.ncbi.nlm.nih.gov/pubmed/23878344",
"http://www.ncbi.nlm.nih.gov/pubmed/19169007",
"http://www.ncbi.nlm.nih.gov/pubmed/35158907",
"https://pubmed.ncbi.nlm.nih.gov/28407090/",
"http://www.ncbi.nlm.nih.gov/pubmed/32138465",
"http://www.ncbi.nlm.nih.gov/pubmed/17823383",
"http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"http://www.ncbi.nlm.nih.gov/pubmed/19638981",
"http://www.ncbi.nlm.nih.gov/pubmed/31252190"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35158907",
"endSection": "abstract",
"offsetInBeginSection": 874,
"offsetInEndSection": 1195,
"text": " Individuals in the highest (vs. lowest) category of fish consumption had a significantly reduced risk of CRC (SRR 0.94, 95%CI 0.89-0.99). In dose-response meta-analysis, a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk (SRR 0.96, 95%CI 0.92-0.99)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35158907",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1196,
"text": "Background: Epidemiological studies on the association between fish consumption and colorectal cancer (CRC) risk have yielded inconsistent results, despite evidence from preclinical studies that long-chain ω-3 polyunsaturated fatty acids inhibit colorectal carcinogenesis. We conducted a meta-analysis of prospective epidemiological studies investigating the association between fish consumption and CRC risk among humans and reviewed studies examining the link between fish components and colorectal carcinogenesis in animal models. Methods: We included studies published until November 2020. We calculated the summary risk ratio (SRR) and 95% confidence intervals (CI) through random effects meta-analysis models in order to summarize evidence from studies among humans. Results: Twenty-five prospective epidemiological studies encompassing 25,777 CRC cases were included. Individuals in the highest (vs. lowest) category of fish consumption had a significantly reduced risk of CRC (SRR 0.94, 95%CI 0.89-0.99). In dose-response meta-analysis, a 50-g increment in the daily consumption of fish was associated with a statistically significant 4% reduction in CRC risk (SRR 0.96, 95%CI 0.92-0.99)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31252190",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1739,
"text": "BACKGROUND & AIMS: There is an unclear association between intake of fish and long-chain n-3 polyunsaturated fatty acids (n-3 LC-PUFAs) and colorectal cancer (CRC). We examined the association between fish consumption, dietary and circulating levels of n-3 LC-PUFAs, and ratio of n-6:n-3 LC-PUFA with CRC using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.METHODS: Dietary intake of fish (total, fatty/oily, lean/white) and n-3 LC-PUFA were estimated by food frequency questionnaires given to 521,324 participants in the EPIC study; among these, 6291 individuals developed CRC (median follow up, 14.9 years). Levels of phospholipid LC-PUFA were measured by gas chromatography in plasma samples from a sub-group of 461 CRC cases and 461 matched individuals without CRC (controls). Multivariable Cox proportional hazards and conditional logistic regression models were used to calculate hazard ratios (HRs) and odds ratios (ORs), respectively, with 95% CIs.RESULTS: Total intake of fish (HR for quintile 5 vs 1, 0.88; 95% CI, 0.80-0.96; Ptrend = .005), fatty fish (HR for quintile 5 vs 1, 0.90; 95% CI, 0.82-0.98; Ptrend = .009), and lean fish (HR for quintile 5 vs 1, 0.91; 95% CI, 0.83-1.00; Ptrend = .016) were inversely associated with CRC incidence. Intake of total n-3 LC-PUFA (HR for quintile 5 vs 1, 0.86; 95% CI, 0.78-0.95; Ptrend = .010) was also associated with reduced risk of CRC, whereas dietary ratio of n-6:n-3 LC-PUFA was associated with increased risk of CRC (HR for quintile 5 vs 1, 1.31; 95% CI, 1.18-1.45; Ptrend < .001). Plasma levels of phospholipid n-3 LC-PUFA was not associated with overall CRC risk, but an inverse trend was observed for proximal compared with distal co"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35458225",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1122,
"text": "Fish is among the foods exerting favourable effects on colorectal cancer (CRC), but the possible role of canned fish has been insufficiently investigated. We aimed to investigate the relationship between canned fish consumption and CRC risk. We analysed data from two case−control studies conducted between 1992 and 2010 in several Italian areas, comprising a total of 2419 incident cases and 4723 hospital controls. Canned fish consumption was analysed according to the weekly frequency of consumption as <1 serving per week (s/w) (reference category), 1 < 2 s/w, and ≥2 s/w. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression models, adjusting for several recognised confounding factors. Overall, canned fish consumption was lower among cases than among controls (23.8% vs. 28.6%). An inverse association was found between canned fish consumption and CRC risk with a significant trend in risk (OR = 0.81, 95% CI: 0.71−0.92 for intermediate consumption and OR = 0.66, 95% CI: 0.51−0.85 for the highest one), which was consistent across strata of several covariates."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32138465",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 629,
"text": "PURPOSE: We aimed to assess the association between the dietary intake of fish-derived omega-3 polyunsaturated fatty acids and the risk of colorectal cancer among Swedish women.MATERIALS AND METHODS: A total of 48,233 women with information on dietary intake were included in the analysis. Participants were followed for incident colorectal cancer until 31 December 2012. Cox proportional hazard models were used to assess the association between baseline fatty acid intake and colorectal cancer risk. All analyses were stratified by colon and rectal cancers.RESULTS: During a median of 21.3 years of follow-up, a total of 344 co"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28804436",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 907,
"text": "Background : Colorectal cancer (CRC) is considered one of the most common forms of cancer in the Western world. High intake of red and processed meat is considered to increase CRC development. Objective : This study examined associations between intake of red meats, poultry, and fish and incident CRC, and if weight status modifies the associations. Design : In the Malmö Diet and Cancer Study, dietary data was collected through a modified diet history method. Via the Swedish Cancer Registry, 728 cases of CRC were identified during 428 924 person-years of follow-up of 16 944 women and 10 987 men. Results : Beef intake was inversely associated with colon cancer. However, in men high intake of beef was associated with increased risk of rectal cancer. High intake of pork was associated with increased incidence of CRC, and colon cancer. Processed meat was associated with increased risk of CRC in men."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32537063",
"endSection": "abstract",
"offsetInBeginSection": 86,
"offsetInEndSection": 953,
"text": "alth problem. Diet plays a key role in preventing this type of cancer. The purpose of our study was to determine dietary risk factors for colorectal cancer in our Moroccan context.METHODS: we conducted a case-control study including patients with colorectal cancer compared with controls. The statistical analysis of results was carried out using R software.RESULTS: our study included 225 patients treated for cancer at the Mohammed VI Hospital Center and 225 controls. The average age of our study population at the time of diagnosis was 55.49±14.06 years, including 119 men (52.9%) and 106 women (47.1%) with a sex ratio of 1.12. Associations were found between the highest intakes of red meats, cold meats, sausages and the risk of colorectal cancer (p = 0.0001) with F4 (4-7 times / week) vs F1 (never): OR = 4.4 (1.6-11.9); (p = 0.001), OR = 1.7 (0.5-5.7); (p ="
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33998355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 900,
"text": "The incidence and mortality rates of colorectal cancer (CRC) in Northeast Brazil are increasing. To study the association between CRC and diet, data were obtained from 64 patients with CRC and 123 sex- and age-matched controls. The dietary details were recorded using a validated food frequency questionnaire. Nutrient intake was calculated using Dietsys software (National Cancer Institute, Maryland, USA). In a binary logistic regression model of dietary components (model 1), the chance of CRC increased by 0.2% (odds ratio [OR] = 1.002; 95% confidence interval [CI]: 1.000-1.004) for each gram of processed meat intake per week (p < 0.010). Consumption of eggs decreased the chance by 0.1% per gram (OR = 0.999; 95% CI: 0.998-1.000; p < 0.050). The use of oil (including olive oil) for served food decreased the chance by 1.8% (OR = 0.982; 95% CI: 0.970-0.992) for each time consumed (p < 0.010)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36014940",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 772,
"text": "There is limited evidence to support the relationship between the consumption of animal-source foods other than red meat and processed meat and colorectal cancer (CRC) risk. We aimed to examine the recent available evidence from observational studies about the association between these food groups’ intake and CRC risk. For this systematic review, we searched the PubMed database for the last five years. A total of fourteen cohort studies and seven case−control studies comprising a total of >60,000 cases were included. The studies showed a consistent significant decrease in CRC risk, overall and by subsites, associated with a high consumption of total dairy products. Less strong effects associated with the consumption of any subtype of dairy product were observed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37572059",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 514,
"text": "Colorectal cancer (CRC) accounts for considerable mortalities worldwide. Several modifiable risk factors, including a high intake of certain foods and beverages can cause CRC. This review summarized the latest findings on the intake of various foods, nutrients, ingredients, and beverages on CRC development, with the objective of classifying them as a risk or protective factor. High-risk food items include red meat, processed meat, eggs, high alcohol consumption, sugar-sweetened beverages, and chocolate candy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36092326",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1521,
"text": "Background and Objective: Colorectal cancer (CRC) is the third most common cancer worldwide, and the incidence and mortality rates continue to increase annually. Many factors, including genetic, immune, and environmental factors, influence the occurrence and development of CRC. Along with the economic development, changes in lifestyle, especially dietary factors, have been shown to greatly affect the progression of CRC. Increasing evidence showed that dietary patterns influence the risk of CRC and affect CRC treatment. The present review describes the role of diet in the prevention and treatment of CRC with the hope that doctors attach importance to dietary patterns in educating patients with CRC or at risk of CRC and that diet may be regarded as an auxiliary treatment strategy to improve patients' outcomes.Methods: English language articles published from 2000 to December 2021 in PubMed and Embase were identified by searching titles for keywords including \"diet\", \"colorectal cancer\", \"dietary pattern\", and \"dietary factor\"; 101 articles were selected for review.Key Content and Findings: The present review describes the role of different dietary patterns and factors in the prevention and treatment of CRC. We found that dietary intervention is closely related to the occurrence, development, and prognosis of CRC. Adherence to the Mediterranean diet (MD), the Dietary Approaches to Stop Hypertension (DASH) diet, fasting, vegetarian diets and the ketogenic diet (KD) were found to reduce the risk of CR"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21888535",
"endSection": "abstract",
"offsetInBeginSection": 453,
"offsetInEndSection": 874,
"text": "The hypothesis linking fish consumption and low cancer incidence appears to be supported by little epidemiological data. However, there are several factors that may mask potential protective associations with fish intake. The type and the amount of fish eaten, the cooking method, the stage of the cancer and, amongst women, menopausal status may all be important factors that relate to whether fish is protective or not."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21888535",
"endSection": "abstract",
"offsetInBeginSection": 453,
"offsetInEndSection": 674,
"text": "The hypothesis linking fish consumption and low cancer incidence appears to be supported by little epidemiological data. However, there are several factors that may mask potential protective associations with fish intake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 242,
"offsetInEndSection": 399,
"text": " We examined the association between intakes of fish and n-3 fatty acids from fish and colorectal cancer risk in men enrolled in the Physicians' Health Study"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26264963",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 402,
"text": "The association between specific fish intake and colorectal cancer risk remains controversial. This study aimed to examine the association between specific fish intake and colorectal cancer risk in Chinese population in a large case control study. During July 2010 to November 2014, 1189 eligible colorectal cancer cases and 1189 frequency-matched controls (age and sex) completed in-person interviews."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 1217,
"offsetInEndSection": 1638,
"text": "Our findings for n-3 fatty acids were similar to those for fish; the multivariate relative risk (95% confidence interval) of total colorectal cancer for the highest versus lowest quartile of n-3 fatty acids was 0.74 (0.57-0.95; P trend = 0.01).CONCLUSIONS: Our results from this long-term prospective study suggest that intakes of fish and long-chain n-3 fatty acids from fish may decrease the risk for colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 1684,
"offsetInEndSection": 1845,
"text": "This study had no publication bias.CONCLUSION: Our findings from this meta-analysis suggest that fish consumption is inversely associated with colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 672,
"offsetInEndSection": 943,
"text": "Cox proportional hazards models were used to estimate multivariate relative risks for colorectal cancer for the categories of fish intake and quartiles of n-3 fatty acid intake.RESULTS: During 22 years of follow-up, 500 men had a confirmed diagnosis of colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "BACKGROUND: Fish consumption may protect against colorectal cancer, but results from observational studies are inconsistent; therefore, a systematic review with a meta-analysis wa"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 1130,
"offsetInEndSection": 1329,
"text": ", 0.88; 95% CI, 0.80-0.95). The pooled ORs of colorectal cancer for the highest versus lowest fish consumption in case-control studies and cohort studies were 0.83 (95% CI, 0.72-0.95) and 0.93 (95% C"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 1420,
"offsetInEndSection": 1655,
"text": "t not among cohort studies. A significant inverse association was found between fish intake and rectal cancer (summary OR, 0.79; 95% CI, 0.65-0.97), and there was a modest trend seen between fish consumption and colon cancer (summary O"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23878344",
"endSection": "abstract",
"offsetInBeginSection": 643,
"offsetInEndSection": 739,
"text": "l studies were identified. Fish consumption was not significantly associated with colorectal, co"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19169007",
"endSection": "abstract",
"offsetInBeginSection": 1688,
"offsetInEndSection": 1822,
"text": "ion and intake of meat products.CONCLUSIONS: The study results indicate that increased fish intake may have a preventive effect on CRC"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 596,
"text": "Prospective and case-control studies either do not show an association between fish intake and cancer risks or show reduced risks at high fish intakes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19169007",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "BACKGROUND/AIMS: Current epidemiologic studies investigating the effect of fish intake on colorectal cancer (CRC)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24615521",
"endSection": "abstract",
"offsetInBeginSection": 308,
"offsetInEndSection": 529,
"text": "According to our results, the consumption of vegetables, fruits, fish, as well as coffee seems to be protective against digestive cancer, while the consumption of citrus and olive oil is protective against gastric cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37572059",
"endSection": "abstract",
"offsetInBeginSection": 515,
"offsetInEndSection": 824,
"text": "Food items that are protective include milk, cheese and other dairy products, fruits, vegetables (particularly cruciferous), whole grains, legumes (particularly soy beans), fish, tea (particularly green tea), coffee (particularly among Asians), chocolate, and moderate alcohol consumption (particularly wine)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15456633",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1310,
"text": "Although long-chain n-3 polyunsaturated fatty acids (Ln-3 PUFA), which are abundant in fish, have shown protective effects on colorectal cancer in laboratory studies, epidemiological studies to date have not been consistent. We evaluated the relationship of consumption of fish and Ln-3 PUFA to the colon and rectal cancer risk in the two cohorts of the Japan Public Health Center-based prospective study of 42,525 men and 46,133 women. Dietary and other exposure data were obtained between 1990 and 1994. Through December 1999, 705 cases of colon and rectal cancer were documented. When data from the two cohorts were pooled, multivariable relative risks (RRs) for the highest quartile compared with the lowest quartile of fish consumption were 1.07 (95% confidence interval, CI = 0.77-1.48) for colon cancer and 0.95 (95% CI = 0.63-1.43) for rectal cancer with no dose-risk trend. RRs for the highest quartile compared with the lowest quartile of eicosapentaenoic acid consumption were 1.05 (95% CI = 0.76-1.46) for colon cancer and 0.91 (95% CI = 0.60-1.38) for rectal cancer with no dose-risk trend. This study does not support the role of fish and Ln-3 PUFA in the etiology of colon and rectal cancer in this population whose fish consumption was high and the variation in Ln-3 PUFA consumption was large."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17419892",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 444,
"text": "Recent studies have shown a decreased risk of colon cancer with consumption of fish. However, most studies on fish consumption do not distinguish between lean and fatty fish, or between poached and fried fish. The aim of this study was to investigate any association between fish consumption and colon cancer in The Norwegian Women and Cancer (NOWAC) study. We focused mainly on lean fish, which was further divided into poached and fried fish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 230,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies. Human studies have not shown consist"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 1189,
"offsetInEndSection": 1433,
"text": "h colon and rectal cancers. Our findings for n-3 fatty acids were similar to those for fish; the multivariate relative risk (95% confidence interval) of total colorectal cancer for the highest versus lowest quartile of n-3 fatty acids was 0.74 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21888535",
"endSection": "abstract",
"offsetInBeginSection": 300,
"offsetInEndSection": 452,
"text": "Among 273 estimates of association reported by these studies, 53 indicated decreased risk while 12 indicated increased risk associated with fish intake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 916,
"offsetInEndSection": 980,
"text": "nosis of colorectal cancer. Fish intake was inversely associated"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16201848",
"endSection": "abstract",
"offsetInBeginSection": 547,
"offsetInEndSection": 728,
"text": "Fish oil feeding resulted in lower 8-OHdG levels (P = 0.038), higher levels of apoptosis (P = 0.035), and a lower cell proliferative index (P = 0.05) compared with corn oil feeding."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 852,
"text": "Breast and colorectal cancer are main causes of death in industrialized countries. In these cancers dietary factors appear to play beneficial or adverse roles. One of the possible beneficial factors may be fish intake or the n-3 polyunsaturated fatty acids from fish, as found in epidemiological and clinical studies. In population studies, high intake of fish during many years is associated with reduced risks of breast and colorectal cancer. Prospective and case-control studies either do not show an association between fish intake and cancer risks or show reduced risks at high fish intakes. In these studies, fish consumption may have been too low or may not reflect fish consumption over a longer period. In population, case-control, and prospective studies, fish and fish n-3 polyunsaturated fatty acids were not found to increase cancer risks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1419,
"text": "BACKGROUND: Fish consumption may protect against colorectal cancer, but results from observational studies are inconsistent; therefore, a systematic review with a meta-analysis was conducted.METHODS: Relevant studies were identified by a search of MEDLINE and EMBASE databases to May 2011, with no restrictions. Reference lists from retrieved articles also were reviewed. Studies that reported odds ratio (OR) or relative risk estimates with 95% confidence intervals (CIs) for the association between the consumption of fish and the risk of colorectal, colon, or rectal cancer were included. Two authors independently extracted data and assessed study quality. The risk estimate (hazard ratio, relative risk, or OR) of the highest and lowest reported categories of fish intake were extracted from each study and analyzed using a random-effects model.RESULTS: Twenty-two prospective cohort and 19 case-control studies on fish consumption and colorectal cancer risk met the inclusion criteria and were included in the meta-analysis. Our analysis found that fish consumption decreased the risk of colorectal cancer by 12% (summary OR, 0.88; 95% CI, 0.80-0.95). The pooled ORs of colorectal cancer for the highest versus lowest fish consumption in case-control studies and cohort studies were 0.83 (95% CI, 0.72-0.95) and 0.93 (95% CI, 0.86-1.01), respectively. There was heterogeneity among case-control studies (P<.001) b"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 915,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies. Human studies have not shown consistent results. We examined the association between intakes of fish and n-3 fatty acids from fish and colorectal cancer risk in men enrolled in the Physicians' Health Study.METHODS: The Physicians' Health Study began as a randomized trial to examine the effect of aspirin and beta-carotene supplementation on cancer and cardiovascular disease. Fish intake was assessed at the 12-month follow-up with an abbreviated food-frequency questionnaire. Cox proportional hazards models were used to estimate multivariate relative risks for colorectal cancer for the categories of fish intake and quartiles of n-3 fatty acid intake.RESULTS: During 22 years of follow-up, 500 men had a confirmed dia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19169007",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1687,
"text": "BACKGROUND/AIMS: Current epidemiologic studies investigating the effect of fish intake on colorectal cancer (CRC) risk are scarce. Therefore, the aim of this study was to elucidate the relationship between fish consumption and CRC risk.METHODS: This hospital-based case-control study was performed in 548 CRC patients (Surgery Clinic, University Hospital in Krakow, Poland) between November 2000 and May 2008. Histological findings, information on anatomic location and stage of cancer were available for all the patients enrolled in this study. The control group consisted of 745 patients of the same hospital with no history of cancer admitted for treatment of non-neoplastic conditions. During the 5-year study period, the food frequency questionnaire used focused on the reference period that was defined as 1-5 years prior to CRC diagnosis for the CRC cases and the date of hospital admission for the controls.RESULTS: The crude odds ratio (OR) was inversely related to fish consumption (z for trend in quartiles of intake= -2.31, p=0.021; OR=0.89; 95% confidence interval, CI: 0.81-0.98). The risk of CRC increased with intake of stewed or cooked meat (z for trend in quartiles of intake=2.14; p=0.032; OR=1.11; 95% CI: 1.01-1.23). The adjusted OR showed a significant reduction in CRC already at the moderate fish intake of one or two servings per week (OR=0.70; 95% CI: 0.51-0.94), but it was even lower at higher fish intake (OR=0.56; 95% CI: 0.39-0.86). All multivariate statistical models employed in the analysis considered potential confounders, such as demographic characteristics of subjects, body mass index, smoking status, leisure time physical activity, energy consump"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24706410",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 810,
"text": "The association between fish, ω-3 and ω-6 polyunsaturated fatty acid (PUFA) intake and risk of colorectal cancer (CRC) remains inconclusive. Recent prospective studies suggest that the relationship may vary by gender, subsite and duration of follow-up. We followed 123,529 US adults (76,386 women and 47,143 men) without a history of cancer at baseline for 24 to 26 years. Fish and PUFA intake was assessed at baseline and updated every 4 years by using a validated food-frequency questionnaire. We found no overall association between fish, ω-3 and ω-6 PUFA intake and CRC risk with hazard ratio (HR) of 1.03 [95% confidence interval (CI): 0.89-1.20] comparing marine ω-3 intake of ≥ 0.30 g/d versus <0.15 g/d among women and 1.05 (95% CI: 0.85-1.30) comparing intake of ≥ 0.41 g/d versus <0.16 g/d among men."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35158907",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 272,
"text": "Background: Epidemiological studies on the association between fish consumption and colorectal cancer (CRC) risk have yielded inconsistent results, despite evidence from preclinical studies that long-chain ω-3 polyunsaturated fatty acids inhibit colorectal carcinogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28804436",
"endSection": "abstract",
"offsetInBeginSection": 908,
"offsetInEndSection": 972,
"text": "Fish intake was inversely associated with risk of rectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 399,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies. Human studies have not shown consistent results. We examined the association between intakes of fish and n-3 fatty acids from fish and colorectal cancer risk in men enrolled in the Physicians' Health Study"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies. Human studies have not shown consistent results"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18483335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "BACKGROUND: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17425596",
"endSection": "abstract",
"offsetInBeginSection": 1544,
"offsetInEndSection": 1748,
"text": "Our findings do not support the hypothesis that consumption of red meat increases colorectal cancer risk but do suggest that high intake of fish may decrease the risk, particularly of distal colon cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26264963",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Higher freshwater fish and sea fish intake is inversely associated with colorectal cancer risk among Chinese population: a case-control study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 596,
"text": "One of the possible beneficial factors may be fish intake or the n-3 polyunsaturated fatty acids from fish, as found in epidemiological and clinical studies. In population studies, high intake of fish during many years is associated with reduced risks of breast and colorectal cancer. Prospective and case-control studies either do not show an association between fish intake and cancer risks or show reduced risks at high fish intakes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 712,
"offsetInEndSection": 976,
"text": "In population, case-control, and prospective studies, fish and fish n-3 polyunsaturated fatty acids were not found to increase cancer risks. Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 976,
"text": "In these studies, fish consumption may have been too low or may not reflect fish consumption over a longer period. In population, case-control, and prospective studies, fish and fish n-3 polyunsaturated fatty acids were not found to increase cancer risks. Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 712,
"offsetInEndSection": 1253,
"text": "In population, case-control, and prospective studies, fish and fish n-3 polyunsaturated fatty acids were not found to increase cancer risks. Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk. In several studies in which the effect of fish consumption on cancer risk was investigated, meat and meat products were positively related to cancer risk, suggesting that cancer risks might be reduced more effectively when meat and meat products in meals are replaced by fish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 444,
"text": "One of the possible beneficial factors may be fish intake or the n-3 polyunsaturated fatty acids from fish, as found in epidemiological and clinical studies. In population studies, high intake of fish during many years is associated with reduced risks of breast and colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 853,
"offsetInEndSection": 1473,
"text": "Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk. In several studies in which the effect of fish consumption on cancer risk was investigated, meat and meat products were positively related to cancer risk, suggesting that cancer risks might be reduced more effectively when meat and meat products in meals are replaced by fish. In conclusion, the existing knowledge suggests that an increase in the consumption of fish and fish n-3 polyunsaturated fatty acids in industrialized countries may contribute to lower breast and colorectal cancer risks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10443950",
"endSection": "abstract",
"offsetInBeginSection": 853,
"offsetInEndSection": 976,
"text": "Clinical studies on markers of colorectal cancer indicate that fish n-3 polyunsaturated fatty acids may reduce cancer risk."
}
] | 13 |
BioASQ-training13b
| null | null |
66214cc6b9f8b89d7e000003
| 388 |
yesno
|
Are bacteria in the genus Clostridium facultative anaerobes?
|
['no']
|
[
"no"
] |
['Clostridia belong to those bacteria which are considered as obligate anaerobe, e.g. oxygen is harmful or lethal to these bacteria.', 'No, bacteria in the genus Clostridium are obligate anaerobes']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26231446",
"http://www.ncbi.nlm.nih.gov/pubmed/25700419",
"http://www.ncbi.nlm.nih.gov/pubmed/31076745",
"http://www.ncbi.nlm.nih.gov/pubmed/20526574",
"http://www.ncbi.nlm.nih.gov/pubmed/31991218",
"http://www.ncbi.nlm.nih.gov/pubmed/18430081",
"http://www.ncbi.nlm.nih.gov/pubmed/21067677"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18430081",
"endSection": "title",
"offsetInBeginSection": 50,
"offsetInEndSection": 92,
"text": "strict anaerobe Clostridium acetobutylicum"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18430081",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Clostridia belong to those bacteria which are considered as obligate anaerobe, e.g. oxygen is harmful or lethal to these bacteria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25700419",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "We report here the closed genome of Clostridium pasteurianum ATCC 6013, a saccharolytic, nitrogen-fixing, and spore-forming Gram-positive obligate anaerobe"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21067677",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Clostridium pasteurianum BB, a saccharolytic and spore-forming obligate anaerobe"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26231446",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "Clostridium difficile is a spore-forming obligate anaerobe that is a leading cause of healthcare-associated infections"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31991218",
"endSection": "abstract",
"offsetInBeginSection": 537,
"offsetInEndSection": 682,
"text": "However, the discovery of antimicrobials has been biased towards aerobes and facultative anaerobes, and strict anaerobes such as Clostridium spp."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31076745",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Clostridium is a large genus of obligate anaerobes belonging to the Firmicutes phylum of bacteria, most of which have a Gram-positive cell wall structure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20526574",
"endSection": "abstract",
"offsetInBeginSection": 515,
"offsetInEndSection": 665,
"text": "Such bacteria are either obligate anaerobic bacteria like Clostridium or Bifidobacterium or facultative anaerobic like Escherichia coli or Salmonella."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31991218",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Antimicrobial production by strictly anaerobic Clostridium spp."
}
] | 11 |
BioASQ-training11b
| null | null |
5e6f774ec6a8763d23000009
| 389 |
yesno
|
Are there any statistical methods for normalizing and identifying differential regions in histone modification ChIP-seq data?
|
['yes']
|
[
"yes"
] |
['Yes. ChIPnorm is a two-stage statistical method to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22870189"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 444,
"offsetInEndSection": 1264,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types. We show that the ChIPnorm method removes most of the noise and bias in the data and outperforms other normalization methods. We correlate the histone marks with gene expression data and confirm that histone modifications H3K27me3 and H3K4me3 act as respectively a repressor and an activator of genes. Compared to what was previously reported in the literature, we find that a substantially higher fraction of bivalent marks in ES cells for H3K27me3 and H3K4me3 move into a K27-only state. We find that most of the promoter regions in protein-coding genes have differential histone-modification sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 660,
"offsetInEndSection": 879,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 660,
"offsetInEndSection": 879,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 444,
"offsetInEndSection": 664,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 444,
"offsetInEndSection": 664,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 444,
"offsetInEndSection": 664,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 444,
"offsetInEndSection": 789,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types. We show that the ChIPnorm method removes most of the noise and bias in the data and outperforms other normalization methods. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 444,
"offsetInEndSection": 664,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 444,
"offsetInEndSection": 663,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 789,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types. We show that the ChIPnorm method removes most of the noise and bias in the data and outperforms other normalization methods."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 295,
"offsetInEndSection": 664,
"text": "This problem turns out to be surprisingly difficult, even in simple pairwise comparisons, because of the significant level of noise in ChIP-seq data. In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 664,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 664,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 664,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "ChIPnorm: a statistical method for normalizing and identifying differential regions in histone modification ChIP-seq libraries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870189",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 664,
"text": "In this paper we propose a two-stage statistical method, called ChIPnorm, to normalize ChIP-seq data, and to find differential regions in the genome, given two libraries of histone modifications of different cell types."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4278518",
"http://amigo.geneontology.org/amigo/term/GO:0016570"
] |
[] |
56b29bf545561f0573000003
| 390 |
yesno
|
Can MVA85A confer immunity against smallpox?
|
['no']
|
[
"no"
] |
['No MVA85A is a candidate tuberculosis vaccine.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25726088"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25726088",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 326,
"text": "We assessed the safety, immunogenicity, and efficacy of a candidate tuberculosis vaccine, modified vaccinia virus Ankara expressing antigen 85A (MVA85A), in adults infected with HIV-1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25726088",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 169,
"text": "Safety, immunogenicity, and efficacy of the candidate tuberculosis vaccine MVA85A in healthy adults infected with HIV-1: a randomised, placebo-controlled, phase 2 trial."
}
] | 11 |
BioASQ-training11b
| null | null |
5e776541835f4e4777000009
| 391 |
yesno
|
Does erythromycin increase risk of hypertrophic pyloric stenosis?
|
['yes']
|
[
"yes"
] |
['Yes, post-natal erythromycin exposure is associated with increased risk of hypertrophic pyloric stenosis. The association is stronger when exposure occurs in the first 2 weeks of life.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27655365",
"http://www.ncbi.nlm.nih.gov/pubmed/12100810",
"http://www.ncbi.nlm.nih.gov/pubmed/12693559",
"http://www.ncbi.nlm.nih.gov/pubmed/11562617",
"http://www.ncbi.nlm.nih.gov/pubmed/25687145",
"http://www.ncbi.nlm.nih.gov/pubmed/23558266"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27655365",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Post-natal erythromycin exposure and risk of infantile hypertrophic pyloric stenosis: a systematic review and meta-analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27655365",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "PURPOSE: Macrolide antibiotics, erythromycin, in particular, have been linked to the development of infantile hypertrophic pyloric stenosis (IHPS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27655365",
"endSection": "abstract",
"offsetInBeginSection": 813,
"offsetInEndSection": 932,
"text": " Overall, erythromycin exposure was significantly associated with development of IHPS [OR 2.45 (1.12-5.35), p = 0.02]. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27655365",
"endSection": "abstract",
"offsetInBeginSection": 1020,
"offsetInEndSection": 1443,
"text": "Data on erythromycin exposure in the first 14 days of life was extracted from 4/9 studies and identified a strong association between erythromycin exposure and subsequent development IHPS [OR 12.89 (7.67-2167), p < 0.00001].CONCLUSION: This study demonstrates a significant association between post-natal erythromycin exposure and development of IHPS, which seems stronger when exposure occurs in the first 2 weeks of life."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687145",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "BACKGROUND AND OBJECTIVE: Use of oral erythromycin in infants is associated with infantile hypertrophic pyloric stenosis (IHPS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687145",
"endSection": "abstract",
"offsetInBeginSection": 1266,
"offsetInEndSection": 1385,
"text": "CONCLUSIONS: Ingestion of oral azithromycin and erythromycin places young infants at increased risk of developing IHPS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687145",
"endSection": "abstract",
"offsetInBeginSection": 972,
"offsetInEndSection": 1188,
"text": "An association between erythromycin and IHPS was also confirmed. Exposure to erythromycin in the first 14 days of life had an aOR of 13.3 (95% CI, 6.80-25.9), and 15 to 42 days of life, aOR 4.10 (95% CI, 1.69-9.91). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23558266",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 406,
"text": "Early exposure to oral erythromycin in young infants, particularly in the first 2 weeks of life, has previously been associated with the development of hypertrophic pyloric stenosis. We report a case of an infant who received an abbreviated 4-day course of oral erythromycin for suspected Chlamydia conjunctivitis at 5 days of life then underwent pyloromyotomy for pyloric stenosis less than 2 weeks later."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11562617",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Maternal and infant use of erythromycin and other macrolide antibiotics as risk factors for infantile hypertrophic pyloric stenosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12693559",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "A case report has suggested that exposure to erythromycin through breast milk might cause infantile hypertrophic pyloric stenosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27655365",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Macrolide antibiotics, erythromycin, in particular, have been linked to the development of infantile hypertrophic pyloric stenosis (IHPS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11562617",
"endSection": "abstract",
"offsetInBeginSection": 425,
"offsetInEndSection": 622,
"text": "Infants prescribed systemic erythromycin had increased risk of IHPS, with the highest risk in the first 2 weeks of age (relative risk = 10.51 for erythromycin in first 2 weeks, 95% CI 4.48, 24.66)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12100810",
"endSection": "abstract",
"offsetInBeginSection": 1157,
"offsetInEndSection": 1476,
"text": "There was an association between maternal prescriptions for nonerythromycin macrolides and infantile hypertrophic pyloric stenosis (adjusted odds ratio 2.77, 95% confidence interval 1.22, 6.30, P =.01).<br><b>CONCLUSION</b>: The hypothesized association between erythromycin and infantile pyloric stenosis was not seen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27655365",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 147,
"text": "Macrolide antibiotics, erythromycin, in particular, have been linked to the development of infantile hypertrophic pyloric stenosis (IHPS)."
}
] | 11 |
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D046248",
"https://meshb.nlm.nih.gov/record/ui?ui=D012306",
"https://meshb.nlm.nih.gov/record/ui?ui=D004917"
] | null |
5a67ade5b750ff445500000c
| 392 |
yesno
|
Are G-quadruplexes(G4) possible drug targets for glioblastoma?
|
['yes']
|
[
"yes"
] |
['The 2H2-6M(4)-oxazole telomestatin derivative (6OTD) targets Glioma stem cells through G4 stabilization and promotion of DNA damage responses. Therefore, G4s are promising therapeutic targets for glioblastoma.', 'G-quadruplex DNA structures (G4 DNA) are a promising therapeutic target for glioblastoma because of their ability to stabilize DNA damage and promote DNA damage response in response to 6-oxazole 6-methyl-CoA reductase inhibitors (6OTD).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33213893",
"http://www.ncbi.nlm.nih.gov/pubmed/34459951",
"http://www.ncbi.nlm.nih.gov/pubmed/28620243",
"http://www.ncbi.nlm.nih.gov/pubmed/26845351",
"http://www.ncbi.nlm.nih.gov/pubmed/26908447",
"http://www.ncbi.nlm.nih.gov/pubmed/24030712"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28620243",
"endSection": "abstract",
"offsetInBeginSection": 1204,
"offsetInEndSection": 1385,
"text": "These observations indicate that 6OTD targets GSCs through G4 stabilization and promotion of DNA damage responses. Therefore, G4s are promising therapeutic targets for glioblastoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28620243",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Targeting glioma stem cells in vivo by a G-quadruplex-stabilizing synthetic macrocyclic hexaoxazole."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34459951",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 390,
"text": "G-quadruplex (G4) DNA is a type of quadruple helix structure formed by a continuous guanine-rich DNA sequence. Emerging evidence in recent years authenticated that G4 DNA structures exist both in cell-free and cellular systems, and function in different diseases, especially in various cancers, aging, neurological diseases, and have been considered novel promising targets for drug design."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28620243",
"endSection": "abstract",
"offsetInBeginSection": 1319,
"offsetInEndSection": 1385,
"text": "Therefore, G4s are promising therapeutic targets for glioblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24030712",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Guanine-rich oligonucleotides (GROs) are promising therapeutic candidate for cancer treatment and other biomedical application."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24030712",
"endSection": "abstract",
"offsetInBeginSection": 1173,
"offsetInEndSection": 1315,
"text": "These findings are valuable to the design and rationale behind the possible targeted drug delivery to specific cellular organelles using GROs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33213893",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "The G-quadruplex (G4) DNA, which has been developed as a potential anticancer target in drug screening and design, plays a crucial role in the oncogene transcription and translation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26845351",
"endSection": "abstract",
"offsetInBeginSection": 1647,
"offsetInEndSection": 1750,
"text": "Therefore, a novel G4-directed therapeutic strategy could specifically target cancer stem cells in GBM."
}
] | 11 |
BioASQ-training11b
| null | null |
62211b973a8413c65300006c
| 393 |
yesno
|
Is the protein ABCG2 (ATP-Binding Cassette, subfamily G, member 2, transporter) excreting uric acid?
|
['yes']
|
[
"yes"
] |
['Yes,\r\nABCG2 plays a central role on extra-renal uric acid excretion']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29264928",
"http://www.ncbi.nlm.nih.gov/pubmed/28566086"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29264928",
"endSection": "abstract",
"offsetInBeginSection": 255,
"offsetInEndSection": 453,
"text": "TP-binding cassette transporter, sub-family G, member 2 (ABCG2/BCRP) is a well-studied urate transporter expressed on apical membranes in several tissues, including the intestine, liver, and kidney."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28566086",
"endSection": "abstract",
"offsetInBeginSection": 248,
"offsetInEndSection": 329,
"text": "the discovery that ABCG2 plays a central role on extra-renal uric acid excretion,"
}
] | 11 |
BioASQ-training11b
| null | null |
5e5b5c6fb761aafe0900000a
| 394 |
yesno
|
Does Groucho related gene 5 (GRG5) have a role only in late development?
|
['no']
|
[
"no"
] |
['Groucho related gene 5 (GRG5) has been described as a multifunctional protein that has been implicated in late embryonic and postnatal mouse development. By both loss and gain of function approaches ablation of GRG5 has been shown to deregulate the Embryonic Stem Cell (ESC) pluripotent state whereas its overexpression leads to enhanced self-renewal and acquisition of cancer cell-like properties. The malignant characteristics of teratomas generated by ESCs that overexpress GRG5 reveal its pro-oncogenic potential.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30214018"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30214018",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 638,
"text": "Groucho related gene 5 (GRG5) is a multifunctional protein that has been implicated in late embryonic and postnatal mouse development. Here, we describe a previously unknown role of GRG5 in early developmental stages by analyzing its function in stem cell fate decisions. By both loss and gain of function approaches we demonstrate that ablation of GRG5 deregulates the Embryonic Stem Cell (ESC) pluripotent state whereas its overexpression leads to enhanced self-renewal and acquisition of cancer cell-like properties. The malignant characteristics of teratomas generated by ESCs that overexpress GRG5 reveal its pro-oncogenic potential."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30214018",
"endSection": "abstract",
"offsetInBeginSection": 135,
"offsetInEndSection": 271,
"text": "Here, we describe a previously unknown role of GRG5 in early developmental stages by analyzing its function in stem cell fate decisions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30214018",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "Groucho related gene 5 (GRG5) is involved in embryonic and neural stem cell state decisions.Groucho related gene 5 (GRG5) is a multifunctional protein that has been implicated in late embryonic and postnatal mouse development. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c629fffe842deac67000009
| 395 |
yesno
|
Was golimumab tested for diabetes?
|
['yes']
|
[
"yes"
] |
['Yes, among children and young adults with newly diagnosed overt type 1 diabetes, golimumab resulted in better endogenous insulin production and less exogenous insulin use than placebo.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33207093"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33207093",
"endSection": "abstract",
"offsetInBeginSection": 2481,
"offsetInEndSection": 2674,
"text": "CONCLUSIONS: Among children and young adults with newly diagnosed overt type 1 diabetes, golimumab resulted in better endogenous insulin production and less exogenous insulin use than placebo. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33207093",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Golimumab and Beta-Cell Function in Youth with New-Onset Type 1 Diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33207093",
"endSection": "abstract",
"offsetInBeginSection": 450,
"offsetInEndSection": 737,
"text": "lticenter, placebo-controlled, double-blind, parallel-group trial, we randomly assigned, in a 2:1 ratio, children and young adults (age range, 6 to 21 years) with newly diagnosed overt type 1 diabetes to receive subcutaneous golimumab or placebo for 52 weeks. The primary end point was e"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33207093",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "Golimumab and Beta-Cell Function in Youth with New-Onset Type 1 Diabetes"
}
] | 11 |
BioASQ-training11b
| null | null |
601c46f61cb411341a00001d
| 396 |
yesno
|
Is shotgun lipidomics the direct infusion of a lipid sample into a mass spectrometer?
|
['yes']
|
[
"yes"
] |
Yes, shotgun lipidomics relies on direct infusion of total lipid extracts into a high-resolution tandem mass spectrometer.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23825371",
"http://www.ncbi.nlm.nih.gov/pubmed/22946708",
"http://www.ncbi.nlm.nih.gov/pubmed/22282095",
"http://www.ncbi.nlm.nih.gov/pubmed/21755525",
"http://www.ncbi.nlm.nih.gov/pubmed/21207296",
"http://www.ncbi.nlm.nih.gov/pubmed/22629264",
"http://www.ncbi.nlm.nih.gov/pubmed/19408941",
"http://www.ncbi.nlm.nih.gov/pubmed/17920553"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23825371",
"endSection": "abstract",
"offsetInBeginSection": 70,
"offsetInEndSection": 122,
"text": "In direct infusion/injection (or shotgun) lipidomics"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22946708",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 374,
"text": "An efficient shotgun lipidomics strategy was established and optimized for fast phospholipid profiling of viscera from three fish species: Lateolabrax japonicas, Ctenopharyngodon idellus, and Carassius auratus. This strategy relies on direct infusion of total lipid extracts into a tandem mass spectrometer without additional separation of the individual molecular species. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22282095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Top-down shotgun lipidomics relies on direct infusion of total lipid extracts into a high-resolution tandem mass spectrometer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21755525",
"endSection": "abstract",
"offsetInBeginSection": 264,
"offsetInEndSection": 317,
"text": "shotgun lipidomic approaches that use direct infusion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21207296",
"endSection": "abstract",
"offsetInBeginSection": 304,
"offsetInEndSection": 341,
"text": "direct infusion (shotgun lipidomics) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22629264",
"endSection": "abstract",
"offsetInBeginSection": 694,
"offsetInEndSection": 745,
"text": "direct infusion-based shotgun lipidomics approaches"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19408941",
"endSection": "abstract",
"offsetInBeginSection": 201,
"offsetInEndSection": 306,
"text": "shotgun lipidomics (MDMS-SL) data, which are acquired directly from lipid extracts after direct infusion "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17920553",
"endSection": "abstract",
"offsetInBeginSection": 799,
"offsetInEndSection": 1123,
"text": "Through direct infusion of the resultant enriched solution, we identified and quantitated a variety of very-low-abundance sphingolipid classes (e.g., sphingosine, psychosine, and lysosphingomyelin) and molecular species (e.g., sphingomyelin) using electrospray ionization mass spectrometry (i.e., shotgun sphingolipidomics)."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008055",
"http://www.biosemantics.org/jochem#4269483",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013057",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D053719",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013058",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007260"
] |
[] |
532f3e08d6d3ac6a34000034
| 397 |
yesno
|
Is autosomal dominant inheritanced form of Osteogenesis imperfecta caused by mutations in the genes associated with collagen production?
|
['yes']
|
[
"yes"
] |
['Osteogenesis imperfecta (OI), also known as brittle bone disease, is a group of genetic disorders that mainly affect the bones. The autosomal dominant form of the disease is cause by a mutation in the COL1A1 or COL1A2 genes which produce type I collagen.', 'steogenesis imperfecta (OI) is a heterogeneous bone disorder characterized by recurrent fractures. Although most cases of OI have heterozygous mutations inCOL1A1orCOL1A2and show autosomal dominant inheritance,']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27312322",
"http://www.ncbi.nlm.nih.gov/pubmed/2992938",
"http://www.ncbi.nlm.nih.gov/pubmed/27677223",
"http://www.ncbi.nlm.nih.gov/pubmed/21567925",
"http://www.ncbi.nlm.nih.gov/pubmed/22863195",
"http://www.ncbi.nlm.nih.gov/pubmed/28116328",
"http://www.ncbi.nlm.nih.gov/pubmed/18566967",
"http://www.ncbi.nlm.nih.gov/pubmed/27510842",
"http://www.ncbi.nlm.nih.gov/pubmed/21341209",
"http://www.ncbi.nlm.nih.gov/pubmed/28820180",
"http://www.ncbi.nlm.nih.gov/pubmed/12362985",
"http://www.ncbi.nlm.nih.gov/pubmed/2886666",
"http://www.ncbi.nlm.nih.gov/pubmed/24928016",
"http://www.ncbi.nlm.nih.gov/pubmed/29150909",
"http://www.ncbi.nlm.nih.gov/pubmed/2037280",
"http://www.ncbi.nlm.nih.gov/pubmed/27762305",
"http://www.ncbi.nlm.nih.gov/pubmed/21667357",
"http://www.ncbi.nlm.nih.gov/pubmed/19533842",
"http://www.ncbi.nlm.nih.gov/pubmed/25402547",
"http://www.ncbi.nlm.nih.gov/pubmed/20839288",
"http://www.ncbi.nlm.nih.gov/pubmed/8456806"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28116328",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 222,
"text": "steogenesis imperfecta (OI) is a heterogeneous bone disorder characterized by recurrent fractures. Although most cases of OI have heterozygous mutations inCOL1A1orCOL1A2and show autosomal dominant inheritance,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27762305",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 274,
"text": "Osteogenesis imperfecta (OI) is a group of hereditary disorders characterized by decreased bone mass and increased fracture risk. The majority of OI cases have an autosomal dominant pattern of inheritance and are usually caused by mutations in genes encoding type I collagen"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27312322",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 281,
"text": " Osteogenesis imperfecta (OI) is a group of hereditary disorders characterized by low bone mass and recurrent fractures. Most OI cases follow an autosomal dominant pattern of inheritance and are attributed to mutations in genes encoding type I collagen (COL1A1/COL1A2). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27677223",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 268,
"text": "Osteogenesis imperfecta (OI) is a genetic disorder characterised by low bone mineral density resulting in fractures. 85-90% of patients with OI carry a variant in the type 1 collagen genes, COL1A1 and COL1A2, which follows an autosomal dominant pattern of inheritance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25402547",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 385,
"text": "Osteogenesis imperfecta (OI) comprises a heterogeneous group of disorders that are characterized by susceptibility to bone fractures, and range in severity from a subtle increase in fracture frequency to death in the perinatal period. Most patients have defects in type I collagen biosynthesis with autosomal-dominant inheritance, but many autosomal-recessive genes have been reported."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24928016",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 159,
"text": "To investigate mutation of COL1A1 gene and analyze the relationship between genotype and clinical phenotype in a family with osteogenesis imperfecta"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21667357",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Dominant inheritance of osteogenesis imperfecta (OI) is caused by mutations in COL1A1 or COL1A2, the genes that encode type I collagen,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21567925",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 805,
"text": "Osteogenesis imperfecta (OI) is a heterogeneous group of inherited disorders of bone formation, resulting in low bone mass and an increased propensity to fracture. It exhibits a broad spectrum of clinical severity, ranging from multiple fractures in utero and perinatal death, to normal adult stature and low fracture incidence. Extra-skeletal features of OI include blue sclera, hearing loss, skin hyperlaxity, joint hyperextensibility, and dentinogenesis imperfecta. The proα1(I) and proα2(I) chains of collagen 1 are encoded by the COL1A1 and COL1A2 genes, respectively; quantitative or qualitative defects in type I collagen synthesis usually manifest as types of OI or some sub-types of EDS. The majority of patients (about 90%) with a clinical diagnosis of OI have a mutation in the COL1A1 or COL1A2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8456806",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 478,
"text": "Osteogenesis imperfecta (OI) type I is characterized by bone fragility without significant deformity, osteopenia, normal stature, blue sclerae, and autosomal dominant inheritance. Dermal fibroblasts from most affected individuals produce about half the expected amount of type I collagen, suggesting that the OI type I phenotype results from a variety of mutations which alter the apparent expression of either COL1A1 or COL1A2, the genes encoding the chains of type I collagen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2886666",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Autosomal dominant osteogenesis imperfecta is caused by mutations in the COL1A2 and COL1A1 genes of type I collagen. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28820180",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 544,
"text": "Osteogenesis imperfecta is caused by dominant autosomal mutations in the type I collagen coding genes (COL1A1 and COL1A2) in about 85% of individuals, affecting collagen quantity or structure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27510842",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Osteogenesis imperfecta (OI) is a heterogeneous group of disorders of connective tissue, mainly caused by mutations in the collagen type I genes (COL1A1 and COL1A2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18566967",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Autosomal dominant osteogenesis imperfecta (OI) is caused by mutations in the genes (COL1A1 or COL1A2) encoding the chains of type I collagen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19533842",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 326,
"text": "In approximately 90% of individuals with osteogenesis imperfecta, mutations in either of the genes encoding the pro-alpha1 or pro-alpha2 chains of type I collagen (COL1A1 or COL1A2) can be identified."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20839288",
"endSection": "abstract",
"offsetInBeginSection": 187,
"offsetInEndSection": 303,
"text": "Autosomal dominant OI is caused by mutations in the genes (COL1A1 or COL1A2) encoding the chains of type I collagen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29150909",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 659,
"text": "ext-generation sequencing technology was used to screen a panel of known OI genes.RESULTS: In 41 probands, we identified 28 different disease-causing variants of 9 different known OI genes. Eleven of the variants are novel. Ten of the 28 variants are located in COL1A1, five in COL1A2, three in BMP1, three in FKBP10, two in TMEM38B, two in P3H1, and one each in CRTAP, SERPINF1, and SERPINH1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22863195",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 307,
"text": "Osteogenesis imperfecta (OI) is a clinically and genetically heterogeneous disorder associated with bone fragility and susceptibility to fractures after minimal trauma. OI type V has an autosomal-dominant pattern of inheritance and is not caused by mutations in the type I collagen genes COL1A1 and COL1A2. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2992938",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Detection of a high frequency RsaI polymorphism in the human pro alpha 2(I) collagen gene which is linked to an autosomal dominant form of osteogenesis imperfecta."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2037280",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Osteogenesis imperfecta due to recurrent point mutations at CpG dinucleotides in the COL1A1 gene of type I collagen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12362985",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 375,
"text": "Osteogenesis imperfecta (OI), commonly known as \"brittle bone disease\", is a dominant autosomal disorder characterized by bone fragility and abnormalities of connective tissue. Biochemical and molecular genetic studies have shown that the vast majority of affected individuals have mutations in either the COL1A1 or COL1A2 genes that encode the chains of type I procollagen. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21341209",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Osteogenesis imperfecta is normally caused by an autosomal dominant mutation in the type I collagen genes COL1A1 and COL1A2."
}
] | 11 |
BioASQ-training11b
|
[
"http://www.biosemantics.org/jochem#4249099",
"http://www.disease-ontology.org/api/metadata/DOID:0110341",
"http://www.disease-ontology.org/api/metadata/DOID:0110340",
"http://www.disease-ontology.org/api/metadata/DOID:0110343",
"http://www.disease-ontology.org/api/metadata/DOID:0110337",
"http://www.disease-ontology.org/api/metadata/DOID:0110338",
"http://www.disease-ontology.org/api/metadata/DOID:0110342",
"http://www.disease-ontology.org/api/metadata/DOID:0110336",
"https://meshb.nlm.nih.gov/record/ui?ui=D010013",
"https://meshb.nlm.nih.gov/record/ui?ui=D005799",
"http://www.disease-ontology.org/api/metadata/DOID:0110334",
"http://www.disease-ontology.org/api/metadata/DOID:12347",
"http://www.disease-ontology.org/api/metadata/DOID:0110335"
] | null |
5a6f77d7b750ff4455000051
| 398 |
yesno
|
Do IEG create a ripple effect of transcription?
|
['yes']
|
[
"yes"
] |
['Rapid induction of immediate-early genes (IEGs) in response to growth factor stimulations is accompanied by co-upregulation of their neighbouring genes. Profiling the primary transcripts in the nucleus with whole-genome tiling arrays delineated simultaneous activation of transcription centred on IEGs.', 'rapid induction of immediate-early genes (iegs) in response to growth factor stimulations is accompanied by co-upregulation of their neighbouring genes.', 'Rapid induction of immediate-early genes (IEGs) in response to growth factor stimulations is accompanied by co-upregulation of their neighbouring genes. Even in surrounding intergenic regions, transcriptional activation took place at the same time.', 'Rapid induction of immediate-early genes (IEGs) in response to growth factor stimulations is accompanied by co-upregulation of their neighbouring genes.', 'Here we show that intensive transcription at one locus frequently spills over into its physical neighbouring loci. Rapid induction of immediate-early genes (IEGs) in response to growth factor stimulations is accompanied by co-upregulation of their neighbouring genes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19160492"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19160492",
"endSection": "abstract",
"offsetInBeginSection": 524,
"offsetInEndSection": 676,
"text": "Rapid induction of immediate-early genes (IEGs) in response to growth factor stimulations is accompanied by co-upregulation of their neighbouring genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19160492",
"endSection": "abstract",
"offsetInBeginSection": 827,
"offsetInEndSection": 923,
"text": "Even in surrounding intergenic regions, transcriptional activation took place at the same time. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19160492",
"endSection": "abstract",
"offsetInBeginSection": 409,
"offsetInEndSection": 523,
"text": "Here we show that intensive transcription at one locus frequently spills over into its physical neighbouring loci."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19160492",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 40,
"text": "Ripples from neighbouring transcription."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19160492",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 41,
"text": "Ripples from neighbouring transcription."
}
] | 6 |
BioASQ-training6b
| null | null |
58c276bc02b8c60953000020
| 399 |
yesno
|
Is the gene MAOA epigenetically modified by methylation?
|
['yes']
|
[
"yes"
] |
['In recent years, the role of epigenetic phenomenon, such as methylation, in mediating vulnerability to behavioral illness has become increasingly appreciated. One prominent locus at which epigenetic phenomena are thought to be in play is the monoamine oxidase A (MAOA) locus.\nWe conclude that methylation of MAOA may play a significant role in common psychiatric illness and that further examination of epigenetic processes at this locus is in order.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22948232",
"http://www.ncbi.nlm.nih.gov/pubmed/22436428",
"http://www.ncbi.nlm.nih.gov/pubmed/22906985",
"http://www.ncbi.nlm.nih.gov/pubmed/23116433",
"http://www.ncbi.nlm.nih.gov/pubmed/22198720",
"http://www.ncbi.nlm.nih.gov/pubmed/22139575",
"http://www.ncbi.nlm.nih.gov/pubmed/19777560",
"http://www.ncbi.nlm.nih.gov/pubmed/20421737",
"http://www.ncbi.nlm.nih.gov/pubmed/20505345",
"http://www.ncbi.nlm.nih.gov/pubmed/18454435",
"http://www.ncbi.nlm.nih.gov/pubmed/16893905"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22948232",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Evidence that the methylation state of the monoamine oxidase A (MAOA) gene predicts brain activity of MAO A enzyme in healthy men."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22948232",
"endSection": "abstract",
"offsetInBeginSection": 765,
"offsetInEndSection": 888,
"text": "We found significant interindividual differences in methylation status and methylation patterns of the core MAOA promoter. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22436428",
"endSection": "abstract",
"offsetInBeginSection": 115,
"offsetInEndSection": 349,
"text": "In the present study, DNA methylation patterns in the MAOA regulatory and exon 1/intron 1 region were investigated for association with panic disorder with particular attention to possible effects of gender and environmental factors. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22436428",
"endSection": "abstract",
"offsetInBeginSection": 1251,
"offsetInEndSection": 1468,
"text": " The present pilot data suggest a potential role of MAOA gene hypomethylation in the pathogenesis of panic disorder particularly in female patients, possibly mediating a detrimental influence of negative life events. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22906985",
"endSection": "abstract",
"offsetInBeginSection": 987,
"offsetInEndSection": 1148,
"text": "The MAOA promoter was hypermethylated immediately upstream of the start codon in cholangiocarcinoma samples and cell lines but not in nonmalignant counterparts. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23116433",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "MAOA promoter methylation and susceptibility to carotid atherosclerosis: role of familial factors in a monozygotic twin sample."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23116433",
"endSection": "abstract",
"offsetInBeginSection": 1400,
"offsetInEndSection": 1601,
"text": "Because twins reared together share early life experience, which may leave a long-lasting epigenetic mark, aberrant MAOA methylation may represent an early biomarker for unhealthy familial environment."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22198720",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Effects of MAOA promoter methylation on susceptibility to paranoid schizophrenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22198720",
"endSection": "abstract",
"offsetInBeginSection": 1339,
"offsetInEndSection": 1454,
"text": "In conclusion, abnormalities of DNA methylation at the MAOA promoter may be associated with schizophrenia in males."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22139575",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 383,
"text": "In our study we analyzed DNA methylation patterns of 14 neuropsychiatric genes (COMT, DAT1, GABRA1, GNB3, GRIN2B, HTR1B, HTR2A, 5-HTT, MAOA, MAOB, NOS1, NR3C1, TPH1 and TH). D"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22139575",
"endSection": "abstract",
"offsetInBeginSection": 1599,
"offsetInEndSection": 1720,
"text": "Our data suggest that aberrant epigenetic regulation of neuropsychiatric genes may contribute to the pathogenesis of BPD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19777560",
"endSection": "abstract",
"offsetInBeginSection": 923,
"offsetInEndSection": 1174,
"text": "We conclude that smoking reliably decreases MAOA methylation, but exact characterization of effects on level of methylation depend on genotype, smoking history, current smoking status, gender, and region of the promoter-associated CpG Island examined."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20421737",
"endSection": "abstract",
"offsetInBeginSection": 593,
"offsetInEndSection": 742,
"text": "Given that DNA methylation is linked to the regulation of gene expression, we hypothesized that epigenetic mechanisms factor into the MAOA expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20421737",
"endSection": "abstract",
"offsetInBeginSection": 1263,
"offsetInEndSection": 1489,
"text": " the extended MAOA regulatory region contains two CpG islands (CGIs), one of which overlaps with the canonical MAOA promoter and the other is located further upstream; both CGIs exhibit sensitivity to differential methylation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20421737",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Identification and characterization of putative methylation targets in the MAOA locus using bioinformatic approaches."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20505345",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "DNA methylation is a key epigenetic mechanism involved in the developmental regulation of gene expression. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18454435",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "MAOA methylation is associated with nicotine and alcohol dependence in women."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18454435",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "In recent years, the role of epigenetic phenomenon, such as methylation, in mediating vulnerability to behavioral illness has become increasingly appreciated. One prominent locus at which epigenetic phenomena are thought to be in play is the monoamine oxidase A (MAOA) locus. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18454435",
"endSection": "abstract",
"offsetInBeginSection": 1092,
"offsetInEndSection": 1266,
"text": "We conclude that methylation of MAOA may play a significant role in common psychiatric illness and that further examination of epigenetic processes at this locus is in order."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16893905",
"endSection": "abstract",
"offsetInBeginSection": 612,
"offsetInEndSection": 729,
"text": "Analysis of CpG methylation in the MAOA promoter region revealed substantial methylation in females but not in males."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16893905",
"endSection": "abstract",
"offsetInBeginSection": 1371,
"offsetInEndSection": 1519,
"text": "Therefore, allelic mRNA expression is affected by genetic and epigenetic events, both with the potential to modulate biogenic amine tone in the CNS."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008745",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019175",
"http://www.uniprot.org/uniprot/AOFA_SHEEP",
"http://www.uniprot.org/uniprot/AOFA_CANFA",
"http://www.uniprot.org/uniprot/AOFA_PONAB",
"http://www.uniprot.org/uniprot/AOFA_PIG",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0032259",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0006306"
] |
[] |
56cf50253975bb303a00000b
| 400 |
yesno
|
Is AZD5153 active in prostate cancer?
|
['yes']
|
[
"yes"
] |
['Yes, AZD5153 was shown to be effective in treatment of prostate cancer.', 'Yes. AZD5153, a novel BRD4 inhibitor, inhibits prostate cancer cell growth in vitro and in vivo. AZD5153 induced apoptosis activation and cell cycle arrest in prostate cancer cells. AZD5153 was non-cytotoxic to the prostate epithelial cells.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30308485"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "AZD5153 Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 18,
"offsetInEndSection": 1666,
"text": "Bromodomain-containing protein 4 (BRD4) overexpression participates in prostate cancer progression by enhancing the transcriptional activity and expression of several key oncogenes. AZD5153 is a novel BRD4 inhibitor.METHODS: Prostate cancer cells were treated with AZD5153. Cell survival was tested by MTT assay and clonogenicity assay. Cell proliferation was tested by [H3] DNA incorporation assay. Cell apoptosis was tested by caspase-3/-9 activity assay, Histone DNA ELISA assay, Annexin V FACS assay and TUNEL staining assay. Cell cycle progression was tested by propidium iodide (PI) FACS assay. Signaling was tested by Western blotting assay. The nude mice PC-3 xenograft model was applied to test AZD5153's activity in vivo.RESULTS: AZD5153 inhibited proliferation and survival of established and primary prostate cancer cells. AZD5153 induced apoptosis activation and cell cycle arrest in prostate cancer cells. AZD5153 was non-cytotoxic to the prostate epithelial cells. AZD5153 downregulated BRD4 targets (cyclin D1, Myc, Bcl-2, FOSL1 and CDK4) in PC-3 and primary prostate cancer cells. Further studies show that AKT could be the primary resistance factor of AZD5153. Pharmacological inhibition or genetic depletion of AKT induced BRD4 downregulation, sensitizing AZD5153-induced cytotoxicity in PC-3 cells. In vivo, AZD5153 oral administration inhibited PC-3 xenograft tumor growth in nude mice. Its anti-tumor activity was further enhanced with co-treatment of the AKT specific inhibitor MK-2206.CONCLUSION: Together, our results indicate a promising therapeutic value of the novel BRD4 inhibitor AZD5153 against prostate cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 857,
"offsetInEndSection": 941,
"text": "AZD5153 induced apoptosis activation and cell cycle arrest in prostate cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 1533,
"offsetInEndSection": 1672,
"text": "CONCLUSION\n\nTogether, our results indicate a promising therapeutic value of the novel BRD4 inhibitor AZD5153 against prostate cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 1002,
"offsetInEndSection": 1119,
"text": "AZD5153 downregulated BRD4 targets (cyclin D1, Myc, Bcl-2, FOSL1 and CDK4) in PC-3 and primary prostate cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 753,
"offsetInEndSection": 856,
"text": "RESULTS\n\nAZD5153 inhibited proliferation and survival of established and primary prostate cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 749,
"offsetInEndSection": 851,
"text": "RESULTS AZD5153 inhibited proliferation and survival of established and primary prostate cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 852,
"offsetInEndSection": 936,
"text": "AZD5153 induced apoptosis activation and cell cycle arrest in prostate cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 997,
"offsetInEndSection": 1114,
"text": "AZD5153 downregulated BRD4 targets (cyclin D1, Myc, Bcl-2, FOSL1 and CDK4) in PC-3 and primary prostate cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 1527,
"offsetInEndSection": 1665,
"text": "CONCLUSION Together, our results indicate a promising therapeutic value of the novel BRD4 inhibitor AZD5153 against prostate cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "AZD5153 Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308485",
"endSection": "abstract",
"offsetInBeginSection": 856,
"offsetInEndSection": 941,
"text": "AZD5153 induced apoptosis activation and cell cycle arrest in prostate cancer cells."
}
] | 11 |
BioASQ-training11b
| null | null |
5e2b253ffbd6abf43b000006
| 402 |
yesno
|
Is Enlimomab effective for stroke treatment?
|
['no']
|
[
"no"
] |
['No. Anti-ICAM therapy with enlimomab is not an effective treatment for ischemic stroke in and may significantly worsen stroke outcome.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/9744839",
"http://www.ncbi.nlm.nih.gov/pubmed/9693236",
"http://www.ncbi.nlm.nih.gov/pubmed/11692032",
"http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"http://www.ncbi.nlm.nih.gov/pubmed/19849665"
] |
[
{
"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/9693236",
"endSection": "abstract",
"offsetInBeginSection": 1185,
"offsetInEndSection": 1498,
"text": "There was no increase in the frequency of adverse events with increasing doses of enlimomab.CONCLUSIONS: Doses 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": "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/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": "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/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1034,
"offsetInEndSection": 1359,
"text": "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": 0,
"offsetInEndSection": 258,
"text": "Patients experiencing fever were more likely to have a poor outcome or die.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": 1178,
"offsetInEndSection": 1271,
"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/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1388,
"offsetInEndSection": 1674,
"text": "Patients experiencing fever were more likely to have a poor outcome or die.<br><b>CONCLUSIONS</b>: 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.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19849665",
"endSection": "abstract",
"offsetInBeginSection": 1934,
"offsetInEndSection": 2068,
"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/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1440,
"offsetInEndSection": 1635,
"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/11692032",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"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": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11673584",
"endSection": "abstract",
"offsetInBeginSection": 1407,
"offsetInEndSection": 1591,
"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
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D016896",
"http://www.biosemantics.org/jochem#4002166",
"https://meshb.nlm.nih.gov/record/ui?ui=D020521"
] | null |
58ec6eb5eda5a5767200000c
| 403 |
yesno
|
Are there any HCV replication inhibitors available?
|
['yes']
|
[
"yes"
] |
Chronic hepatitis C virus (HCV) infection is a worldwide health problem causing serious complications, such as liver cirrhosis and hepatoma. Small interfering RNAs (siRNAs) and short hairpin RNAs (shRNAs) have been reported to suppress gene expression significantly. HCV seems a suitable candidate for targets of siRNAs, as HCV is a positive single-strand RNA virus and replicates in the cytoplasm. Based on results, nowadays there are few HCV replication inhibitors such as GS-563253, PSI-6130, NA-808, BMS-790052, GS-9132 and BMS-788329.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24165192",
"http://www.ncbi.nlm.nih.gov/pubmed/24154738",
"http://www.ncbi.nlm.nih.gov/pubmed/23791700",
"http://www.ncbi.nlm.nih.gov/pubmed/23745769",
"http://www.ncbi.nlm.nih.gov/pubmed/23688081",
"http://www.ncbi.nlm.nih.gov/pubmed/23896953",
"http://www.ncbi.nlm.nih.gov/pubmed/23896281",
"http://www.ncbi.nlm.nih.gov/pubmed/23629709",
"http://www.ncbi.nlm.nih.gov/pubmed/23453230",
"http://www.ncbi.nlm.nih.gov/pubmed/23466233",
"http://www.ncbi.nlm.nih.gov/pubmed/23454058",
"http://www.ncbi.nlm.nih.gov/pubmed/23440335",
"http://www.ncbi.nlm.nih.gov/pubmed/23431163",
"http://www.ncbi.nlm.nih.gov/pubmed/23384816",
"http://www.ncbi.nlm.nih.gov/pubmed/21331152",
"http://www.ncbi.nlm.nih.gov/pubmed/21694902",
"http://www.ncbi.nlm.nih.gov/pubmed/23230455"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24165192",
"endSection": "abstract",
"offsetInBeginSection": 778,
"offsetInEndSection": 925,
"text": "We report here the discovery of the first small-molecule HCV infectivity inhibitor, GS-563253, also called HCV infectivity inhibitor 1 (HCV II-1). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24154738",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 140,
"text": "Resistance to mericitabine (prodrug of HCV NS5B polymerase inhibitor PSI-6130) is rare and conferred by the NS5B S282T mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23791700",
"endSection": "abstract",
"offsetInBeginSection": 525,
"offsetInEndSection": 616,
"text": "We tested the ability of NA808 to inhibit SPT's enzymatic activity in FLR3-1 replicon cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23791700",
"endSection": "abstract",
"offsetInBeginSection": 1488,
"offsetInEndSection": 1631,
"text": "The SPT inhibitor NA808 prevents replication of HCV genotypes 1a, 1b, 2a, 3a, and 4a in cultured hepatocytes and in mice with humanized livers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23745769",
"endSection": "abstract",
"offsetInBeginSection": 123,
"offsetInEndSection": 263,
"text": "Vaniprevir (phase III clinical trials) and MK-5172 (phase II clinical trials) are two potent antiviral compounds that target NS3/4A protease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23688081",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 200,
"text": "treatment for hepatitis C virus (HCV) infection has been significantly improved with the approval of the first two HCV NS3/4A protease inhibitors, telaprevir (Incivek) and boceprevir (Victrelis). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23896953",
"endSection": "abstract",
"offsetInBeginSection": 717,
"offsetInEndSection": 1271,
"text": "Combination therapy with telaprevir and BMS-788329 (NS5A inhibitor) reduced serum HCV RNA to undetectable levels. The presence of an NS3-V36A telaprevir resistance mutation resulted in poor response to telaprevir monotherapy but showed significant HCV reduction when telaprevir was combined with BMS-788329. However, a BMS-788329-resistant strain emerged at low frequency. Infection with a BMS-788329-resistant NS5A-L31V mutation rapidly resulted in gain of an additional NS5A-Y93A mutation that conferred telaprevir resistance during combination therapy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23896281",
"endSection": "abstract",
"offsetInBeginSection": 130,
"offsetInEndSection": 240,
"text": "HCV NS5A replication complex inhibitors, exemplified by Daclatasvir (BMS-790052), represent a new class of DAA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23629709",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 265,
"text": "ACH-806 (or GS-9132) is a novel, small-molecule inhibitor specific for hepatitis C virus (HCV). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23453230",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 329,
"text": "Telaprevir and boceprevir are the first two protease inhibitor (PI) DAAs to be approved for combination therapy with pegylated interferon (PEG-IFN) and ribavirin (RBV). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23466233",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 130,
"text": "symmetrical bidentate structure of the NS5A inhibitor BMS-790052, a series of new monodentate molecules were designed"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23454058",
"endSection": "abstract",
"offsetInBeginSection": 1040,
"offsetInEndSection": 1204,
"text": "In vitro, boceprevir is more active than telaprevir against the HCV G3 NS3/4A enzyme in cell-based and biochemical assays and against G3 isolates in replicon assays"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23440335",
"endSection": "abstract",
"offsetInBeginSection": 351,
"offsetInEndSection": 577,
"text": "Alisporivir is the most advanced host-targeting antiviral in clinical development. Alisporivir blocks HCV replication by neutralizing the peptidyl-prolyl isomerase activity of the abundant host cytosolic protein, cyclophilin A"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23431163",
"endSection": "abstract",
"offsetInBeginSection": 102,
"offsetInEndSection": 264,
"text": "Interestingly, the NS5A inhibitor daclatasvir (BMS-790052) caused a decrease in serum HCV RNA levels by about two orders of magnitude within 6 h of administration"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014779",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004364"
] |
[
{
"o": "Drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_type",
"s": "http://data.linkedct.org/resource/intervention/24334"
},
{
"o": "Intervention #24334 (Drug:HCV polymerase inhibitor pro-drug)",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://data.linkedct.org/resource/intervention/24334"
},
{
"o": "HCV polymerase inhibitor pro-drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_name",
"s": "http://data.linkedct.org/resource/intervention/24334"
},
{
"o": "Drug",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A10759582"
},
{
"o": "Drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_type",
"s": "http://data.linkedct.org/resource/intervention/23449"
},
{
"o": "Intervention #23449 (Drug:HCV polymerase inhibitor pro-drug)",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://data.linkedct.org/resource/intervention/23449"
},
{
"o": "HCV polymerase inhibitor pro-drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_name",
"s": "http://data.linkedct.org/resource/intervention/23449"
},
{
"o": "Drug",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A10759582"
},
{
"o": "Drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_type",
"s": "http://data.linkedct.org/resource/intervention/26936"
},
{
"o": "HCV polymerase inhibitor pro-drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_name",
"s": "http://data.linkedct.org/resource/intervention/26936"
},
{
"o": "Drug",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A10759582"
},
{
"o": "Intervention #26936 (Drug:HCV polymerase inhibitor pro-drug)",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://data.linkedct.org/resource/intervention/26936"
},
{
"o": "Drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_type",
"s": "http://data.linkedct.org/resource/intervention/28754"
},
{
"o": "Intervention #28754 (Drug:HCV polymerase inhibitor pro-drug)",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://data.linkedct.org/resource/intervention/28754"
},
{
"o": "Drug",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A10759582"
},
{
"o": "HCV polymerase inhibitor pro-drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_name",
"s": "http://data.linkedct.org/resource/intervention/28754"
},
{
"o": "Drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_type",
"s": "http://data.linkedct.org/resource/intervention/24333"
},
{
"o": "Intervention #24333 (Drug:HCV polymerase inhibitor pro-drug)",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://data.linkedct.org/resource/intervention/24333"
},
{
"o": "HCV polymerase inhibitor pro-drug",
"p": "http://data.linkedct.org/resource/linkedct/intervention_name",
"s": "http://data.linkedct.org/resource/intervention/24333"
},
{
"o": "Drug",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A10759582"
}
] |
53353927d6d3ac6a34000043
| 404 |
yesno
|
Does CRISPR inversion of CTCF sites alter genome topology?
|
['yes']
|
[
"yes"
] |
['Yes. CRISPR inversion of CTCF sites alters genome topology.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26276636"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26276636",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26276636",
"endSection": "abstract",
"offsetInBeginSection": 258,
"offsetInEndSection": 1185,
"text": "To test the functional significance of this observation, we combined CRISPR/Cas9-based genomic-DNA-fragment editing with chromosome-conformation-capture experiments to show that the location and relative orientations of CBSs determine the specificity of long-range chromatin looping in mammalian genomes, using protocadherin (Pcdh) and β-globin as model genes. Inversion of CBS elements within the Pcdh enhancer reconfigures the topology of chromatin loops between the distal enhancer and target promoters and alters gene-expression patterns. Thus, although enhancers can function in an orientation-independent manner in reporter assays, in the native chromosome context, the orientation of at least some enhancers carrying CBSs can determine both the architecture of topological chromatin domains and enhancer/promoter specificity. These findings reveal how 3D chromosome architecture can be encoded by linear genome sequences"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26276636",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26276636",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D064113",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D064112"
] | null |
587e440f2420191125000005
| 405 |
yesno
|
Can discharge destinations be accurately predicted using the Risk Assessment and Prediction Tool (RAPT)?
|
['yes']
|
[
"yes"
] |
['Yes. The Risk Assessment and Prediction Tool (RAPT) appears to be a valuable predictor of discharge destination after orthopedic surgery and neurosurgical procedures.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26305296",
"http://www.ncbi.nlm.nih.gov/pubmed/24717404",
"http://www.ncbi.nlm.nih.gov/pubmed/31327649",
"http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"http://www.ncbi.nlm.nih.gov/pubmed/29788192"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29788192",
"endSection": "abstract",
"offsetInBeginSection": 1380,
"offsetInEndSection": 1640,
"text": "CONCLUSION: Our analysis identified age, lower lumbar/lumbosacral surgery, and RAPT walk score as independent predictors of discharge to SNF, and demonstrated superior predictive power compared with the total RAPT Score when combined in a novel grading scale. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26305296",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "PURPOSE: The aim of this study was to evaluate the value of conventional factors, the Risk Assessment and Predictor Tool (RAPT) and performance-based functional tests as predictors of delayed recovery after total hip arthroplasty (THA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 1939,
"offsetInEndSection": 2051,
"text": "CONCLUSIONS: The RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 2311,
"offsetInEndSection": 2647,
"text": "The RAPT allows for identification of patients who are likely to be discharged home or to rehabilitation, which may facilitate preoperative planning of postoperative care. Additionally, it identifies intermediate-risk patients and could be used to implement targeted interventions to facilitate discharge home in this group of patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 1518,
"offsetInEndSection": 1564,
"text": "RESULTS: Overall predictive accuracy was 78%. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24717404",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "OBJECTIVE: To assess the relevance of the RAPT (Risk Assessment and Prediction Tool), among a cohort of patients undergoing total hip arthroplasty (THA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24717404",
"endSection": "abstract",
"offsetInBeginSection": 1239,
"offsetInEndSection": 1369,
"text": "CONCLUSION: This study confirmed the usefulness of the RAPT to help in patient orientation decision after total hip arthroplasty. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 1947,
"offsetInEndSection": 2058,
"text": "CONCLUSIONS\n\nThe RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 1570,
"offsetInEndSection": 1690,
"text": "RAPT scores<6 and >10 (of 12) predicted with >90% accuracy discharge to inpatient rehabilitation and home, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 2319,
"offsetInEndSection": 2490,
"text": "The RAPT allows for identification of patients who are likely to be discharged home or to rehabilitation, which may facilitate preoperative planning of postoperative care."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 312,
"offsetInEndSection": 466,
"text": "The Risk Assessment and Prediction Tool (RAPT) is a preoperative survey constructed to predict discharge disposition after total joint arthroplasty (TJA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 1939,
"offsetInEndSection": 2049,
"text": "CONCLUSIONS The RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 312,
"offsetInEndSection": 467,
"text": "The Risk Assessment and Prediction Tool (RAPT) is a preoperative survey constructed to predict discharge disposition after total joint arthroplasty (TJA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 620,
"offsetInEndSection": 773,
"text": "A low RAPT score is reported to indicate a high risk of needing any form of inpatient rehabilitation after TJA, including short-term nursing facilities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 1947,
"offsetInEndSection": 2058,
"text": "CONCLUSIONS\nThe RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 1887,
"offsetInEndSection": 1998,
"text": "CONCLUSIONS: The RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31327649",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "BACKGROUND: The Risk Assessment and Prediction Tool (RAPT) is used to predict patient discharge disposition after total joint arthroplasty."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25106801",
"endSection": "abstract",
"offsetInBeginSection": 1943,
"offsetInEndSection": 2054,
"text": "CONCLUSIONS: The RAPT accurately predicted discharge disposition for high- and low-risk patients in our cohort."
}
] | 11 |
BioASQ-training11b
| null | null |
5e2b0d71fbd6abf43b000001
| 406 |
yesno
|
Are the Fanconi anemia genes a part of the same signalling pathway?
|
['yes']
|
[
"yes"
] |
['The Fanconi anemia genes code for proteins that act in complexes to coordinate the repair of damaged DNA.', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNAMutations in at least 14 different genes have been shown to cause FA', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNAMutations in at least 14 different genes have been shown to cause FA', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNAMutations in at least 14 different genes have been shown to cause FA', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA ', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA ', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA ', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA ', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA ', 'Mutations in at least 14 different genes have been shown to cause FA. The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA. ', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA. Mutations in at least 14 different genes have been shown to cause FA. ', 'The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA. Mutations in at least 14 different genes have been shown to cause FA. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21557222",
"http://www.ncbi.nlm.nih.gov/pubmed/10088637",
"http://www.ncbi.nlm.nih.gov/pubmed/15611632",
"http://www.ncbi.nlm.nih.gov/pubmed/11157805",
"http://www.ncbi.nlm.nih.gov/pubmed/20407210",
"http://www.ncbi.nlm.nih.gov/pubmed/23333482",
"http://www.ncbi.nlm.nih.gov/pubmed/17387268"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21557222",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 285,
"text": "Mutations in at least 14 different genes have been shown to cause FA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21557222",
"endSection": "abstract",
"offsetInBeginSection": 427,
"offsetInEndSection": 519,
"text": "The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10088637",
"endSection": "abstract",
"offsetInBeginSection": 428,
"offsetInEndSection": 630,
"text": " The current review describes the structure and function of the Fanconi anemia genes and describes the role of the encoded Fanconi anemia proteins in a cellular pathway controlling chromosome stability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20407210",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Fanconi anemia (FA) is a rare human genetic disease caused by mutations in any one of 13 known genes that encode proteins functioning in one common signaling pathway, the FA pathway, or in unknown genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23333482",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Fanconi anemia (FA) is a rare inherited recessive disease caused by mutations in one of fifteen genes known to encode FA pathway components."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15611632",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Fanconi anemia (FA) proteins function in a DNA damage response pathway that appears to be part of the network including breast cancer susceptibility gene products, BRCA1 and BRCA2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15611632",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Fanconi anemia (FA) proteins function in a DNA damage response pathway that appears to be part of the network including breast cancer susceptibility gene products, BRCA1 and BRCA2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20407210",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "Fanconi anemia (FA) is a rare human genetic disease caused by mutations in any one of 13 known genes that encode proteins functioning in one common signaling pathway, the FA pathway, or in unknown genes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15611632",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Fanconi anemia (FA) proteins function in a DNA damage response pathway that appears to be part of the network including breast cancer susceptibility gene products, BRCA1 and BRCA2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15611632",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Fanconi anemia (FA) proteins function in a DNA damage response pathway that appears to be part of the network including breast cancer susceptibility gene products, BRCA1 and BRCA2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17387268",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "The Fanconi anemia (FA) gene family comprises at least 12 genes interacting in a common pathway involved in DNA repair"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11157805",
"endSection": "abstract",
"offsetInBeginSection": 1171,
"offsetInEndSection": 1396,
"text": "These findings show that the newly identified FANCE protein is an integral part of the FA pathway, and support the concept of a functional link between all known proteins encoded by the genes that are mutated in this disorder"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15611632",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Fanconi anemia (FA) proteins function in a DNA damage response pathway that appears to be part of the network including breast cancer susceptibility gene products, BRCA1 and BRCA2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17387268",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "The Fanconi anemia (FA) gene family comprises at least 12 genes interacting in a common pathway involved in DNA repair"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11157805",
"endSection": "abstract",
"offsetInBeginSection": 1171,
"offsetInEndSection": 1396,
"text": "These findings show that the newly identified FANCE protein is an integral part of the FA pathway, and support the concept of a functional link between all known proteins encoded by the genes that are mutated in this disorder"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15611632",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Fanconi anemia (FA) proteins function in a DNA damage response pathway that appears to be part of the network including breast cancer susceptibility gene products, BRCA1 and BRCA2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20407210",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "Fanconi anemia (FA) is a rare human genetic disease caused by mutations in any one of 13 known genes that encode proteins functioning in one common signaling pathway, the FA pathway, or in unknown genes"
}
] | 5 |
BioASQ-training5b
|
[
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007165",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005199",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015398",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051856",
"http://www.disease-ontology.org/api/metadata/DOID:13636",
"http://www.disease-ontology.org/api/metadata/DOID:1062"
] |
[] |
54f42f2764850a5854000005
| 407 |
yesno
|
Is calcium overload involved in the development of diabetic cardiomyopathy?
|
['yes']
|
[
"yes"
] |
['Yes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22402252",
"http://www.ncbi.nlm.nih.gov/pubmed/8761317",
"http://www.ncbi.nlm.nih.gov/pubmed/3850773",
"http://www.ncbi.nlm.nih.gov/pubmed/10359740",
"http://www.ncbi.nlm.nih.gov/pubmed/8864644",
"http://www.ncbi.nlm.nih.gov/pubmed/3384188"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22402252",
"endSection": "sections.0",
"offsetInBeginSection": 800,
"offsetInEndSection": 1107,
"text": "High-glucose treatment resulted in increased intracellular calcium ([Ca2+]i) which was mobilized to the mitochondria. Concomitant intra-mitochondrial calcium ([Ca2+]m) increase resulted in enhanced reactive oxygen and nitrogen species generation. These events led to mitochondrial dysfunction and apoptosis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22402252",
"endSection": "sections.0",
"offsetInBeginSection": 1788,
"offsetInEndSection": 1965,
"text": "The novel findings of the study reveal that high glucose induces apoptosis by both mitochondria-dependent and independent pathways via concomitant rise in intracellular calcium."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8761317",
"endSection": "sections.0",
"offsetInBeginSection": 107,
"offsetInEndSection": 224,
"text": "Diabetes-induced myocardial dysfunction has been attributed, in part, to calcium overload within individual myocytes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3850773",
"endSection": "sections.0",
"offsetInBeginSection": 1136,
"offsetInEndSection": 1250,
"text": "It seems that intracellular calcium overload is intimately involved in the development of diabetic cardiomyopathy;"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10359740",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "BACKGROUND: It has been suggested that intracellular Ca2+ overload in cardiac myocytes leads to the development of diabetic cardiomyopathy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8864644",
"endSection": "sections.0",
"offsetInBeginSection": 858,
"offsetInEndSection": 1089,
"text": "The results from the alloxan-rat model of diabetes support the view that membrane abnormalities with respect to Ca2+ handling may lead to the occurrence of intracellular Ca2+ overload and the development of diabetic cardiomyopathy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3850773",
"endSection": "sections.0",
"offsetInBeginSection": 1136,
"offsetInEndSection": 1403,
"text": "It seems that intracellular calcium overload is intimately involved in the development of diabetic cardiomyopathy; however, a concentrated research effort is required to understand the primary biochemical lesion in the pathogenesis of cardiac dysfunction in diabetes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3384188",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "It has been suggested that the occurrence of an intracellular Ca2+ overload may result in the development of diabetic cardiomyopathy, which is associated with depletion of high-energy phosphate stores and a derangement of ultrastructure and cardiac dysfunction."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D058065",
"http://www.disease-ontology.org/api/metadata/DOID:9351",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002118",
"http://www.biosemantics.org/jochem#4071295"
] | null |
517139098ed59a060a000004
| 408 |
yesno
|
Are paralog genes co-regulated?
|
['yes']
|
[
"yes"
] |
['Paralog genes arise from gene duplication events during evolution, which often lead to similar proteins that cooperate in common pathways and in protein complexes. Consequently, paralogs show correlation in gene expression.', 'Co-regulation of paralog genes in the three-dimensional chromatin architecture. This enables concerted expression of paralogs over diverse cell-types and indicate evolutionary constraints in functional genome organization.', 'Co-regulation of paralog genes in the three-dimensional chromatin architecture. Consequently, paralogs show correlation in gene expression whereby the mechanisms of co-regulation remain unclear.', 'Co-regulation of paralog genes in the three-dimensional chromatin architecture. Consequently, paralogs show correlation in gene expression whereby the mechanisms of co-regulation remain unclear. In eukaryotes, genes are regulated in part by distal enhancer elements through looping interactions with gene promoters.', 'Yes. Paralogs share common regulatory mechanisms and cluster not only in the linear genome but also in the three-dimensional chromatin architecture. This enables concerted expression of paralogs over diverse cell-types and indicate evolutionary constraints in functional genome organization.', 'yes', 'Co-regulation of paralog genes in the three-dimensional chromatin architecture. In eukaryotes, genes are regulated in part by distal enhancer elements through looping interactions with gene promoters.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28667373",
"http://www.ncbi.nlm.nih.gov/pubmed/18493055",
"http://www.ncbi.nlm.nih.gov/pubmed/20621981",
"http://www.ncbi.nlm.nih.gov/pubmed/27634932",
"http://www.ncbi.nlm.nih.gov/pubmed/16860306",
"http://www.ncbi.nlm.nih.gov/pubmed/20482863"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27634932",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "Co-regulation of paralog genes in the three-dimensional chromatin architecture."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27634932",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 1452,
"text": "Consequently, paralogs show correlation in gene expression whereby the mechanisms of co-regulation remain unclear. In eukaryotes, genes are regulated in part by distal enhancer elements through looping interactions with gene promoters. These looping interactions can be measured by genome-wide chromatin conformation capture (Hi-C) experiments, which revealed self-interacting regions called topologically associating domains (TADs). We hypothesize that paralogs share common regulatory mechanisms to enable coordinated expression according to TADs. To test this hypothesis, we integrated paralogy annotations with human gene expression data in diverse tissues, genome-wide enhancer-promoter associations and Hi-C experiments in human, mouse and dog genomes. We show that paralog gene pairs are enriched for co-localization in the same TAD, share more often common enhancer elements than expected and have increased contact frequencies over large genomic distances. Combined, our results indicate that paralogs share common regulatory mechanisms and cluster not only in the linear genome but also in the three-dimensional chromatin architecture. This enables concerted expression of paralogs over diverse cell-types and indicate evolutionary constraints in functional genome organization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27634932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Paralog genes arise from gene duplication events during evolution, which often lead to similar proteins that cooperate in common pathways and in protein complexes. Consequently, paralogs show correlation in gene expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27634932",
"endSection": "abstract",
"offsetInBeginSection": 598,
"offsetInEndSection": 713,
"text": "We hypothesize that paralogs share common regulatory mechanisms to enable coordinated expression according to TADs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18493055",
"endSection": "abstract",
"offsetInBeginSection": 1240,
"offsetInEndSection": 1489,
"text": "Further, interspecific changes in testis bias of expression are generally correlated within the co-regulated pairs and are anti-correlated within the anti-regulated pairs, suggesting coordinated regulation within both types of paralogous gene pairs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18493055",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Analysis of the Drosophila melanogaster testes transcriptome reveals coordinate regulation of paralogous genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18493055",
"endSection": "abstract",
"offsetInBeginSection": 1240,
"offsetInEndSection": 1493,
"text": "Further, interspecific changes in testis bias of expression are generally correlated within the co-regulated pairs and are anti-correlated within the anti-regulated pairs, suggesting coordinated regulation within both types of paralogous gene pairs.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27634932",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 278,
"text": "Consequently, paralogs show correlation in gene expression whereby the mechanisms of co-regulation remain unclear."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27634932",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Co-regulation of paralog genes in the three-dimensional chromatin architecture."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18493055",
"endSection": "abstract",
"offsetInBeginSection": 1240,
"offsetInEndSection": 1490,
"text": "Further, interspecific changes in testis bias of expression are generally correlated within the co-regulated pairs and are anti-correlated within the anti-regulated pairs, suggesting coordinated regulation within both types of paralogous gene pairs.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27634932",
"endSection": "abstract",
"offsetInBeginSection": 923,
"offsetInEndSection": 1130,
"text": "We show that paralog gene pairs are enriched for co-localization in the same TAD, share more often common enhancer elements than expected and have increased contact frequencies over large genomic distances. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28667373",
"endSection": "abstract",
"offsetInBeginSection": 308,
"offsetInEndSection": 494,
"text": "MiRNA genes are often subject to co-evolutionary changes together with their target transcripts, which may be reflected by differences between paralog mouse and primate miRNA/mRNA pairs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20482863",
"endSection": "abstract",
"offsetInBeginSection": 506,
"offsetInEndSection": 626,
"text": "We characterize the collapse over time through the distribution of runs of reduced paralog pairs in duplicated segments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20621981",
"endSection": "abstract",
"offsetInBeginSection": 610,
"offsetInEndSection": 869,
"text": "In addition, we identified 81 co-regulated regions on the human genome (RIDGEs) by using expression data from all cancers. Some RIDGEs (28%) consist of paralog genes while another subset (30%) are specifically dysregulated in tumors but not in normal tissues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16860306",
"endSection": "abstract",
"offsetInBeginSection": 1254,
"offsetInEndSection": 1410,
"text": "We conclude that the similarity of hoxb3a/Hoxa3 regulatory mechanisms reflect the shared descent of both genes from a single ancestral paralog group 3 gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16860306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "Conserved co-regulation and promoter sharing of hoxb3a and hoxb4a in zebrafish."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18493055",
"endSection": "abstract",
"offsetInBeginSection": 511,
"offsetInEndSection": 839,
"text": "By analyzing paralogs of testis-biased genes, we identified \"co-regulated\" paralogous pairs in which both genes are testis biased, \"anti-regulated\" pairs in which one paralog is testis biased and the other downregulated in testes, and \"neutral\" pairs in which one paralog is testis biased and the other constitutively expressed."
}
] | 11 |
BioASQ-training11b
| null | null |
5a6e21b4b750ff445500003a
| 409 |
yesno
|
Is it safe to use Abatacept during pregnancy?
|
['no']
|
[
"no"
] |
Prophylactic withdrawal of drugs before pregnancy is mandatory for abatacept.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23292481",
"http://www.ncbi.nlm.nih.gov/pubmed/22772888",
"http://www.ncbi.nlm.nih.gov/pubmed/21985166",
"http://www.ncbi.nlm.nih.gov/pubmed/21346578",
"http://www.ncbi.nlm.nih.gov/pubmed/21120498",
"http://www.ncbi.nlm.nih.gov/pubmed/19506586",
"http://www.ncbi.nlm.nih.gov/pubmed/18504282"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23292481",
"endSection": "abstract",
"offsetInBeginSection": 480,
"offsetInEndSection": 777,
"text": "These patients were exposed to rituximab (anti-CD20 monoclonal antibody) or abatacept (fusion protein CTLA4Ig) during the first trimester of their pregnancies. No significant adverse effects or complications were observed during the pregnancies, and all three patients delivered healthy newborns. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23292481",
"endSection": "abstract",
"offsetInBeginSection": 947,
"offsetInEndSection": 1214,
"text": "Despite these favorable outcomes, the use of these two biological agents must follow international recommendations. Their use is not currently allowed during pregnancy except in cases where the potential benefit to the mother justifies the potential risk to the fetus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22772888",
"endSection": "abstract",
"offsetInBeginSection": 951,
"offsetInEndSection": 1265,
"text": "PREGNANCY: Azathioprine, chloroquine, cyclosporin A, prednisolone, sulfasalazine, tacrolimus and cyclophosphamide (only after the second trimester) may be administered during pregnancy. Biologics should be avoided unless there is a treatment need in cases of uncontrolled disease activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21985166",
"endSection": "abstract",
"offsetInBeginSection": 1052,
"offsetInEndSection": 1244,
"text": "As such, it is recommended that abatacept, rituximab and tocilizumab be withheld prior to pregnancy; however, tumour necrosis factor inhibitors and anakinra may be continued until conception. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21346578",
"endSection": "abstract",
"offsetInBeginSection": 843,
"offsetInEndSection": 926,
"text": "Case reports on abatacept, tocilizumab or anakinra in pregnancy are not conclusive."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21346578",
"endSection": "abstract",
"offsetInBeginSection": 1111,
"offsetInEndSection": 1333,
"text": "The very limited experience with abatacept, tocilizumab or anakinra in pregnancy allows no statement as to their compatibility with pregnancy. At present use of biological agents throughout pregnancy cannot be recommended."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21120498",
"endSection": "abstract",
"offsetInBeginSection": 494,
"offsetInEndSection": 642,
"text": "Drugs recommended to be stopped before pregnancy include methotrexate and leflunomide, plus the biologics: anti-TNF agents, rituximab and abatacept."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19506586",
"endSection": "abstract",
"offsetInBeginSection": 449,
"offsetInEndSection": 641,
"text": "Whereas methotrexate, leflunomide, abatacept and rituximab must be withdrawn before a planned pregnancy, tumor necrosis factor inhibitors and bisphosphonates can be continued until conception."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18504282",
"endSection": "abstract",
"offsetInBeginSection": 435,
"offsetInEndSection": 604,
"text": "Pregnancy experience with abatacept and rituximab is still too limited to prove their safety for the developing fetus. They must be withdrawn before a planned pregnancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18504282",
"endSection": "abstract",
"offsetInBeginSection": 874,
"offsetInEndSection": 976,
"text": "Prophylactic withdrawal of drugs before pregnancy is mandatory for abatacept, rituximab, LEF and MMF. "
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011247",
"http://www.biosemantics.org/jochem#4002070",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007565",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0060136"
] |
[] |
52bf1aa503868f1b06000006
| 410 |
yesno
|
Is the crystal structure of Pim-1 available?
|
['yes']
|
[
"yes"
] |
['Yes,\nThe crystal structures of Pim1 in apo form and bound with AMPPNP have been solved']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25575657",
"http://www.ncbi.nlm.nih.gov/pubmed/30033129",
"http://www.ncbi.nlm.nih.gov/pubmed/16227208",
"http://www.ncbi.nlm.nih.gov/pubmed/22339127",
"http://www.ncbi.nlm.nih.gov/pubmed/15808862",
"http://www.ncbi.nlm.nih.gov/pubmed/23936194",
"http://www.ncbi.nlm.nih.gov/pubmed/22926267"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16227208",
"endSection": "abstract",
"offsetInBeginSection": 505,
"offsetInEndSection": 673,
"text": "Recent crystallographic studies of Pim-1 have identified unique structural features but have not provided insight into how the kinase recognizes its target substrates. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30033129",
"endSection": "abstract",
"offsetInBeginSection": 351,
"offsetInEndSection": 454,
"text": "a co-crystal structure of lead molecule (HS38) in complex with DAPK3, a dual Pim/DAPK3 inhibitor (HS56)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25575657",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 425,
"text": "The crystal structure of this compound with PIM1 confirmed the predicted binding mode and protein-ligand interactions except those in the acidic ribose pocket. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22926267",
"endSection": "abstract",
"offsetInBeginSection": 422,
"offsetInEndSection": 690,
"text": "Using the determined X-ray crystal structure of PIM1 complexed to the compound 1-R as a control, we discuss the importance of including the protein flexibility inherent in the ensemble docking protocol, for the accuracy of the structure prediction of the bound state. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23936194",
"endSection": "abstract",
"offsetInBeginSection": 391,
"offsetInEndSection": 530,
"text": "Here, we describe the crystal structure of Pim1 in complex with a newly developed pyrido[4,3-d]pyrimidine-derivative inhibitor (SKI-O-068)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22339127",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 211,
"text": "Crystallographic and docking data analyses have been undertaken using inhibitor complexes "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15808862",
"endSection": "abstract",
"offsetInBeginSection": 378,
"offsetInEndSection": 459,
"text": "The crystal structures of Pim1 in apo form and bound with AMPPNP have been solved"
}
] | 11 |
BioASQ-training11b
| null | null |
5cb380b8ecadf2e73f00005d
| 413 |
yesno
|
Is there a role of regorafenib for sarcoma treatment?
|
['yes']
|
[
"yes"
] |
['Yes, there is evidence to suggest that regorafenib can be effective for sarcoma treatment. Clinical trials are under-way.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24266804",
"http://www.ncbi.nlm.nih.gov/pubmed/26266019",
"http://www.ncbi.nlm.nih.gov/pubmed/25301268",
"http://www.ncbi.nlm.nih.gov/pubmed/27751846",
"http://www.ncbi.nlm.nih.gov/pubmed/26907871",
"http://www.ncbi.nlm.nih.gov/pubmed/24756792",
"http://www.ncbi.nlm.nih.gov/pubmed/25884155"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26907871",
"endSection": "abstract",
"offsetInBeginSection": 809,
"offsetInEndSection": 862,
"text": "Regorafenib has been approved for third-line therapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25884155",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Study protocol of REGOSARC trial: activity and safety of regorafenib in advanced soft tissue sarcoma: a multinational, randomized, placebo-controlled, phase II trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25884155",
"endSection": "abstract",
"offsetInBeginSection": 1795,
"offsetInEndSection": 1972,
"text": "DISCUSSION: The design of this trial allows an assessment of regorafenib activity over placebo in four sarcoma strata and might provide evidence for launching a phase III trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26266019",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 533,
"text": "This case provides rationale for adding a Ewing sarcoma arm to SARC024, a phase II study of regorafenib, another multi-targeted kinase inhibitor, in patients with liposarcoma, osteosarcoma and Ewing and Ewing-like sarcomas (NCT02048371)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24266804",
"endSection": "abstract",
"offsetInBeginSection": 525,
"offsetInEndSection": 718,
"text": "Thus, the Phase III studies with pazopanib, regorafenib, muramyl tripeptide (MTP) and ridaforolimus are extensively discussed as well as the biological rationale for the use of these compounds."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24756792",
"endSection": "abstract",
"offsetInBeginSection": 726,
"offsetInEndSection": 935,
"text": "Currently, regorafenib is examined in several clinical trials (mostly phase II) in different tumor entities, including renal cell carcinoma (RCC), hepatocellular carcinoma (HCC), and soft tissue sarcoma (STS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301268",
"endSection": "abstract",
"offsetInBeginSection": 1674,
"offsetInEndSection": 1852,
"text": "Analysis of primary human sarcoma samples revealed direct cytotoxicity following exposure to sorafenib and regorafenib with a corresponding increase in ALDHbright cells (P<0.05)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301268",
"endSection": "abstract",
"offsetInBeginSection": 954,
"offsetInEndSection": 1299,
"text": "Parametric and non-parametric statistical analyses were performed as appropriate.RESULTS: After functionally validating the CSC phenotype of ALDHbright sarcoma cells, we observed that sorafenib and regorafenib were cytotoxic to sarcoma cell lines (P<0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P<0.05)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301268",
"endSection": "abstract",
"offsetInBeginSection": 595,
"offsetInEndSection": 1299,
"text": "We evaluated survival and CSC phenotype in mice harboring sarcoma metastases after TKI therapy. We exposed dissociated primary sarcoma tumors to sorafenib, regorafenib, and pazopanib, and we used tissue microarray (TMA) and primary sarcoma samples to evaluate the frequency and intensity of CSC markers after neoadjuvant therapy with sorafenib and pazopanib. Parametric and non-parametric statistical analyses were performed as appropriate.RESULTS: After functionally validating the CSC phenotype of ALDHbright sarcoma cells, we observed that sorafenib and regorafenib were cytotoxic to sarcoma cell lines (P<0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P<0.05)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301268",
"endSection": "abstract",
"offsetInBeginSection": 691,
"offsetInEndSection": 1299,
"text": "We exposed dissociated primary sarcoma tumors to sorafenib, regorafenib, and pazopanib, and we used tissue microarray (TMA) and primary sarcoma samples to evaluate the frequency and intensity of CSC markers after neoadjuvant therapy with sorafenib and pazopanib. Parametric and non-parametric statistical analyses were performed as appropriate.RESULTS: After functionally validating the CSC phenotype of ALDHbright sarcoma cells, we observed that sorafenib and regorafenib were cytotoxic to sarcoma cell lines (P<0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P<0.05)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301268",
"endSection": "abstract",
"offsetInBeginSection": 691,
"offsetInEndSection": 1396,
"text": "We exposed dissociated primary sarcoma tumors to sorafenib, regorafenib, and pazopanib, and we used tissue microarray (TMA) and primary sarcoma samples to evaluate the frequency and intensity of CSC markers after neoadjuvant therapy with sorafenib and pazopanib. Parametric and non-parametric statistical analyses were performed as appropriate.RESULTS: After functionally validating the CSC phenotype of ALDHbright sarcoma cells, we observed that sorafenib and regorafenib were cytotoxic to sarcoma cell lines (P<0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P<0.05). In contrast, we observed negligible effects on viability and CSC sub-populations with pazopanib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301268",
"endSection": "abstract",
"offsetInBeginSection": 1016,
"offsetInEndSection": 1275,
"text": "After functionally validating the CSC phenotype of ALDHbright sarcoma cells, we observed that sorafenib and regorafenib were cytotoxic to sarcoma cell lines (P < 0.05), with a corresponding 1.4 - 2.8 fold increase in ALDHbright cells from baseline (P < 0.05)."
}
] | 6 |
BioASQ-training6b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:1115",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012509",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012380"
] | null |
58848a13e56acf517600000d
| 414 |
yesno
|
Is amoxicillin used for treatment of malnutrition in children?
|
['yes']
|
[
"yes"
] |
['Yes, amoxicillin is used for treatment of malnutrition in children.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23326395",
"http://www.ncbi.nlm.nih.gov/pubmed/21836758",
"http://www.ncbi.nlm.nih.gov/pubmed/23755286",
"http://www.ncbi.nlm.nih.gov/pubmed/23363496",
"http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"http://www.ncbi.nlm.nih.gov/pubmed/18318945"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23326395",
"endSection": "abstract",
"offsetInBeginSection": 879,
"offsetInEndSection": 1478,
"text": " Another RCT did not show superiority of ceftriaxone over amoxicilllin for these same outcomes, but adressed SAM children with and without complications (p = 0.27). Another RCT showed no difference between amoxicillin and cotrimoxazole efficacies for pneumonia in underweight, but not SAM. Our meta-analysis of 12 pooled susceptibility-studies for all types of bacterial isolates, including 2767 stricly SAM children, favoured amoxicillin over cotrimoxazole for susceptibility medians: 42% (IQR 27-55%) vs 22% (IQR 17-23%) and population-weighted-means 52.9% (range 23-57%) vs 35.4% (range 6.7-42%)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23326395",
"endSection": "abstract",
"offsetInBeginSection": 1812,
"offsetInEndSection": 1875,
"text": " Susceptibility-studies favour amoxicillin over cotrimoxazole. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21836758",
"endSection": "abstract",
"offsetInBeginSection": 733,
"offsetInEndSection": 918,
"text": "Oral amoxicillin for 5 days was as effective as intramuscular ceftriaxone for 2 days (1 RCT). For uncomplicated SAM, amoxicillin showed no benefit over placebo (1 retrospective study). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23755286",
"endSection": "abstract",
"offsetInBeginSection": 1658,
"offsetInEndSection": 1864,
"text": "Children who took amoxicillin and de-worming had 95% (HR = 1.95, 95%-CI = 1.17, 3.23) and 74% (HR = 1.74, 95%-CI = 1.07, 2.83) more probability to recover from SAM as compared to those who didn't take them."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23363496",
"endSection": "abstract",
"offsetInBeginSection": 273,
"offsetInEndSection": 610,
"text": "METHODS: In this randomized, double-blind, placebo-controlled trial, we randomly assigned Malawian children, 6 to 59 months of age, with severe acute malnutrition to receive amoxicillin, cefdinir, or placebo for 7 days in addition to ready-to-use therapeutic food for the outpatient treatment of uncomplicated severe acute malnutrition. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23363496",
"endSection": "abstract",
"offsetInBeginSection": 772,
"offsetInEndSection": 1304,
"text": "In the amoxicillin, cefdinir, and placebo groups, 88.7%, 90.9%, and 85.1% of the children recovered, respectively (relative risk of treatment failure with placebo vs. amoxicillin, 1.32; 95% confidence interval [CI], 1.04 to 1.68; relative risk with placebo vs. cefdinir, 1.64; 95% CI, 1.27 to 2.11). The mortality rates for the three groups were 4.8%, 4.1%, and 7.4%, respectively (relative risk of death with placebo vs. amoxicillin, 1.55; 95% CI, 1.07 to 2.24; relative risk with placebo vs. cefdinir, 1.80; 95% CI, 1.22 to 2.64)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute malnutrition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 191,
"text": "OBJECTIVE: To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute malnutrition with ready-to-use therapeutic food."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 457,
"text": "The standard protocol group received a 7-day course of amoxicillin at the onset of treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 696,
"offsetInEndSection": 882,
"text": "RESULTS: Four hundred and ninety-eight children were treated according to the standard protocol with amoxicillin, and 1955 were treated under the alternate protocol without antibiotics. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 978,
"offsetInEndSection": 1179,
"text": "The recovery rate for children who received amoxicillin was worse at 4 weeks (40%vs. 71%) but similar after up to 12 weeks of therapy (84%vs. 86%), compared to the children treated without antibiotics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 1304,
"offsetInEndSection": 1500,
"text": "CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute malnutrition who were treated without amoxicillin did not have an inferior rate of recovery."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute malnutrition."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18318945",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Treatment of severe malnutrition with 2-day intramuscular ceftriaxone vs 5-day amoxicillin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute malnutrition with ready-to-use therapeutic food."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute malnutrition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute malnutrition with ready-to-use therapeutic food."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18318945",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Treatment of severe malnutrition with 2-day intramuscular ceftriaxone vs 5-day amoxicillin."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute malnutrition"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute malnutrition."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18318945",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Treatment of severe malnutrition with 2-day intramuscular ceftriaxone vs 5-day amoxicillin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 365,
"text": "OBJECTIVE: To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute malnutrition with ready-to-use therapeutic food. METHODS: This retrospective cohort study compared data from the treatment of two groups of children in Malawi aged 6-59 months with uncomplicated severe acute malnutrition. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 982,
"offsetInEndSection": 1506,
"text": "The recovery rate for children who received amoxicillin was worse at 4 weeks (40%vs. 71%) but similar after up to 12 weeks of therapy (84%vs. 86%), compared to the children treated without antibiotics. Regression modelling indicated that this difference at 4 weeks was most strongly associated with the receipt of amoxicillin. CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute malnutrition who were treated without amoxicillin did not have an inferior rate of recovery. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute malnutrition."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18318945",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Treatment of severe malnutrition with 2-day intramuscular ceftriaxone vs 5-day amoxicillin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 1309,
"offsetInEndSection": 1506,
"text": "CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute malnutrition who were treated without amoxicillin did not have an inferior rate of recovery. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute malnutrition."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18318945",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Treatment of severe malnutrition with 2-day intramuscular ceftriaxone vs 5-day amoxicillin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 365,
"text": "OBJECTIVE: To determine whether the inclusion of amoxicillin correlates with better recovery rates in the home-based treatment of severe acute malnutrition with ready-to-use therapeutic food. METHODS: This retrospective cohort study compared data from the treatment of two groups of children in Malawi aged 6-59 months with uncomplicated severe acute malnutrition. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 982,
"offsetInEndSection": 1506,
"text": "The recovery rate for children who received amoxicillin was worse at 4 weeks (40%vs. 71%) but similar after up to 12 weeks of therapy (84%vs. 86%), compared to the children treated without antibiotics. Regression modelling indicated that this difference at 4 weeks was most strongly associated with the receipt of amoxicillin. CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute malnutrition who were treated without amoxicillin did not have an inferior rate of recovery. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute malnutrition."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18318945",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Treatment of severe malnutrition with 2-day intramuscular ceftriaxone vs 5-day amoxicillin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 1309,
"offsetInEndSection": 1506,
"text": "CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute malnutrition who were treated without amoxicillin did not have an inferior rate of recovery. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Evaluation of the routine use of amoxicillin as part of the home-based treatment of severe acute malnutrition."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18318945",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Treatment of severe malnutrition with 2-day intramuscular ceftriaxone vs 5-day amoxicillin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20545919",
"endSection": "abstract",
"offsetInBeginSection": 1309,
"offsetInEndSection": 1506,
"text": "CONCLUSIONS: This review of two therapeutic feeding programmes suggests that children with severe acute malnutrition who were treated without amoxicillin did not have an inferior rate of recovery. "
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000658",
"http://www.biosemantics.org/jochem#4248866",
"http://www.biosemantics.org/jochem#4134180",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D044342",
"http://www.biosemantics.org/jochem#http://www.biosemantics.org/jochem#:4248866",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002648"
] |
[] |
56bb69d0ac7ad1001900000c
| 415 |
yesno
|
Are genes that escape X-chromosome inactivation related to mental impairment?
|
['yes']
|
[
"yes"
] |
['Yes. Genes that escape X-inactivation in humans have high intraspecific variability in expression, are associated with mental impairment but are not slow evolving.', 'Yes, most of the X-chromosome inactivation genes shown to be associated with mental retardation are those encoding transcription factors involved in intellectual disability, such as X-linked Na(+) /H(+) exchanger 2 (NHE2), Sox 10, Endothelin-3 (EDN3) and SOX10. Some X- chromosome inactivation gene variants are associated with intellectual disability but not others.', 'Genes that escape X-inactivation in humans have high intraspecific variability in expression, are associated with mental impairment but are not slow evolving. The newly described escape genes cluster on the X chromosome in the same chromosomal regions as the previously known escapees. There is an excess of escaping genes associated with mental retardation, consistent with this being a common phenotype of polyX phenotypes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24023392",
"http://www.ncbi.nlm.nih.gov/pubmed/17383248"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17383248",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Mutation screening of the MECP2 gene in a large cohort of 613 fragile-X negative patients with mental retardation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17383248",
"endSection": "abstract",
"offsetInBeginSection": 821,
"offsetInEndSection": 1079,
"text": "The first one, the double nucleotide substitution c.1162_1163delinsTA leading to a premature stop codon (p.Pro388X) was found in a female patient with random X-inactivation, presenting with borderline mental impairment without any features of Rett syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17383248",
"endSection": "abstract",
"offsetInBeginSection": 1095,
"offsetInEndSection": 1386,
"text": "the c.679C>G substitution, changing a glutamine to a glutamate in the transcriptional repression functional domain (p.Gln227Glu), was found in a female patient with a moderately biased X-chromosome inactivation profile and presenting with mild intellectual delay and minor psychotic features"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24023392",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Genes that escape X-inactivation in humans have high intraspecific variability in expression, are associated with mental impairment but are not slow evolving."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24023392",
"endSection": "abstract",
"offsetInBeginSection": 901,
"offsetInEndSection": 1168,
"text": " The newly described escape genes cluster on the X chromosome in the same chromosomal regions as the previously known escapees. There is an excess of escaping genes associated with mental retardation, consistent with this being a common phenotype of polyX phenotypes."
}
] | 11 |
BioASQ-training11b
| null | null |
5c72768a7c78d6947100006c
| 416 |
yesno
|
Are epigenetic changes heritable?
|
['yes']
|
[
"yes"
] |
['Epigenetics is defined as heritable changes in gene expression that are, unlike mutations, not attributable to alterations in the sequence of DNA. The predominant epigenetic mechanisms are DNA methylation, modifications to chromatin, loss of imprinting, and non-coding RNA. These epigenetic programs may account for a significant fraction of the "missing heritability" problem that is observed in genome-wide association studies.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31526982",
"http://www.ncbi.nlm.nih.gov/pubmed/24678826",
"http://www.ncbi.nlm.nih.gov/pubmed/29312436",
"http://www.ncbi.nlm.nih.gov/pubmed/33767749",
"http://www.ncbi.nlm.nih.gov/pubmed/29233676",
"http://www.ncbi.nlm.nih.gov/pubmed/18704881",
"http://www.ncbi.nlm.nih.gov/pubmed/30160987",
"http://www.ncbi.nlm.nih.gov/pubmed/22567405",
"http://www.ncbi.nlm.nih.gov/pubmed/34489118",
"http://www.ncbi.nlm.nih.gov/pubmed/27341739",
"http://www.ncbi.nlm.nih.gov/pubmed/10479537",
"http://www.ncbi.nlm.nih.gov/pubmed/19416939",
"http://www.ncbi.nlm.nih.gov/pubmed/27730435",
"http://www.ncbi.nlm.nih.gov/pubmed/32992597",
"http://www.ncbi.nlm.nih.gov/pubmed/27649584",
"http://www.ncbi.nlm.nih.gov/pubmed/25191382",
"http://www.ncbi.nlm.nih.gov/pubmed/17413852",
"http://www.ncbi.nlm.nih.gov/pubmed/20620207",
"http://www.ncbi.nlm.nih.gov/pubmed/30963999",
"http://www.ncbi.nlm.nih.gov/pubmed/18331347",
"http://www.ncbi.nlm.nih.gov/pubmed/21941617",
"http://www.ncbi.nlm.nih.gov/pubmed/20003072",
"http://www.ncbi.nlm.nih.gov/pubmed/26216216",
"http://www.ncbi.nlm.nih.gov/pubmed/33866814",
"http://www.ncbi.nlm.nih.gov/pubmed/22975443",
"http://www.ncbi.nlm.nih.gov/pubmed/25778758",
"http://www.ncbi.nlm.nih.gov/pubmed/20599773",
"http://www.ncbi.nlm.nih.gov/pubmed/21734376",
"http://www.ncbi.nlm.nih.gov/pubmed/25421652",
"http://www.ncbi.nlm.nih.gov/pubmed/34070712",
"http://www.ncbi.nlm.nih.gov/pubmed/29732172",
"http://www.ncbi.nlm.nih.gov/pubmed/20399890",
"http://www.ncbi.nlm.nih.gov/pubmed/20627830",
"http://www.ncbi.nlm.nih.gov/pubmed/30414795",
"http://www.ncbi.nlm.nih.gov/pubmed/33809396",
"http://www.ncbi.nlm.nih.gov/pubmed/22125494",
"http://www.ncbi.nlm.nih.gov/pubmed/32868918",
"http://www.ncbi.nlm.nih.gov/pubmed/11597505",
"http://www.ncbi.nlm.nih.gov/pubmed/33612870",
"http://www.ncbi.nlm.nih.gov/pubmed/17684399",
"http://www.ncbi.nlm.nih.gov/pubmed/27591071",
"http://www.ncbi.nlm.nih.gov/pubmed/34058565",
"http://www.ncbi.nlm.nih.gov/pubmed/22419988",
"http://www.ncbi.nlm.nih.gov/pubmed/27312865",
"http://www.ncbi.nlm.nih.gov/pubmed/24768945",
"http://www.ncbi.nlm.nih.gov/pubmed/20416204",
"http://www.ncbi.nlm.nih.gov/pubmed/18042143",
"http://www.ncbi.nlm.nih.gov/pubmed/14652236",
"http://www.ncbi.nlm.nih.gov/pubmed/35484099",
"http://www.ncbi.nlm.nih.gov/pubmed/17413847",
"http://www.ncbi.nlm.nih.gov/pubmed/36057300",
"http://www.ncbi.nlm.nih.gov/pubmed/32445090",
"http://www.ncbi.nlm.nih.gov/pubmed/31431820",
"http://www.ncbi.nlm.nih.gov/pubmed/23580343",
"http://www.ncbi.nlm.nih.gov/pubmed/32319122",
"http://www.ncbi.nlm.nih.gov/pubmed/31301046",
"http://www.ncbi.nlm.nih.gov/pubmed/25104823",
"http://www.ncbi.nlm.nih.gov/pubmed/18550486",
"http://www.ncbi.nlm.nih.gov/pubmed/34493403"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21734376",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 272,
"text": "Epigenetics is defined as heritable changes in gene expression that are, unlike mutations, not attributable to alterations in the sequence of DNA. The predominant epigenetic mechanisms are DNA methylation, modifications to chromatin, loss of imprinting and non-coding RNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26216216",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 665,
"text": "Genome-wide association studies of complex physiological traits and diseases consistently found that associated genetic factors, such as allelic polymorphisms or DNA mutations, only explained a minority of the expected heritable fraction. This discrepancy is known as \"missing heritability\", and its underlying factors and molecular mechanisms are not established. Epigenetic programs may account for a significant fraction of the \"missing heritability.\" Epigenetic modifications, such as DNA methylation and chromatin assembly states, reflect the high plasticity of the genome and contribute to stably alter gene expression without modifying genomic DNA sequences."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17413852",
"endSection": "abstract",
"offsetInBeginSection": 1385,
"offsetInEndSection": 1493,
"text": "Epigenetics is defined as heritable changes in gene expression that do not involve a change in DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17413852",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Epigenetics is defined as mitotically and meiotically heritable changes in gene expression that do not involve a change in the DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20620207",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Epigenetic changes refer to heritable changes that may modulate gene expression without affecting DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18042143",
"endSection": "abstract",
"offsetInBeginSection": 706,
"offsetInEndSection": 954,
"text": "Epigenetic alterations, which, by definition, comprise mitotically and meiotically heritable changes in gene expression that are not caused by changes in the primary DNA sequence, are increasingly being recognized for their roles in carcinogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32319122",
"endSection": "abstract",
"offsetInBeginSection": 378,
"offsetInEndSection": 597,
"text": "Unlike heritable genetic changes, which are always associated with mutations in gene sequence, heritable epigenetic changes can be associated with physical or chemical changes in molecules or only changes in the system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20416204",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "Epigenetic alterations are defined as heritable changes in gene expression mediated through mechanisms other than alterations in the DNA sequence itself, including DNA promoter methylation and various histone covalent modifications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18331347",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Epigenetics refers to heritable phenotypic alterations in the absence of DNA sequence changes, and DNA methylation is one of the extensively studied epigenetic alterations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25191382",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Epigenetics is defined as heritable changes that affect gene expression without altering the DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25104823",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "Epigenetics refers to heritable changes in patterns of gene expression that occur without alterations in DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27591071",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Epigenetic modifications are classified as heritable and reversible chemical modifications of chromatin that do not cause changes in DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33866814",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Epigenetics is the study of changes in gene activity that can be transmitted through cell divisions but cannot be explained by changes in the DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33866814",
"endSection": "abstract",
"offsetInBeginSection": 624,
"offsetInEndSection": 728,
"text": "First, some epigenetic states are transmitted intergenerationally and affect the phenotype of offspring."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33767749",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 379,
"text": "One possible but largely unexplored explanation is that exposure to sublethal doses of insecticides may alter epigenetic patterns that are heritable."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20620207",
"endSection": "abstract",
"offsetInBeginSection": 112,
"offsetInEndSection": 270,
"text": "DNA methylation is one such heritable epigenetic change, which is causally associated with the transcription regulation of many genes in the mammalian genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32319122",
"endSection": "abstract",
"offsetInBeginSection": 837,
"offsetInEndSection": 982,
"text": "As a result, heritable epigenetic changes can include any that can alter a wave such as changes in form, midline, frequency, amplitude, or phase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31431820",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 230,
"text": "Epigenetics has been defined as 'a stably heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence' and several epigenetic regulators are recurrently mutated in hematological malignancies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32868918",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 461,
"text": "Epigenetic alterations (epimutations) could thus contribute to heritable variation within populations and be subject to evolutionary processes such as natural selection and drift."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17684399",
"endSection": "abstract",
"offsetInBeginSection": 431,
"offsetInEndSection": 487,
"text": "Some of these epigenetic changes appear to be heritable."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33866814",
"endSection": "abstract",
"offsetInBeginSection": 623,
"offsetInEndSection": 728,
"text": " First, some epigenetic states are transmitted intergenerationally and affect the phenotype of offspring."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20003072",
"endSection": "abstract",
"offsetInBeginSection": 1301,
"offsetInEndSection": 1380,
"text": " First, stress-induced methylation changes are common and are mostly heritable."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10479537",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Epigenetic inheritance systems enable the environmentally induced phenotypes to be transmitted between generations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33612870",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 274,
"text": " Epigenetic changes enforced by various environmental and lifestyle factors lead to heritable modifications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27312865",
"endSection": "abstract",
"offsetInBeginSection": 293,
"offsetInEndSection": 417,
"text": " Transient epigenetic changes across the entire genome can influence metabolic outcomes and might or might not be heritable."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29233676",
"endSection": "abstract",
"offsetInBeginSection": 175,
"offsetInEndSection": 279,
"text": " More interestingly, epigenetic changes are reversible heritable changes which pass through generations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29312436",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 330,
"text": " However, it is unclear whether the active changes mediated by variations in DNA methyltransferase activity are heritable."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35484099",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 250,
"text": "Epigenetic modification refers to heritable changes in the genetic material without any changes in the nucleic acid sequence and results in heritable phenotypic changes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18550486",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "Epigenetics refers to the heritable, but reversible, regulation of various biological functions mediated principally through changes in DNA methylation and chromatin structure derived from histone modification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19416939",
"endSection": "abstract",
"offsetInBeginSection": 760,
"offsetInEndSection": 958,
"text": "Although epigenetic modifications may contribute substantially to average risk, they will not contribute much to recurrence risk and heritability unless they persist on average for many generations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24768945",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Epigenetic processes, defined as heritable changes in gene expression that occur without changes to the DNA sequence, have emerged as a promising area of cardiovascular disease research."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20627830",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 279,
"text": "Epigenetic changes can be defined as stable molecular alterations of a cellular phenotype such as the gene expression profile of a cell that are heritable during somatic cell divisions (and sometimes germ line transmissions) but do not involve changes of the DNA sequence itself."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21941617",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Epigenetic modifications are heritable changes in gene expression not encoded by the DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34058565",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Epigenetics is defined as the study of changes in gene function that are mitotically or meiotically heritable and do not lead to a change in DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11597505",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Epigenetic mechanisms are heritable traits that are mediated by changes in a genetic locus that do not involve a modification at the nucleotide level."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27649584",
"endSection": "abstract",
"offsetInBeginSection": 88,
"offsetInEndSection": 238,
"text": "ssion, notably during embryonic development. New research indicates that epigenetic factors are heritable, which is why paternal lifestyle may affect "
}
] | 12 |
BioASQ-training12b
| null | null |
644efd5157b1c7a315000086
| 417 |
yesno
|
Does triiodothyronine (T3) has cardiac angiogenic effects?
|
['Yes']
|
[
"Yes"
] |
['T3-induced cardiac sprouting angiogenesis in adult hypothyroid mice was associated with PDGF-BB, PDGFR-β and downstream activation of Akt.\nT(3) administration restored TRbeta mRNA expression level in AAC hearts to the control level.\nTRbeta in the coronary ECs regulates capillary density during cardiac development, and down-regulation of TRbeta results in coronary microvascular rarefaction during pathological hypertrophy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22681587",
"http://www.ncbi.nlm.nih.gov/pubmed/20100314",
"http://www.ncbi.nlm.nih.gov/pubmed/19286941",
"http://www.ncbi.nlm.nih.gov/pubmed/19074585",
"http://www.ncbi.nlm.nih.gov/pubmed/2530972"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22681587",
"endSection": "sections.0",
"offsetInBeginSection": 1664,
"offsetInEndSection": 1802,
"text": "T3-induced cardiac sprouting angiogenesis in adult hypothyroid mice was associated with PDGF-BB, PDGFR-β and downstream activation of Akt."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20100314",
"endSection": "sections.0",
"offsetInBeginSection": 916,
"offsetInEndSection": 1073,
"text": "L-T3 significantly increased angiogenesis and cell survival and enhanced the expression of nuclear-encoded transcription factors involved in these processes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074585",
"endSection": "sections.0",
"offsetInBeginSection": 761,
"offsetInEndSection": 854,
"text": "T(3) administration restored TRbeta mRNA expression level in AAC hearts to the control level."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074585",
"endSection": "sections.0",
"offsetInBeginSection": 907,
"offsetInEndSection": 1049,
"text": "Rbeta knockout and TRalpha/TRbeta double-knockout mice both exhibited significantly less capillary density in LV compared with wild-type mice."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074585",
"endSection": "sections.0",
"offsetInBeginSection": 1406,
"offsetInEndSection": 1597,
"text": "TRbeta in the coronary ECs regulates capillary density during cardiac development, and down-regulation of TRbeta results in coronary microvascular rarefaction during pathological hypertrophy."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014284",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0045766",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0045765",
"http://www.biosemantics.org/jochem#4275389",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D043925",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018919",
"http://www.biosemantics.org/jochem#4005955",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D043924",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011988",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0002040"
] | null |
513f4892bee46bd34c000014
| 418 |
yesno
|
Is mitofusin 2 a receptor for parkin?
|
['yes']
|
[
"yes"
] |
Yes, Mfn2 functions as a mitochondrial receptor for Parkin.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23958438",
"http://www.ncbi.nlm.nih.gov/pubmed/23845246",
"http://www.ncbi.nlm.nih.gov/pubmed/23620051",
"http://www.ncbi.nlm.nih.gov/pubmed/22914740",
"http://www.ncbi.nlm.nih.gov/pubmed/22807239",
"http://www.ncbi.nlm.nih.gov/pubmed/21252228",
"http://www.ncbi.nlm.nih.gov/pubmed/19076450",
"http://www.ncbi.nlm.nih.gov/pubmed/20871098"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23845246",
"endSection": "abstract",
"offsetInBeginSection": 113,
"offsetInEndSection": 283,
"text": "Recent work demonstrates that a phosphorylated form of the mitochondrial fusion protein Mitofusin 2 serves as a receptor for Parkin translocation to damaged mitochondria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23620051",
"endSection": "abstract",
"offsetInBeginSection": 421,
"offsetInEndSection": 563,
"text": "We show that the mitochondrial outer membrane guanosine triphosphatase mitofusin (Mfn) 2 mediates Parkin recruitment to damaged mitochondria. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23620051",
"endSection": "abstract",
"offsetInBeginSection": 1087,
"offsetInEndSection": 1201,
"text": "Mfn2 functions as a mitochondrial receptor for Parkin and is required for quality control of cardiac mitochondria."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20871098",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/MFN2_RAT",
"http://www.uniprot.org/uniprot/MFN2_HUMAN",
"http://www.uniprot.org/uniprot/MFN2_MOUSE",
"http://www.uniprot.org/uniprot/MARF_DROME",
"http://www.uniprot.org/uniprot/PACRG_HUMAN",
"http://www.uniprot.org/uniprot/PACRG_MOUSE"
] |
[
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},
{
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"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0673396"
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{
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{
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] |
5318352fb166e2b806000011
| 419 |
yesno
|
Can clonidine be used to reduce agitation in children.
|
['yes']
|
[
"yes"
] |
['Yes, clonidine is effective in prevention of post-anesthesia agitation in children.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23394604",
"http://www.ncbi.nlm.nih.gov/pubmed/21150631",
"http://www.ncbi.nlm.nih.gov/pubmed/20514964",
"http://www.ncbi.nlm.nih.gov/pubmed/18095969",
"http://www.ncbi.nlm.nih.gov/pubmed/17986032",
"http://www.ncbi.nlm.nih.gov/pubmed/17416907",
"http://www.ncbi.nlm.nih.gov/pubmed/17019218",
"http://www.ncbi.nlm.nih.gov/pubmed/16677266",
"http://www.ncbi.nlm.nih.gov/pubmed/16632814",
"http://www.ncbi.nlm.nih.gov/pubmed/16301230",
"http://www.ncbi.nlm.nih.gov/pubmed/14977793",
"http://www.ncbi.nlm.nih.gov/pubmed/12173195",
"http://www.ncbi.nlm.nih.gov/pubmed/11473855"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23394604",
"endSection": "sections.0",
"offsetInBeginSection": 861,
"offsetInEndSection": 1089,
"text": "Children receiving clonidine immediately after anesthesia induction had statistically significant improvement in postoperative agitation at the 15-minute mark (P = .096) and last score obtained (P = .095) using the Watcha scale."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21150631",
"endSection": "sections.0",
"offsetInBeginSection": 204,
"offsetInEndSection": 330,
"text": "Clonidine has proven to be effective in reducing the incidence of post-operative agitation at a higher dose (3 and 2 μg kg⁻¹)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21150631",
"endSection": "sections.0",
"offsetInBeginSection": 1200,
"offsetInEndSection": 1396,
"text": "Post-anaesthetic agitation was observed in two patients (6.6%) in group 1, eight patients (26.6%) in group 2 as compared to 12 patients (40%) in group 3 after 15 min of post-operative observation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21150631",
"endSection": "sections.0",
"offsetInBeginSection": 1397,
"offsetInEndSection": 1503,
"text": "The mean scores in group 1 at 15 and 30 min were significantly lower than those in group 3 (P value <0.05)"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21150631",
"endSection": "sections.0",
"offsetInBeginSection": 1630,
"offsetInEndSection": 1860,
"text": "Caudal clonidine at a lower dose (1 μg kg⁻¹) could be effective in reducing the incidence of sevoflurane-induced emergence agitation in children undergoing urogenital and lower limb surgery without any significant adverse effects."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17416907",
"endSection": "sections.0",
"offsetInBeginSection": 770,
"offsetInEndSection": 878,
"text": "Only the 4 microg kg-1 dose of clonidine was associated with a significant reduction in emergence agitation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17416907",
"endSection": "sections.0",
"offsetInBeginSection": 879,
"offsetInEndSection": 1001,
"text": "Fewer children in the clonidine 4 microg kg-1 group displayed agitation (25%) than in the midazolam group (60%) (P=0.025)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17416907",
"endSection": "sections.0",
"offsetInBeginSection": 1128,
"offsetInEndSection": 1276,
"text": "In comparison with midazolam, clonidine 4 microg kg-1 reduced sevoflurane-induced emergence agitation without increasing postoperative side-effects."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17019218",
"endSection": "sections.0",
"offsetInBeginSection": 1336,
"offsetInEndSection": 1450,
"text": "Prophylactic use of clonidine against sevoflurane-induced agitation may represent a new and promising application."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16677266",
"endSection": "sections.0",
"offsetInBeginSection": 888,
"offsetInEndSection": 1125,
"text": "One hundred and twenty children were included in this study: 59 of whom received clonidine, and 61 placebo; 41% of those in the placebo group exhibited moderate-severe EA compared with only 22% of those in the clonidine group (P < 0.03)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16677266",
"endSection": "sections.0",
"offsetInBeginSection": 1495,
"offsetInEndSection": 1690,
"text": "Findings demonstrate that i.v. clonidine administered after induction of anesthesia significantly reduces the incidence of EA in young children, but is associated with sleepiness postoperatively."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16632814",
"endSection": "sections.0",
"offsetInBeginSection": 921,
"offsetInEndSection": 981,
"text": "Clonidine could not prevent agitation (incidence 54%, 13/24)"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16632814",
"endSection": "sections.0",
"offsetInBeginSection": 1245,
"offsetInEndSection": 1337,
"text": "Clonidine 1.5 microg/kg did not differ from placebo with respect to postoperative agitation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16301230",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Clonidine is effective in treating sevoflurane-induced postanesthesia agitation in children."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16301230",
"endSection": "sections.0",
"offsetInBeginSection": 527,
"offsetInEndSection": 866,
"text": "Pain and discomfort scores were significantly decreased in the clonidine group; the incidence of agitation was reduced by 57% (P = 0.029) and the incidence of severe agitation by 67% (P = 0.064). Relative risks for developing agitation and severe agitation were 0.43 (95% confidence interval, 0.24-0.78) and 0.32 (0.09-1.17), respectively."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16301230",
"endSection": "sections.0",
"offsetInBeginSection": 867,
"offsetInEndSection": 963,
"text": "Clonidine produces a substantial reduction in the risk of postsevoflurane agitation in children."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14977793",
"endSection": "sections.0",
"offsetInBeginSection": 1011,
"offsetInEndSection": 1103,
"text": "Agitation was observed in 12 midazolam-treated and five clonidine-treated patients (P=0.05)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14977793",
"endSection": "sections.0",
"offsetInBeginSection": 1649,
"offsetInEndSection": 1745,
"text": "Compared with midazolam, clonidine premedication reduced agitation during sevoflurane induction."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12173195",
"endSection": "sections.0",
"offsetInBeginSection": 1351,
"offsetInEndSection": 1590,
"text": "Clonidine 3 micrograms kg-1 prevented agitation after sevoflurane anaesthesia, independently of the route of administration. The effect of clonidine appears to be dose-dependent, as an epidural dose of 1 microgram kg-1 failed to reduce it."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11473855",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "Clonidine prevents sevoflurane-induced agitation in children."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11473855",
"endSection": "sections.0",
"offsetInBeginSection": 482,
"offsetInEndSection": 563,
"text": "In 16 placebo and 2 clonidine-treated patients agitation was observed (P < 0.001)"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11473855",
"endSection": "sections.0",
"offsetInBeginSection": 565,
"offsetInEndSection": 723,
"text": "In 6 patients of the Placebo group, agitation was graded as severe, whereas none of the patients in the Clonidine group developed severe agitation (P = 0.02)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11473855",
"endSection": "sections.0",
"offsetInBeginSection": 857,
"offsetInEndSection": 944,
"text": "We conclude that clonidine effectively prevents agitation after sevoflurane anesthesia."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11473855",
"endSection": "sections.0",
"offsetInBeginSection": 1071,
"offsetInEndSection": 1239,
"text": "Clonidine 2 microg/kg IV after anesthetic induction effectively reduces the incidence of agitation without resulting in clinically relevant bradycardia and hypotension."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23394604",
"endSection": "sections.0",
"offsetInBeginSection": 1496,
"offsetInEndSection": 1730,
"text": "Children receiving clonidine prior to undergoing strabismus surgery have a small but noticeable reduction in postoperative agitation, stay slightly longer in the post-anesthesia care unit, and have higher rates of parent satisfaction."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18095969",
"endSection": "sections.0",
"offsetInBeginSection": 147,
"offsetInEndSection": 599,
"text": "We report three cases of preoperative use of intranasal clonidine in pediatric patients, all for different indications. One patient was treated for preoperative agitation and hallucinations associated with oral midazolam. One patient was given clonidine as a premedicant. The third patient was treated for preoperative agitation and hypertension. All three patients had subjective resolution of indicated symptoms and none experienced adverse outcomes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17019218",
"endSection": "sections.0",
"offsetInBeginSection": 389,
"offsetInEndSection": 532,
"text": "Oral or intravenous clonidine has been successfully used for the prevention of sevoflurane-induced agitation during emergence from anaesthesia."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003000",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002648",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011595"
] | null |
515df89e298dcd4e5100002f
| 420 |
yesno
|
Does GRHL2 over-expression lead to EMT?
|
['no']
|
[
"no"
] |
['Grainyhead-like 2 (Grhl2), a transcription factor, has been reported to be associated with several tumor processes including EMT. Grhl2 antagonizes transforming growth factor-b (TGFb)-induced EMT', 'The transcription factor--Grainyhead-like 2 (GRHL2) maintains the epithelial phenotype. Grhl2 is a suppressor of EMT. Grhl2 antagonizes transforming growth factor-b (TGFb)-induced EMT.', 'The transcription factor grainyhead-like 2 (GRHL2) plays a crucial role in various developmental processes Grhl2 antagonizes transforming growth factor-b (TGFb)-induced EMT']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26355710",
"http://www.ncbi.nlm.nih.gov/pubmed/26887977",
"http://www.ncbi.nlm.nih.gov/pubmed/27402864",
"http://www.ncbi.nlm.nih.gov/pubmed/28960866",
"http://www.ncbi.nlm.nih.gov/pubmed/23814079",
"http://www.ncbi.nlm.nih.gov/pubmed/23284647",
"http://www.ncbi.nlm.nih.gov/pubmed/28067907"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23284647",
"endSection": "abstract",
"offsetInBeginSection": 562,
"offsetInEndSection": 720,
"text": "Grhl2 is down-regulated in disseminated cancer cells that have undergone EMT, and over-expression of Grhl2 is sufficient to induce epithelial gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23284647",
"endSection": "abstract",
"offsetInBeginSection": 1239,
"offsetInEndSection": 1360,
"text": " Grhl2 plays an essential role in the determination of epithelial phenotype of breast cancers, EMT and tumor progression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23814079",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 955,
"text": "In breast cancer cell lines, shRNA-mediated knockdown of GRHL2 expression or functional inactivation of GRHL2 using dominant negative GRHL2 proteins induces down-regulation of ERBB3 gene expression, a striking reduction in cell proliferation, and morphological and phenotypical alterations characteristic of an epithelial-to-mesenchymal transition (EMT), thus implying contradictory roles of GRHL2 in breast carcinogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23814079",
"endSection": "abstract",
"offsetInBeginSection": 956,
"offsetInEndSection": 1312,
"text": "Interestingly, we could further demonstrate that expression of GRHL2 is directly suppressed by the transcription factor zinc finger enhancer-binding protein 1 (ZEB1), which in turn is a direct target for repression by GRHL2, suggesting that the EMT transcription factors GRHL2 and ZEB1 form a double negative regulatory feedback loop in breast cancer cells"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27402864",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Mesenchymal-Epithelial Transition in Sarcomas Is Controlled by the Combinatorial Expression of MicroRNA 200s and GRHL2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26887977",
"endSection": "abstract",
"offsetInBeginSection": 259,
"offsetInEndSection": 341,
"text": "transcription factor--Grainyhead-like 2 (GRHL2) maintains the epithelial phenotype"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28960866",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 262,
"text": "We explored the role of grainyhead-like 2 (GRHL2), a suppressor of EMT, in the progression of PDAC"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28960866",
"endSection": "abstract",
"offsetInBeginSection": 878,
"offsetInEndSection": 1009,
"text": "GRHL2 knockdown CFPAC-1 cells demonstrated morphological changes into mesenchymal appearances and reduced proliferation through EMT"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26355710",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "The transcription factor grainyhead-like 2 (GRHL2) plays a crucial role in various developmental processes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28067907",
"endSection": "abstract",
"offsetInBeginSection": 248,
"offsetInEndSection": 378,
"text": "Grainyhead-like 2 (Grhl2), a transcription factor, has been reported to be associated with several tumor processes including EMT. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28067907",
"endSection": "abstract",
"offsetInBeginSection": 957,
"offsetInEndSection": 1022,
"text": "Grhl2 antagonizes transforming growth factor-β (TGFβ)-induced EMT"
}
] | 11 |
BioASQ-training11b
| null | null |
5d384ce87bc3fee31f000013
| 421 |
yesno
|
Is there increased incidence of incontinence in athletes?
|
['yes']
|
[
"yes"
] |
['There is a very high prevalence of urinary incontinence in women athletes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23687004",
"http://www.ncbi.nlm.nih.gov/pubmed/23361854",
"http://www.ncbi.nlm.nih.gov/pubmed/23122895",
"http://www.ncbi.nlm.nih.gov/pubmed/21571270",
"http://www.ncbi.nlm.nih.gov/pubmed/21501085",
"http://www.ncbi.nlm.nih.gov/pubmed/20890872",
"http://www.ncbi.nlm.nih.gov/pubmed/20390664",
"http://www.ncbi.nlm.nih.gov/pubmed/19415493",
"http://www.ncbi.nlm.nih.gov/pubmed/18506324",
"http://www.ncbi.nlm.nih.gov/pubmed/17390923",
"http://www.ncbi.nlm.nih.gov/pubmed/16953954",
"http://www.ncbi.nlm.nih.gov/pubmed/15385857",
"http://www.ncbi.nlm.nih.gov/pubmed/15233598",
"http://www.ncbi.nlm.nih.gov/pubmed/11999199",
"http://www.ncbi.nlm.nih.gov/pubmed/11689727",
"http://www.ncbi.nlm.nih.gov/pubmed/10932809",
"http://www.ncbi.nlm.nih.gov/pubmed/8684695",
"http://www.ncbi.nlm.nih.gov/pubmed/8041527"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23687004",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 482,
"text": "Urinary incontinence affects women of all ages, including top female athletes, but is often under-reported. The highest prevalence of urinary incontinence is reported in those participating in high impact sports."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23361854",
"endSection": "abstract",
"offsetInBeginSection": 29,
"offsetInEndSection": 196,
"text": "The prevalence of female stress urinary incontinence is high, and young adults are also affected, including athletes, especially those involved in \"high-impact\" sports"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23122895",
"endSection": "abstract",
"offsetInBeginSection": 1841,
"offsetInEndSection": 2074,
"text": "Analysis of these data suggests that perineal pressure is decreased in female athletes compared with nonathlete women. A lower perineal pressure correlates with increased symptoms of urinary incontinence and pelvic floor dysfunction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21571270",
"endSection": "abstract",
"offsetInBeginSection": 943,
"offsetInEndSection": 1033,
"text": "Urinary incontinence is a prevalent condition among athletes that is not openly discussed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21501085",
"endSection": "abstract",
"offsetInBeginSection": 1464,
"offsetInEndSection": 1564,
"text": "High-level sport appears to be a significant independent risk factor for AI in healthy young women. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20890872",
"endSection": "abstract",
"offsetInBeginSection": 604,
"offsetInEndSection": 671,
"text": "The prevalence of LUTS was 54.7%, and 30% for urinary incontinence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20890872",
"endSection": "abstract",
"offsetInBeginSection": 1528,
"offsetInEndSection": 1583,
"text": "LUTS and incontinence are prevalent in female athletes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20390664",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "A relationship between sport or fitness activities and urinary incontinence (UI) previously has been described in women. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19415493",
"endSection": "abstract",
"offsetInBeginSection": 203,
"offsetInEndSection": 294,
"text": "studies have also shown a high prevalence of SUI in young, physically fit female athletes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18506324",
"endSection": "abstract",
"offsetInBeginSection": 727,
"offsetInEndSection": 830,
"text": "There was urinary incontinence in female long-distance runners and a correlation with eating disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17390923",
"endSection": "abstract",
"offsetInBeginSection": 31,
"offsetInEndSection": 136,
"text": "young female athletes participating in high-impact sports may be at higher risk for urinary incontinence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17390923",
"endSection": "abstract",
"offsetInBeginSection": 363,
"offsetInEndSection": 631,
"text": "Results indicated that more than 25% of those completing surveys experienced incontinence and that more than 90% had never told anyone about their problem and had no knowledge of preventive measures; 16% reported incontinence negatively impacted their quality of life."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16953954",
"endSection": "abstract",
"offsetInBeginSection": 1303,
"offsetInEndSection": 1377,
"text": "There is a very high prevalence of urinary incontinence in women athletes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15385857",
"endSection": "abstract",
"offsetInBeginSection": 697,
"offsetInEndSection": 832,
"text": "Women athletes should be counseled about the increased risk of urinary incontinence with ultra high-impact sports and eating disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15233598",
"endSection": "abstract",
"offsetInBeginSection": 606,
"offsetInEndSection": 1036,
"text": "Stress urinary incontinence is a barrier to women's participation in sport and fitness activities and, therefore, it may be a threat to women's health, self-esteem and well-being. The prevalence during sports among young, nulliparous elite athletes varies between 0% (golf) and 80% (trampolinists). The highest prevalence is found in sports involving high impact activities such as gymnastics, track and field, and some ball games"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11999199",
"endSection": "abstract",
"offsetInBeginSection": 1202,
"offsetInEndSection": 1330,
"text": "Urinary leakage is common among elite athletes and dancers, particularly during training, but also during daily life activities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11689727",
"endSection": "abstract",
"offsetInBeginSection": 1850,
"offsetInEndSection": 2064,
"text": "There is a high prevalence of stress and urge incontinence in female elite athletes. The frequency of SUI and urge incontinence was significantly higher in eating disordered athletes compared with healthy athletes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10932809",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1419,
"text": "High impact sports activities may produce urinary incontinence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8684695",
"endSection": "abstract",
"offsetInBeginSection": 825,
"offsetInEndSection": 906,
"text": "Urinary incontinence during physical stresses is common in young nulliparous wome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8041527",
"endSection": "abstract",
"offsetInBeginSection": 1307,
"offsetInEndSection": 1395,
"text": "Incontinence during physical stresses is common in young, highly fit, nulliparous women."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D056352",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014549",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014550"
] |
[] |
5361677c7d100faa09000008
| 423 |
yesno
|
Is pimavanserin a typical antipsychotic?
|
['no']
|
[
"no"
] |
['No, pimavanserin is an atypical antipsychotic.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29047301"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29047301",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 193,
"text": "Pimavanserin is the first FDA-approved atypical antipsychotic drug indicated for the treatment of hallucinations and delusions associated with Parkinson's disease psychosis (PDP)."
}
] | 11 |
BioASQ-training11b
| null | null |
5e2dbd0afbd6abf43b000017
| 424 |
yesno
|
Have chimeric antigen receptor (CAR)-T cell therapies been approved for the treatment of B cell malignancies?
|
['yes']
|
[
"yes"
] |
['Yes, four chimeric antigen receptor (CAR)-T cell therapies now approved for the treatment of B cell malignancies.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33833444"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33833444",
"endSection": "abstract",
"offsetInBeginSection": 345,
"offsetInEndSection": 592,
"text": "Engineered T cells have achieved success in the treatment of blood cancers, with four chimeric antigen receptor (CAR)-T cell therapies now approved for the treatment of B cell malignancies based on their unprecedented efficacy in clinical trials. "
}
] | 12 |
BioASQ-training12b
| null | null |
6415ca99690f196b51000019
| 425 |
yesno
|
Is BCL11B involved in schizophrenia?
|
['yes']
|
[
"yes"
] |
['Yes, BCL11B is associated with attention, memory, executive function and antipsychotic-induced schizophrenia.', 'Yes. SATB2 is associated with schizophrenia and is an important transcription factor regulating neocortical organization and circuitry. Rare mutations in SATB2 cause a syndrome that includes developmental delay, and mouse studies identify an important role for SATB2 in learning and memory. Interacting partners BCL11B and GATAD2A are also schizophrenia risk genes.', 'Yes. Exome sequencing studies have identified multiple genes harboring de novo loss-of-function (LoF) variants in individuals with schizophrenia, including BCL11B, a master regulator of cortical development, in patients with schizophrenia. BCL 11B is involved in the development of the central nervous system, and its deficiency or pharmacological neutralization may contribute to the onset of schizophrenia.', 'Yes. BCL11B is a transcriptional repressor essential for schizophrenia.', 'Yes. BCL11B is associated with early as well as with late onset schizophrenia.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30040823"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30040823",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 493,
"text": "Interacting partners BCL11B and GATAD2A are also schizophrenia risk genes indicating that other genes interacting with or are regulated by SATB2 are making a contribution to schizophrenia and cognition . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30040823",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 489,
"text": "Interacting partners BCL11B and GATAD2A are also schizophrenia risk genes indicating that other genes interacting with or are regulated by SATB2 are making a contribution to schizophrenia and cognition."
}
] | 11 |
BioASQ-training11b
| null | null |
5e2e0fa2fbd6abf43b00001f
| 426 |
yesno
|
Is nicotinamide effective for skin cancer prevention?
|
['yes']
|
[
"yes"
] |
['Yes, oral nicotinamide is safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"http://www.ncbi.nlm.nih.gov/pubmed/24798949",
"http://www.ncbi.nlm.nih.gov/pubmed/23349012",
"http://www.ncbi.nlm.nih.gov/pubmed/19804594",
"http://www.ncbi.nlm.nih.gov/pubmed/25561219"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 341,
"text": "Nicotinamide (vitamin B3) has been shown to have protective effects against damage caused by UV radiation and to reduce the rate of new premalignant actinic keratoses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1151,
"offsetInEndSection": 1820,
"text": "ESULTS: At 12 months, the rate of new nonmelanoma skin cancers was lower by 23% (95% confidence interval [CI], 4 to 38) in the nicotinamide group than in the placebo group (P=0.02). Similar differences were found between the nicotinamide group and the placebo group with respect to new basal-cell carcinomas (20% [95% CI, -6 to 39]lower rate with nicotinamide, P=0.12) and new squamous-cell carcinomas (30% [95% CI, 0 to 51] lower rate, P=0.05). The number of actinic keratoses was 11% lower in the nicotinamide group than in the placebo group at 3 months (P=0.01), 14% lower at 6 months (P<0.001), 20% lower at 9 months (P<0.001), and 13% lower at 12 months (P=0.001)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 2040,
"offsetInEndSection": 2192,
"text": "CONCLUSIONS: Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24798949",
"endSection": "abstract",
"offsetInBeginSection": 70,
"offsetInEndSection": 281,
"text": "Nicotinamide is a safe, widely available vitamin that reduces the immune suppressive effects of UV, enhances DNA repair in keratinocytes and has shown promise in the chemoprevention of non-melanoma skin cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24798949",
"endSection": "abstract",
"offsetInBeginSection": 871,
"offsetInEndSection": 1005,
"text": " In summary, nicotinamide, by enhancing DNA repair in melanocytes, is a potential agent for the chemoprevention of cutaneous melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23349012",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 385,
"text": "Recent double-blinded randomized controlled Phase 2 studies in heavily sun-damaged individuals have shown that oral nicotinamide significantly reduces premalignant actinic keratoses, and may reduce new non-melanoma skin cancers. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19804594",
"endSection": "abstract",
"offsetInBeginSection": 201,
"offsetInEndSection": 357,
"text": "Nicotinamide (vitamin B3) prevents UV-induced immunosuppression and carcinogenesis in mice, and solar-simulated (ss) UV-induced immunosuppression in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23349012",
"endSection": "abstract",
"offsetInBeginSection": 1714,
"offsetInEndSection": 1940,
"text": "These results show that nicotinamide enhances two different pathways for repair of UV-induced photolesions, supporting nicotinamide's potential as an inexpensive, convenient and non-toxic agent for skin cancer chemoprevention."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23349012",
"endSection": "abstract",
"offsetInBeginSection": 383,
"offsetInEndSection": 611,
"text": "Recent double-blinded randomized controlled Phase 2 studies in heavily sun-damaged individuals have shown that oral nicotinamide significantly reduces premalignant actinic keratoses, and may reduce new non-melanoma skin cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1821,
"offsetInEndSection": 2193,
"text": "No noteworthy between-group differences were found with respect to the number or types of adverse events during the 12-month intervention period, and there was no evidence of benefit after nicotinamide was discontinued.CONCLUSIONS: Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 612,
"text": "Nicotinamide (vitamin B3) has been shown to have protective effects against damage caused by UV radiation and to reduce the rate of new premalignant actinic keratoses.METHODS: In this phase 3, double-blind, randomized, controlled trial, we randomly assigned, in a 1:1 ratio, 386 participants who had had at least two nonmelanoma skin cancers in the previous 5 years to receive 500 mg of nicotinamide twice daily or placebo for 12 months. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1333,
"offsetInEndSection": 1597,
"text": "Similar differences were found between the nicotinamide group and the placebo group with respect to new basal-cell carcinomas (20% [95% CI, -6 to 39]lower rate with nicotinamide, P=0.12) and new squamous-cell carcinomas (30% [95% CI, 0 to 51] lower rate, P=0.05). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1821,
"offsetInEndSection": 2193,
"text": "No noteworthy between-group differences were found with respect to the number or types of adverse events during the 12-month intervention period, and there was no evidence of benefit after nicotinamide was discontinued.CONCLUSIONS: Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 612,
"text": "Nicotinamide (vitamin B3) has been shown to have protective effects against damage caused by UV radiation and to reduce the rate of new premalignant actinic keratoses.METHODS: In this phase 3, double-blind, randomized, controlled trial, we randomly assigned, in a 1:1 ratio, 386 participants who had had at least two nonmelanoma skin cancers in the previous 5 years to receive 500 mg of nicotinamide twice daily or placebo for 12 months. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1333,
"offsetInEndSection": 1597,
"text": "Similar differences were found between the nicotinamide group and the placebo group with respect to new basal-cell carcinomas (20% [95% CI, -6 to 39]lower rate with nicotinamide, P=0.12) and new squamous-cell carcinomas (30% [95% CI, 0 to 51] lower rate, P=0.05). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1821,
"offsetInEndSection": 2193,
"text": "No noteworthy between-group differences were found with respect to the number or types of adverse events during the 12-month intervention period, and there was no evidence of benefit after nicotinamide was discontinued.CONCLUSIONS: Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 612,
"text": "Nicotinamide (vitamin B3) has been shown to have protective effects against damage caused by UV radiation and to reduce the rate of new premalignant actinic keratoses.METHODS: In this phase 3, double-blind, randomized, controlled trial, we randomly assigned, in a 1:1 ratio, 386 participants who had had at least two nonmelanoma skin cancers in the previous 5 years to receive 500 mg of nicotinamide twice daily or placebo for 12 months. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1333,
"offsetInEndSection": 1597,
"text": "Similar differences were found between the nicotinamide group and the placebo group with respect to new basal-cell carcinomas (20% [95% CI, -6 to 39]lower rate with nicotinamide, P=0.12) and new squamous-cell carcinomas (30% [95% CI, 0 to 51] lower rate, P=0.05). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1821,
"offsetInEndSection": 2193,
"text": "No noteworthy between-group differences were found with respect to the number or types of adverse events during the 12-month intervention period, and there was no evidence of benefit after nicotinamide was discontinued.CONCLUSIONS: Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 612,
"text": "Nicotinamide (vitamin B3) has been shown to have protective effects against damage caused by UV radiation and to reduce the rate of new premalignant actinic keratoses.METHODS: In this phase 3, double-blind, randomized, controlled trial, we randomly assigned, in a 1:1 ratio, 386 participants who had had at least two nonmelanoma skin cancers in the previous 5 years to receive 500 mg of nicotinamide twice daily or placebo for 12 months. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1333,
"offsetInEndSection": 1597,
"text": "Similar differences were found between the nicotinamide group and the placebo group with respect to new basal-cell carcinomas (20% [95% CI, -6 to 39]lower rate with nicotinamide, P=0.12) and new squamous-cell carcinomas (30% [95% CI, 0 to 51] lower rate, P=0.05). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 1821,
"offsetInEndSection": 2193,
"text": "No noteworthy between-group differences were found with respect to the number or types of adverse events during the 12-month intervention period, and there was no evidence of benefit after nicotinamide was discontinued.CONCLUSIONS: Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 2021,
"offsetInEndSection": 2160,
"text": "Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Nicotinamide has shown potential as a safe and effective intervention for the prevention of malignant and premalignant skin lesions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 2021,
"offsetInEndSection": 2160,
"text": "Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Nicotinamide has shown potential as a safe and effective intervention for the prevention of malignant and premalignant skin lesions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 2021,
"offsetInEndSection": 2160,
"text": "Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Nicotinamide has shown potential as a safe and effective intervention for the prevention of malignant and premalignant skin lesions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19804594",
"endSection": "abstract",
"offsetInBeginSection": 1749,
"offsetInEndSection": 1853,
"text": "Nicotinamide, which protected against both UVB and UVA, is a promising agent for skin cancer prevention."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 2021,
"offsetInEndSection": 2160,
"text": "Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Nicotinamide has shown potential as a safe and effective intervention for the prevention of malignant and premalignant skin lesions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26488693",
"endSection": "abstract",
"offsetInBeginSection": 2021,
"offsetInEndSection": 2160,
"text": "Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25561219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Nicotinamide has shown potential as a safe and effective intervention for the prevention of malignant and premalignant skin lesions."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012878",
"http://www.disease-ontology.org/api/metadata/DOID:4159",
"http://www.disease-ontology.org/api/metadata/DOID:3451",
"http://www.biosemantics.org/jochem#http://www.biosemantics.org/jochem#:4273660",
"http://www.biosemantics.org/jochem#4273660"
] |
[] |
56c03d1fef6e39474100001a
| 427 |
yesno
|
Is deletion at 6q24.2-26 associated with longer survival of patients with high-grade serous ovarian carcinoma (HGSOCs)?
|
['yes']
|
[
"yes"
] |
['Yes. Loss at 6q24.2-26 was significantly associated with the cluster of longer survival independently from other confounding factors. The prognostic value of this deletion was validated in two independent series, one consisting of 36 HGSOCs analyzed by fluorescent in situ hybridization (P = 0.04) and another comprised of 411 HGSOCs from the Cancer Genome Atlas study (TCGA) (HR = 0.67, 95%CI = 0.48-0.93, Padj = 0.019).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25454820",
"http://www.ncbi.nlm.nih.gov/pubmed/26463438"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25454820",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Deletion at 6q24.2-26 predicts longer survival of high-grade serous epithelial ovarian cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25454820",
"endSection": "abstract",
"offsetInBeginSection": 602,
"offsetInEndSection": 1882,
"text": "We found that loss at 6q24.2-26 was significantly associated with the cluster of longer survival independently from other confounding factors (HR = 0.06, 95%CI = 0.01-0.43, Padj = 0.005). The prognostic value of this deletion was validated in two independent series, one consisting of 36 HGSOCs analyzed by fluorescent in situ hybridization (P = 0.04) and another comprised of 411 HGSOCs from the Cancer Genome Atlas study (TCGA) (HR = 0.67, 95%CI = 0.48-0.93, Padj = 0.019). In addition, we confirmed the association of low expression of the genes from the region with longer survival in 799 HGSOCs (HR = 0.74, 95%CI = 0.61-0.90, log-rank P = 0.002) and 675 high-FIGO stage HGSOCs (HR = 0.76, 95%CI = 0.61-0.96, log-rank P = 0.02) available from the online tool KM-plotter. Finally, by integrating copy number, RNAseq and survival data of 296 HGSOCs from TCGA we propose a few candidate genes that can potentially explain the association. Altogether our findings indicate that the 6q24.2-26 deletion is an independent marker of favorable outcome in HGSOCs with potential clinical value as it can be analyzed by FISH on tumor sections and guide the selection of patients towards more conservative therapeutic strategies in order to reduce side-effects and improve quality of life."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25454820",
"endSection": "abstract",
"offsetInBeginSection": 1542,
"offsetInEndSection": 1882,
"text": "Altogether our findings indicate that the 6q24.2-26 deletion is an independent marker of favorable outcome in HGSOCs with potential clinical value as it can be analyzed by FISH on tumor sections and guide the selection of patients towards more conservative therapeutic strategies in order to reduce side-effects and improve quality of life."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26463438",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 272,
"text": "OBJECTIVE\nWe aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene GTF2H5, which is localized at the 6q24.2-26 deletion previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26463438",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 272,
"text": "OBJECTIVE We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene GTF2H5, which is localized at the 6q24.2-26 deletion previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25454820",
"endSection": "abstract",
"offsetInBeginSection": 1542,
"offsetInEndSection": 1886,
"text": "Altogether our findings indicate that the 6q24.2-26 deletion is an independent marker of favorable outcome in HGSOCs with potential clinical value as it can be analyzed by FISH on tumor sections and guide the selection of patients towards more conservative therapeutic strategies in order to reduce side-effects and improve quality of life.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26463438",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 508,
"text": "<b>OBJECTIVE</b>: We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene GTF2H5, which is localized at the 6q24.2-26 deletion previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients.<br><b>METHODS</b>: In order to test if protein levels of GTF2H5 are associated with patients' outcome, we performed GTF2H5 immunohistochemical staining in 139 high-grade serous ovarian carcinomas included in tissue microarrays."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26463438",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "We aimed to evaluate the prognostic and predictive value of the nucleotide excision repair-related gene GTF2H5, which is localized at the 6q24.2-26 deletion previously reported by our group to predict longer survival of high-grade serous ovarian cancer patients."
}
] | 11 |
BioASQ-training11b
| null | null |
5c5b52731a4c55d80b000003
| 428 |
yesno
|
Can FOXOs modulate longevity?
|
['yes']
|
[
"yes"
] |
FOXOs are reliable markers of longevity.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22438832",
"http://www.ncbi.nlm.nih.gov/pubmed/22187289",
"http://www.ncbi.nlm.nih.gov/pubmed/21431325",
"http://www.ncbi.nlm.nih.gov/pubmed/21114762",
"http://www.ncbi.nlm.nih.gov/pubmed/21076489",
"http://www.ncbi.nlm.nih.gov/pubmed/20874444",
"http://www.ncbi.nlm.nih.gov/pubmed/20592766",
"http://www.ncbi.nlm.nih.gov/pubmed/19861158",
"http://www.ncbi.nlm.nih.gov/pubmed/19408108",
"http://www.ncbi.nlm.nih.gov/pubmed/19066462",
"http://www.ncbi.nlm.nih.gov/pubmed/18371346",
"http://www.ncbi.nlm.nih.gov/pubmed/18208360",
"http://www.ncbi.nlm.nih.gov/pubmed/18193389",
"http://www.ncbi.nlm.nih.gov/pubmed/15942449",
"http://www.ncbi.nlm.nih.gov/pubmed/15126506"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22438832",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Forkhead box O (FOXO) transcription factors have a conserved function in regulating metazoan lifespan."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22187289",
"endSection": "abstract",
"offsetInBeginSection": 1475,
"offsetInEndSection": 1641,
"text": "In contrast to FoxO1, FoxO3a and FoxO6 were specifically diminished in the CNS of HFD animals possibly contributing to the reduced lifespan observed in these animals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431325",
"endSection": "abstract",
"offsetInBeginSection": 1048,
"offsetInEndSection": 1291,
"text": "Interestingly, many target proteins of AMPK are so-called longevity factors, e.g., SIRT1, p53, and FoxOs, which not only can increase the stress resistance and extend the lifespan of many organisms but also inhibit the inflammatory responses. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21114762",
"endSection": "abstract",
"offsetInBeginSection": 373,
"offsetInEndSection": 437,
"text": "Components of anti-ageing and autophagy include SirTs and FoxOs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21076489",
"endSection": "abstract",
"offsetInBeginSection": 1659,
"offsetInEndSection": 1959,
"text": "Since Sirts and FoxOs are reliable markers of longevity, the results appear to suggest that Longevinex induces longevity after prolonged feeding via induction of autophagy, while it converts death signals into survival signals and provides cardioprotection within a relatively shorter period of time."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20874444",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Forkhead box O (FOXO) transcription factors are involved in various cellular processes, including cell proliferation, stress resistance, metabolism, and longevity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20592766",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 595,
"text": "In this respect, members of the mammalian forkhead transcription factors of the O class (FoxOs) that include FoxO1, FoxO3, FoxO4 and FoxO6 are increasingly being recognized as exciting prospects for multiple disorders. These transcription factors govern development, proliferation, survival and longevity during multiple cellular environments that can involve oxidative stress. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20592766",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1160,
"text": "Here we discuss the fascinating but complex role of FoxOs during cellular injury and oxidative stress, progenitor cell development, fertility, angiogenesis, cardiovascular function, cellular metabolism and diabetes, cell longevity, immune surveillance and cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19861158",
"endSection": "abstract",
"offsetInBeginSection": 813,
"offsetInEndSection": 896,
"text": "Many longevity genes, e.g. FoxOs and SIRT1, are inhibitors of NF-kappaB signaling. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19408108",
"endSection": "abstract",
"offsetInBeginSection": 954,
"offsetInEndSection": 1126,
"text": "Interestingly, several longevity genes such as SIRT1, SIRT6, and FoxOs can clearly suppress NF-kappaB signaling and in this way delay the aging process and extend lifespan."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19066462",
"endSection": "abstract",
"offsetInBeginSection": 548,
"offsetInEndSection": 772,
"text": "Yet, FoxOs also can significantly affect normal cell survival and longevity, requiring new treatments for neoplastic growth to modulate novel pathways that integrate cell proliferation, metabolism, inflammation and survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371346",
"endSection": "abstract",
"offsetInBeginSection": 460,
"offsetInEndSection": 897,
"text": "These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems. Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18208360",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 343,
"text": "Forkhead box O (FoxO) transcription factors are important downstream targets of the PI3K/Akt signaling pathway and crucial regulators of cell fate. This function of FoxOs relies on their ability to control diverse cellular functions, including proliferation, differentiation, apoptosis, DNA repair, defense against oxidative stress and ageing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18208360",
"endSection": "abstract",
"offsetInBeginSection": 619,
"offsetInEndSection": 872,
"text": "This brief review focuses on the molecular mechanisms, cellular effects and resulting organismal phenotypes generated by differentially regulated FoxO proteins and discusses our current understanding of the role of FoxOs in disease and ageing processes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18193389",
"endSection": "abstract",
"offsetInBeginSection": 624,
"offsetInEndSection": 957,
"text": "In this review, we focus on the several interactions of aging-associated signaling cascades regulated either by Sirtuins and FoxOs or NF-kappaB signaling pathways. We provide evidence that signaling via the longevity factors of FoxOs and SIRT1 can inhibit NF-kappaB signaling and simultaneously protect against inflamm-aging process."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15942449",
"endSection": "abstract",
"offsetInBeginSection": 509,
"offsetInEndSection": 846,
"text": "In diverse species transcription factors belonging to the forkhead/winged helix box gene, group O (FOXO) subfamily have been found to be crucial in downstream suppression of the life-shortening effects of insulin/insulin-like growth factor-I receptor signalling pathways that, when upregulated, accelerate ageing by suppression of FOXO. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15942449",
"endSection": "abstract",
"offsetInBeginSection": 1154,
"offsetInEndSection": 1293,
"text": "In humans, FOXO3a, as well as FOXO1 and -4, and their downstream effectors, could hold the key to counteracting ageing and common diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15126506",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "FOXO transcription factors have important roles in metabolism, cellular proliferation, stress tolerance, and aging. "
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008136",
"http://www.uniprot.org/uniprot/FOXO_DROGR",
"http://www.uniprot.org/uniprot/FOXO_DROWI",
"http://www.uniprot.org/uniprot/FOXO_CAEEL",
"http://www.uniprot.org/uniprot/FOXO_DROPS",
"http://www.uniprot.org/uniprot/FOXO_DROME",
"http://www.uniprot.org/uniprot/FOXO_DROAN",
"http://www.uniprot.org/uniprot/FOXO_DROPE",
"http://www.uniprot.org/uniprot/FOXO_DROSE",
"http://www.uniprot.org/uniprot/FOXO_DROVI",
"http://www.uniprot.org/uniprot/FOXO_DROYA",
"http://www.uniprot.org/uniprot/FOXO_DROER",
"http://www.uniprot.org/uniprot/FOXO_DROMO"
] |
[
{
"o": "http://linkedlifedata.com/resource/#_42344D42373800B",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/B4MB78"
},
{
"o": "GJ14344",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_42344D42373800B"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_42344D42373800A"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_42344D42373800B"
},
{
"o": "http://linkedlifedata.com/resource/#_42345054443300D",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/B4PTD3"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_42345054443300C"
},
{
"o": "GE24216",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_42345054443300D"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_42345054443300D"
},
{
"o": "http://linkedlifedata.com/resource/#_42344846363400D",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/B4HF64"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_42344846363400D"
},
{
"o": "GM24148",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_42344846363400D"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_42344846363400C"
},
{
"o": "http://linkedlifedata.com/resource/#_423350304B3600D",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/B3P0K6"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_423350304B3600C"
},
{
"o": "GG16833",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_423350304B3600D"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_423350304B3600D"
},
{
"o": "http://linkedlifedata.com/resource/#_42344B42463600B",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/B4KBF6"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_42344B42463600B"
},
{
"o": "GI21984",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_42344B42463600B"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_42344B42463600A"
},
{
"o": "http://linkedlifedata.com/resource/#_51323938573700B",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/Q298W7"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_51323938573700A"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_51323938573700B"
},
{
"o": "GA16248",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_51323938573700B"
},
{
"o": "http://linkedlifedata.com/resource/#_42344A53433200B",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/B4JSC2"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_42344A53433200A"
},
{
"o": "GH22274",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_42344A53433200B"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_42344A53433200B"
},
{
"o": "http://linkedlifedata.com/resource/#_42344734533800E",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/B4G4S8"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_42344734533800E"
},
{
"o": "GL24235",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_42344734533800E"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_42344734533800D"
},
{
"o": "C477334",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A3832745"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A3832745",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1311653"
},
{
"o": "FOXO protein, Drosophila",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A3832745"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A3832745",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C1311653"
},
{
"o": "MeSH",
"p": "http://www.w3.org/2004/02/skos/core#note",
"s": "http://linkedlifedata.com/resource/umls/label/A3832745"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A3832745",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1311653"
},
{
"o": "FOXO protein, Drosophila",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A3832745"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A3832745",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C1311653"
},
{
"o": "http://linkedlifedata.com/resource/#_42334C59533500D",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/B3LYS5"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_42334C59533500C"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_42334C59533500D"
},
{
"o": "GF16233",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_42334C59533500D"
},
{
"o": "http://linkedlifedata.com/resource/#_42344E46523100B",
"p": "http://purl.uniprot.org/core/encodedBy",
"s": "http://purl.uniprot.org/uniprot/B4NFR1"
},
{
"o": "foxo",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_42344E46523100B"
},
{
"o": "Forkhead box protein O",
"p": "http://purl.uniprot.org/core/fullName",
"s": "http://linkedlifedata.com/resource/#_42344E46523100A"
},
{
"o": "GK22687",
"p": "http://purl.uniprot.org/core/orfName",
"s": "http://linkedlifedata.com/resource/#_42344E46523100B"
}
] |
52b2ec944003448f55000002
| 429 |
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