nirantk/geneticsQA-train huggingface dataset:
Question: What is the effect of ranolazine in diastolic heart failure?

Context:
Data from in vitro and animal studies indicate that ranolazine improves diastolic function by inhibiting the late sodium current. 
Ranolazine is an innovative anti-ischemic and antianginal agent that inhibits the late Na current, thereby reducing the Na-dependent Ca-overload, which improves diastolic tone and oxygen handling during myocardial ischemia. In addition, ranolazine seems to exert beneficial effects on diastolic cardiac function. 
Ranolazine improves cardiac diastolic dysfunction through modulation of myofilament calcium sensitivity
Diastolic dysfunction could be reversed by ranolazine, probably resulting from a direct effect on myofilaments, indicating that cardiac oxidative stress may mediate diastolic dysfunction through altering the contractile apparatus.
Ranolazine (10 microM) significantly reduced the PC-induced increase in LVEDP by 72 +/- 6% (n = 6, p < 0.001), reduced left ventricular wall stiffness, and attenuated the PC-induced increase of CPP by 53 +/- 10% (n = 6-7, p < 0.05). 
 Ranolazine, a specific inhibitor of late INa, reduces Na influx and hence ameliorates disturbed Na and Ca homeostasis.
New clinical and experimental studies even point to potential antiarrhythmic effects, beneficial effects in diastolic heart failure, and under hyperglycemic conditions.

Answer: Data from in vitro and animal studies indicate that ranolazine improves diastolic function by inhibiting the late sodium current. Ranolazine is an innovative anti-ischemic and antianginal agent that reduces the Na-dependent Ca-overload, which improves diastolic tone and oxygen handling during myocardial ischemia. Furthermore, ranolazine improves cardiac diastolic dysfunction through modulation of myofilament calcium sensitivity.
Question: Is tirilazad effective for treatment of aneurysmal subarachnoid haemorrhage?

Context:
There was no significant difference between the two groups at the end of follow up for the primary outcome, death (odds ratio (OR) 0.89, 95% confidence interval (CI) 0.74 to 1.06), or in poor outcome (death, vegetative state or severe disability) (OR 1.04, 95% CI 0.90 to 1.21). During the treatment period, fewer patients developed delayed cerebral ischaemia in the tirilazad group than in the control group (OR 0.80, 95% CI 0.69 to 0.93). Subgroup analyses did not demonstrate any significant difference in effects of tirilazad on clinical outcomes. 
AUTHORS' CONCLUSIONS: There is no evidence that tirilazad, in addition to nimodipine, reduces mortality or improves poor outcome in patients with aneurysmal SAH.
This clinical trial suggest that tirilazad mesylate, at a dosage of 6 mg/kg/day, improves overall outcome in aneurysmal subarachnoid hemorrhage patients.
Tirilazad is ineffective.There are many possible successful treatment options for preventing vasospasm, delayed ischemic neurologic deficits, and poor neurologic outcome following aneurysmal subarachnoid hemorrhage; however, further multicenter RCTs need to be performed to determine if there is a significant benefit from their use
Findings from previous multicenter clinical trials have suggested that tirilazad mesylate, a synthetic nonhormonal 21-aminosteroid, might be effective in preventing delayed cerebral ischemia following subarachnoid hemorrhage (SAH).
This clinical trial suggest that tirilazad mesylate, at a dosage of 6 mg/kg/day, improves overall outcome in aneurysmal subarachnoid hemorrhage patients.

Answer: No. Based on meta-analysis, there is no evidence that tirilazad, in addition to nimodipine, reduces mortality or improves poor outcome in patients with aneurysmal subarachnoid haemorrhage.
Exact answer: no
Question: What do nerve-associated peripheral glial progenitors give rise to?

Context:
Parasympathetic neurons originate from nerve-associated peripheral glial progenitors.
We show that the parasympathetic system in mice--including trunk ganglia and the cranial ciliary, pterygopalatine, lingual, submandibular, and otic ganglia--arise from glial cells in nerves, not neural crest cells. The parasympathetic fate is induced in nerve-associated Schwann cell precursors at distal peripheral sites.
Neurodevelopment. Parasympathetic neurons originate from nerve-associated peripheral glial progenitors.
Parasympathetic neurons originate from nerve-associated peripheral glial progenitors
Neurodevelopment. Parasympathetic neurons originate from nerve-associated peripheral glial progenitors.

Answer: Nerve-associated peripheral glial progenitors give rise to parasympathetic neurons. The parasympathetic system in mice--including trunk ganglia and the cranial ciliary, pterygopalatine, lingual, submandibular, and otic ganglia--arise from glial cells in nerves, not neural crest cells. The parasympathetic fate is induced in nerve-associated Schwann cell precursors at distal peripheral sites.
Parasympathetic neurons originate from nerve-associated peripheral glial progenitors. The parasympathetic fate is induced in nerve-associated Schwann cell precursors at distal peripheral sites.
Parasympathetic neurons originate from nerve-associated peripheral glial progenitors.
Exact answer: Parasympathetic neurons
Question: Which is the  subcellular localization of ERAP2?

Context:
The human endoplasmic reticulum aminopeptidase (ERAP) 1 and 2 proteins 
They are categorized as a unique class of proteases based on their subcellular localization on the luminal side of the endoplasmic reticulum. 
endoplasmic reticulum aminopeptidase 2 (ERAP2) 
ERAP2 is a proteolytic enzyme set in the endoplasmic reticulum (ER) 
both A-LAP and L-RAP are retained in the endoplasmic reticulum

Answer: Endoplasmic reticulum aminopeptidase 2 (ERAP2) is localized to the luminal side of the endoplasmic reticulum.
Exact answer: luminal side of the endoplasmic reticulum
Question: Which genes does thyroid hormone receptor alpha1 regulate in the liver?

Context:
Mice expressing the mutant thyroid hormone receptor TRalpha1R384C, which has a 10-fold reduced affinity to the ligand T(3), exhibit hypermetabolism due to an overactivation of the sympathetic nervous system. To define the consequences in the liver, we analyzed hepatic metabolism and the regulation of liver genes in the mutant mice. Our results showed that hepatic phosphoenolpyruvate-carboxykinase was up-regulated and pyruvate kinase mRNA down-regulated, contrary to what observed after T(3) treatment
Remarkably, there was an obligatory requirement for a TR, whether TRbeta or TRalpha1, for any detectable D1 expression in liver.
Liver and kidney D1 mRNA and activity levels were reduced in TRbeta(-/-) but not TRalpha1(-/-) mice

Answer: phosphoenolpyruvate-carboxykinase"//
"pyruvate kinase"//
"D1", "deiodinase 1"//
Exact answer: phosphoenolpyruvate-carboxykinase, pyruvate kinase, D1, deiodinase 1
Question: Do conserved noncoding elements co-occur with matrix-attachment regions?

Context:
We hypothesized that some of these regions might be matrix-scaffold attachment regions, MARs (or S/MARs). MARs comprise one of the few classes of eukaryotic noncoding DNA with an experimentally characterized function, being involved in the attachment of chromatin to the nuclear matrix, chromatin remodeling and transcription regulation. To test our hypothesis, we analyzed the co-occurrence of predicted MARs with highly conserved noncoding DNA regions in human-mouse genomic alignments. We found that 11% of the conserved noncoding DNA consists of predicted MARs. Conversely, more than half of the predicted MARs co-occur with one or more independently identified conserved sequence blocks. An excess of conserved predicted MARs is seen in intergenic regions preceding 5' ends of genes, suggesting that these MARs are primarily involved in transcriptional control
A significant fraction of conserved noncoding DNA in human and mouse consists of predicted matrix attachment regions.
To test our hypothesis, we analyzed the co-occurrence of predicted MARs with highly conserved noncoding DNA regions in human-mouse genomic alignments.
To test our hypothesis, we analyzed the co-occurrence of predicted MARs with highly conserved noncoding DNA regions in human-mouse genomic alignments

Answer: Yes. It is estimated that 11% of the conserved noncoding DNA consists of predicted MARs. Conversely, more than half of the predicted MARs co-occur with one or more independently identified conserved sequence blocks. An excess of conserved predicted MARs is seen in intergenic regions preceding 5' ends of genes, suggesting that these MARs are primarily involved in transcriptional control.
Exact answer: yes
Question: Is there a relation between ANP and transcapillary albumin escape?

Context:
Thus, in a large ethnically homogeneous cohort of diabetic subjects, our data show: (1) a significant association of C708/T polymorphism with microalbuminuria in long-term diabetes and with both lower plasma ANP levels and widespread albumin leakage
hese results suggest a possible role of PND gene in conferring protection from nephropathy and microvascular damage in type 1 diabetes.
Moreover, the increased susceptibility of the glomerular capillaries in diabetics to ANP seems to be part of a more generalized capillary abnormality, because ANP also increases the transcapillary escape of albumin.
In summary, low dose ANP infusion in healthy subjects caused a shift of plasma water and electrolytes from the circulation, with albumin escape as a secondary phenomenon.

Answer: A possible role of ANP gene in conferring protection from nephropathy and microvascular damage in type 1 diabetes is present.
ANP infusion in healthy subjects caused a shift of plasma water and electrolytes from the circulation, with albumin escape as a secondary phenomenon
Exact answer: yes
Question: LY450139 is investigational name of which drug?

Context:
The outcomes of the clinical trials of the γ-secretase inhibitor Semagacestat (LY-450139) and the γ-secretase modulator (GSM) Tarenflurbil were disappointing, but may not represent the end of the γ-secretase era. 
A selective BACE inhibitor and the γ-secretase inhibitor LY450139 (semagacestat) were used to inhibit respective secretase.
ACS chemical neuroscience molecule spotlight on semagacestat (LY450139).
Semagacestat (LY450139) is a novel γ-secretase inhibitor currently in late-stage development by Eli Lilly and Company as a potential treatment for Alzheimer's disease (AD). 
 The γ-secretase inhibitor LY450139 (semagacestat) lowers plasma Aβ(1-40) and Aβ(1-42) in a dose-dependent manner but has no clear effect on the CSF level of these isoforms. 
TRODUCTION: LY450139 (semagacestat) inhibits gamma-secretase, a key enzyme for generation of amyloid beta (Abeta), the peptide deposited in plaques in Alzheimer disease (AD).
Two potent gamma-secretase inhibitors (GSIs), DAPT (N-[N-(3,5-difluorophenacetyl-L-alanyl)]-S-phenylglycine t-butyl ester) and LY450139 (hydroxylvaleryl monobenzocaprolactam), were found to reduce the density of dendritic spines in wild-type mice. 
velopment of semagacestat (LY450139), a functional gamma-secretase inhibitor, for the treatment of Alzheimer's disease.
OBJECTIVE: This paper reviews the pharmacology and chemical efficacy of an A beta-lowering agent, semagacestat (LY450139).
ACS chemical neuroscience molecule spotlight on semagacestat (LY450139).
 A selective BACE inhibitor and the γ-secretase inhibitor LY450139 (semagacestat) were used to inhibit respective secretase.

Answer: LY450139 is investigational name of Semagacestat. It is a γ-secretase inhibitor developed for treatment for Alzheimer's disease. Chemical name of LY450139 is hydroxylvaleryl monobenzocaprolactam.
Exact answer: semagacestat
Question: What is Creutzfeldt-Jakob Disease (CJD)?

Context:
Creutzfeldt-Jakob disease (CJD) is a rare, rapidly progressive, and fatal neurodegenerative disease affecting the central nervous system
Creutzfeldt-Jakob disease (sCJD) is the most prevalent of the human prion diseases, which are fatal and transmissible neurodegenerative diseases caused by the infectious prion protein (PrP(Sc)
The origin of sCJD is unknown, although the initiating event is thought to be the stochastic misfolding of endogenous prion protein (PrP(C)) into infectious PrP(Sc).
Creutzfeldt-Jakob disease (CJD) is a progressive, fatal, neurodegenerative disease classified under transmissible spongiform encephalopathies (TSE) or prion diseases
Sporadic Creutzfeldt-Jakob disease (CJD) is the most prevalent manifestation of the transmissible spongiform encephalopathies or prion diseases affecting humans
Creutzfeldt-Jakob disease (CJD) is a rare, degenerative and fatal brain disease that appears to be caused by an abnormal form of a protein called a prion.
Creutzfeldt-Jakob disease (CJD) is presumably caused by a slow infectious pathogen or prion. The principal clinical features of Creutzfeldt-Jakob disease are dementia, pyramidal and extrapyramidal symptoms and signs, cerebellar dysfunction, and myoclonus.
Creutzfeldt-Jakob disease (CJD) is a rapidly progressive, neurodegenerative disorder causing dramatic neuromuscular symptoms, profound dementia, and death.
Creutzfeldt-Jakob disease (CJD) is a rare neurodegenerative disorder.
Creutzfeldt-Jakob disease (CJD) is a rare neurodegenerative condition with a rapid disease course and a mortality rate of 100%.
Creutzfeldt-Jakob disease is a rare, but rapidly progressive, up to now untreatable and fatal neurodegenerative disorder
Creutzfeldt-Jakob disease is a rare neurodegenerative disease that belongs to the group of human spongiform encephalopathies and usually affects elderly people.
Creutzfeldt-Jakob disease (CJD) is a transmissible spongiform encephalopathy

Answer: Creutzfeldt-Jakob disease (CJD) is the most prevalent of the human prion diseases, which are fatal and transmissible neurodegenerative diseases caused by the infectious prion protein (PrP(Sc)). The origin of CJD is unknown, although the initiating event is thought to be the stochastic misfolding of endogenous prion protein (PrP(C)) into infectious PrP(Sc).
Creutzfeldt-Jakob disease (CJD) is a rare, rapidly progressive, and fatal neurodegenerative disease affecting the central nervous system Creutzfeldt-Jakob disease (sCJD) is the most prevalent of the human prion diseases, which are fatal and transmissible neurodegenerative diseases caused by the infectious prion protein (PrP(Sc)
Creutzfeldt-Jakob disease (CJD) is a rare, rapidly progressive, and fatal neurodegenerative disease affecting the central nervous system
Question: Is calcium overload involved in the development of diabetic cardiomyopathy?

Context:
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.
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.
Diabetes-induced myocardial dysfunction has been attributed, in part, to calcium overload within individual myocytes.
It seems that intracellular calcium overload is intimately involved in the development of diabetic cardiomyopathy;
BACKGROUND: It has been suggested that intracellular Ca2+ overload in cardiac myocytes leads to the development of diabetic cardiomyopathy.
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.
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.
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.

Answer: Yes.
Exact answer: yes
Question: List all articles on network meta-analysis for smoking cessation

Context:
Cardiovascular events associated with smoking cessation pharmacotherapies: a network meta-analysis.
Pharmacological interventions for smoking cessation: an overview and network meta-analysis.
Effectiveness and cost-effectiveness of computer and other electronic aids for smoking cessation: a systematic review and network meta-analysis.
network meta-analysis on interventions for smoking cessation including over 100 trials
Smoking cessation interventions in COPD: a network meta-analysis of randomised trials.

Answer: Cardiovascular events associated with smoking cessation pharmacotherapies: a network meta-analysis.
Pharmacological interventions for smoking cessation: an overview and network meta-analysis
Effectiveness and cost-effectiveness of computer and other electronic aids for smoking cessation: a systematic review and network meta-analysis.
Smoking cessation interventions in COPD: a network meta-analysis of randomised trials.
Exact answer: Cardiovascular events associated with smoking cessation pharmacotherapies: a network meta-analysis.
Pharmacological interventions for smoking cessation: an overview and network meta-analysis
Effectiveness and cost-effectiveness of computer and other electronic aids for smoking cessation: a systematic review and network meta-analysis.
Smoking cessation interventions in COPD: a network meta-analysis of randomised trials.
Question: What is the suggested clinical management of Fanconi anemia?

Context:
Hematopoietic stem cell transplantation is the only proven cure for the hematopoietic manifestations of FA and aggressive lifelong surveillance for solid tumors is essential.
Bone marrow surveillance is an important part of the clinical management of FA and often reveals cytogenetic aberrations
In patients with FA, there is a high incidence of aggressive HNSCC at a young age. Surgery remains the mainstay of treatment because patients with FA tolerate radiation therapy and chemotherapy poorly, with significant morbidity

Answer: Hematopoietic stem cell transplantation is the only proven cure for the hematopoietic manifestations of FA and aggressive lifelong surveillance for solid tumors is essential.In patients with FA, there is a high incidence of aggressive HNSCC at a young age. Surgery remains the mainstay of treatment because patients with FA tolerate radiation therapy and chemotherapy poorly, with significant morbidity
Hematopoietic stem cell transplantation is the only proven cure for the hematopoietic manifestations of FA and aggressive lifelong surveillance for solid tumors is essential. Surgery remains the mainstay of treatment because patients with FA tolerate radiation therapy and chemotherapy poorly, with significant morbidity. In patients with FA, there is a high incidence of aggressive HNSCC at a young age. Bone marrow surveillance is an important part of the clinical management of FA and often reveals cytogenetic aberrations. 
Hematopoietic stem cell transplantation is the only proven cure for the hematopoietic manifestations of FA and aggressive lifelong surveillance for solid tumors is essential.
Surgery remains the mainstay of treatment because patients with FA tolerate radiation therapy and chemotherapy poorly, with significant morbidity. In patients with FA, there is a high incidence of aggressive HNSCC at a young age. Hematopoietic stem cell transplantation is the only proven cure for the hematopoietic manifestations of FA and aggressive lifelong surveillance for solid tumors is essential. Bone marrow surveillance is an important part of the clinical management of FA and often reveals cytogenetic aberrations.
Question: Is Rheumatoid Arthritis related to myopathy?

Context:
Prevalence of risk factors for statin-induced myopathy in rheumatoid arthritis patients
we describe a patient with rheumatoid arthritis and respiratory failure associated with proximal myopathy secondary to HCQ
Occurrence of chloroquine-induced myopathy after low-dose treatment of rheumatoid arthritis for seven years
a 75 year old female with rheumatoid arthritis treated with daily doses of 250 mg of chloroquine for four years. The patient visited because of several months history of predominantly proximal progressive tetraparesis with areflexia
Myopathy and neuropathy in rheumatoid arthritis
with rheumatoid arthritis (RA) have clinical or subclinical evidence of peripheral neuropathy or myopathy
The study reveals an increased prevalence of neurogenic but not myogenic changes in patients with RA compared with controls

Answer: Vacuolar myopathy and statin-induced myopathy have been reported in rheumatoid arthritis patients, but this association may be due to the anti-malarial treatment received. An increased prevalence of neurogenic but not myogenic changes in patients with RA compared with controls has been reported.
Exact answer: yes
Question: Which histone modifications distinguish between promoters and enhancers?

Context:
Here, we used chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) to measure genome-wide changes in histone H3 acetylation at lysine 27 (H3K27ac), a marker of active enhancers, in unstimulated HUVECs and HUVECs stimulated with VEGFA for 1, 4, and 12 h.
Here we use whole-transcriptome analysis coupled with genome-wide profiling of H3K27ac and H3K27me3 to map chromatin states and enhancers in mouse embryonic forelimb and hindlimb.
Using H3K27ac profiles, we identified 28,377 putative enhancers, many of which are likely to be limb specific based on strong enrichment near genes highly expressed in the limb and comparisons with tissue-specific EP300 sites and known enhancers. 
a chromatin state signature associated with active developmental enhancers, defined by high levels of H3K27ac marking, nucleosome displacement, hypersensitivity to sonication, and strong depletion of H3K27me3
We also find that some developmental enhancers exhibit components of this signature, including hypersensitivity, H3K27ac enrichment, and H3K27me3 depletion, at lower levels in tissues in which they are not active.
At some locations, H3K27 monomethylation was also found to be associated with chromatin signatures of gene enhancers.
Individual chromatin marks, such as H3K27ac and H3K27me3, have been identified to distinguish active from inactive enhancers. 
We find that histone H3K27ac distinguishes active enhancers from inactive/poised enhancer elements containing H3K4me1 alone. 
Although certain chromatin features, such as the histone acetyltransferase P300 and the histone modification H3K4me1, indicate the presence of enhancers, only a fraction of enhancers are functionally active. Individual chromatin marks, such as H3K27ac and H3K27me3, have been identified to distinguish active from inactive enhancers.
We find that histone H3K27ac distinguishes active enhancers from inactive/poised enhancer elements containing H3K4me1 alone.

Answer: H3K27ac is a marker of active enhancers. An enhancer chromatin state signature associated with active developmental enhancers may be defined by high levels of H3K27ac marking, nucleosome displacement, hypersensitivity to sonication, and strong depletion of H3K27me3.
Exact answer: H3K27ac enrichment, H3K27me3 depletion