nirantk/geneticsQA-train huggingface dataset:
Question: What is the mechanism of action of DNA topoisomerase II inhibitors?

Context:
DNA topoisomerase II inhibitors are a major class of cancer chemotherapeutics, which are thought to eliminate cancer cells by inducing DNA double-strand breaks.
We show that anthracyclines promote histone eviction irrespective of their ability to induce DNA double-strand breaks. The histone variant H2AX, which is a key component of the DNA damage response, is also evicted by anthracyclines, and H2AX eviction is associated with attenuated DNA repair.
Induction of apoptotic cell death by DNA topoisomerase II inhibitors
The results we have obtained clearly indicate that topoisomerase II poisons induce cell death by apoptosis.
Histone eviction deregulates the transcriptome in cancer cells
We define a novel mechanism of action of anthracycline anticancer drugs doxorubicin and daunorubicin on chromatin biology, with important consequences for DNA damage responses, epigenetics, transcription

Answer: DNA topoisomerase II inhibitors eliminate cancer cells by causing DNA double-strand breaks, finally leading to apoptotic cell death. Moreover, drug-induced histone eviction was also shown to be associated with attenuated DNA repair, epigenetic changes and transcpription deregulation.
Question: is pharmacological treatment of subclinical hypothyroidism effective in reducing cardiovascular events?

Context:
The decision to treat elderly people is still an unresolved clinical challenge--first, due to a lack of appropriately powered randomized controlled trials of L-T4 in sHT patients, examining cardiovascular hard endpoints in various classes of age; and second, because of the negative effects of possible overtreatment.
The lack of specific randomized trials enrolling either old or very old subjects, aimed at evaluate the efficacy of hormonal replacement on overall survival and cardiovascular risk reduction along with the negative effects of possible over-treatment, makes the decision to treat older people a still unresolved clinical challenge
In patients with type 2 DM, the presence of SH serves as an additional risk factor for endothelial dysfunction.
Treatment of SCH with levothyroxine was associated with fewer IHD events in younger individuals, but this was not evident in older people.
Subclinical hyperthyroidism seems to be a risk factor of developing major cardiovascular events, especially stroke in older adults from the general population with normal left ventricular function.
SCH appears to influence the postoperative outcome for patients by increasing the development of postoperative atrial fibrillation. However, it is still unproven whether preoperative thyroxine replacement therapy for patients with SCH might prevent postoperative atrial fibrillation after CABG.
In CHF patients TSH levels even slightly above normal range are independently associated with a greater likelihood of heart failure progression.
In current RCTs, levothyroxine replacement therapy for subclinical hypothyroidism did not result in improved survival or decreased cardiovascular morbidity. Data on health-related quality of life and symptoms did not demonstrate significant differences between intervention groups.
However, the actual effectiveness of thyroid hormone substitution in reducing the risk of cardiovascular events remains to be elucidated. In conclusion, the multiplicity and the possible reversibility of subclinical hypothyroidism-associated cardiovascular abnormalities suggest that the decision to treat a patient should depend on the presence of risk factors, rather than on a TSH threshold. 
However, whether SH confers a high risk for cardiovascular disease, and whether LT4 therapy has a long-term benefit that clearly outweighs the risks of overzealous treatment in these individuals, remain topics of controversy.

Answer: whether SH confers a high risk for cardiovascular disease, and whether LT4 therapy has a long-term benefit that clearly outweighs the risks of overzealous treatment in these individuals, remain topics of controversy.
Exact answer: no
Question: Describe clinical applications of the PIM2 scoring system.

Context:
In this study, we examine if transfusion is an independent predictor of mortality, or if outcomes are merely a result of the initial severity as predicted by Pediatric Risk of Mortality (PRISM) III, Pediatric Index of Mortality (PIM2), and day 1 Pediatric Logistic Organ Dysfunction (PELOD) scores.
INTRODUCTION: The Pediatric Index of Mortality 2 (PIM2) is one of the most commonly used scoring systems to predict mortality in patients admitted to pediatric intensive care units (PICU) in Argentina.
CONCLUSIONS: The PIM2 score adequately discriminates survivors from non-survivors.
PIM2 scoring did not explain the outcome adequately, suggesting need for recalibration.
CONCLUSION: PIM2 scoring system show adequate discriminatory function and well calibrated for the case mix of patients in PICU of Fayoum, Egypt. It can be used as beneficial tool for evaluation of risk adjusted mortality. 
The aim of the study was to explore the association between Glasgow Coma Scale (GCS), Paediatric Index of Mortality (PIM2) and Injury Severity Score (ISS), and the long-term outcome of children with injuries.
Pediatric index of mortality 2 score as an outcome predictor in pediatric Intensive Care Unit in India.
BACKGROUND AND AIMS: Pediatric index of mortality (PIM) 2 score is one of the severity scoring systems being used for predicting outcome of patients admitted to intensive care units (ICUs).
CONCLUSION: PIM2 score discriminated well between survivors and death at PICU.
OBJECTIVE: A study to validate and calibrate Pediatric Index of Mortality-2 (PIM2) in children admitted to our pediatric intensive care unit (PICU).
CONCLUSION: PIM2 is a good index for prediction of mortality in our pediatric intensive care unit. 
The Pediatric Index of Mortality 2 (PIM2) is one of the most commonly used scoring systems to predict mortality in patients admitted to pediatric intensive care units (PICU) in Argentina.
Pediatric Index of Mortality 2 (PIM2) and Pediatric Risk of Mortality (PRISM) are scoring systems to predict mortality likehood; thus, it is necessary to validate such predictors in Pediatric Intensive Care Units' population.
Although PRISM, PIM and PIM2 have displayed good discrimination and calibration in the present setting, PIM is considered as the most accurate and appropriate tool for predicting mortality in the studied NICU.
The PIM2 score adequately discriminates survivors from non-survivors.

Answer: The Pediatric Index of Mortality 2 (PIM2) is one of the most commonly used scoring systems to predict mortality in patients admitted to pediatric intensive care units. The PIM2 score adequately discriminates survivors from non-survivor
Question: Which substances are dangerous to g6PD deficient individuals?

Context:
The principal clinical manifestation encountered was favism.
G6PD deficiency is the most common enzymopathy of red blood cells. The clinical symptoms of favism are jaundice, hematuria and haemolytic anaemia that seem to affect liver and kidney in long term. Thus we evaluate kidney and liver function of favism patients in an endemic area of the disease with a high rate of fava beans cultivation. 

Answer: Antimalarial drugs (primaquine, pamaquine, chloriquine), fava beans, sulfonamides, some antibiotics( nalidixic acid, nitrofurantoin, isoniazid, dapsone, and furazolidone) and henna
Exact answer: primaquine, pamaquine, chloroquine, fava beans, sulfonamides, antibiotics, henna
Question: Is curcumin a phytochemical?

Context:
we analyzed turmeric from different agroclimatic regions for influence of various factors on its growth and yield of important phytochemicals
The phytochemical, curcumin, has been reported to play many beneficial roles.
Curcumin (CUR), the major component in Curcuma longa, has been shown as a potent chemopreventive phytochemical that modulates various signaling pathways. 
Curcumin (CUR) is a phytochemical that inhibits the xenobiotic ABC efflux transporters implicated in cancer multidrug resistance (MDR), such as P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and multidrug resistance-associated proteins 1 and 5 (MRP1 and MRP5). 
In this study, we tested the efficacy of combining temozolomide with curcumin, a phytochemical known to inhibit glioblastoma growth, and investigated the mechanisms involved.
 In the present study, we investigate whether curcumin (cur), a phytochemical compound with potent anti-inflammatory effect
the Phytochemicals Curcumin 
in combination with the phytochemicals curcumin and quercetin
Curcumin is a phytochemical derived from rhizome of turmeric Curcuma longa, present in the curry spice. 
Curcumin, a naturally occurring polyphenolic phytochemical isolated from the medicinal plant Curcuma longa, has anti-inflammatory activities
In the present study curcumin (CUR), a known anticancer phytochemical, 
 Curcumin, a natural phytochemical, exhibits potent anticancer activities.
hat curcumin, a phytochemical compound with potent anti-inflammatory properties 
curcumin, a phytochemical

Answer: Yes, curcumin is a phytochemical derived from rhizome of turmeric Curcuma longa.
Exact answer: yes
Question: Is there an association between bruxism and reflux

Context:
Rhythmic masticatory muscle activity, including sleep bruxism (SB), can be induced in healthy individuals by experimental esophageal acidification, which plays an important role in the pathogenesis of gastroesophageal reflux disease (GERD). However, no robust evidence supports the association between SB and GERD.
Sleep bruxism is prevalent in GERD patients, and GERD is highly associated with SB.
Our large-scale cross-sectional study found that problem behaviors in adolescents were associated with sleep problems, including sleep bruxism, as well as lifestyle and food habits and GERD symptoms.
The frequencies of EMG bursts, rhythmic masticatory muscle activity (RMMA) episodes, grinding noise, and the RMMA/microarousal ratio were significantly higher in the 20-minute period after acidic infusion than after saline infusion. RMMA episodes including SB were induced by esophageal acidification. 
Direct restorative treatment of dental erosion caused by gastroesophageal reflux disease associated with bruxism:
This article presents a case report of a 27-year-old male smoker with tooth wear and dentin sensitivity caused by GERD associated with bruxism
Dental wear caused by association between bruxism and gastroesophageal reflux disease:
This paper presents a case report in which bruxism associated with acid feeding, smoking habit and episodes of gastric reflow caused severe tooth wear and great muscular discomfort with daily headache episodes.
most jaw muscle activities, ie, RMMA, single short-burst, and clenching episodes, occur in relation to gastroesophageal reflux mainly in the supine position.
Association between nocturnal bruxism and gastroesophageal reflux.
Nocturnal bruxism may be secondary to nocturnal gastroesophageal reflux, occurring via sleep arousal and often together with swallowing.

Answer: There is an association between bruxism and reflux.
Exact answer: yes
Question: What is the mode of inheritance of nemaline myopathy?

Context:
The results indicate that mutations in TPM2 may cause nemaline myopathy as well as cap disease with a dominant mode of inheritance.
Autosomal recessive inheritance had been verified or appeared likely in all nebulin cases
Most cases were sporadic, but in addition there were instances of both autosomal dominant and autosomal recessive inheritance, while two families showed mosaicism for dominant mutations.
Finding the causative mutation(s) determines the mode of inheritance
We conclude that in the Finnish CNM patients, the mode of inheritance appears to be recessive. Apart from a few instances of dominant inheritance, most cases published also seem compatible with recessive inheritance.

Answer: Nemaline  myopathy has a autosomal dominant or recessive mode of inheritance.
Exact answer: autosomal dominant, autosomal recessive
Question: What disease is the drug aducanumab targeting?

Context:
 Most importantly, recent trials of three different Aβ antibodies (solanezumab, crenezumab, and aducanumab) have suggested a slowing of cognitive decline in post hoc analyses of mild AD subjects. 
ecent results from trials of agents such as aducanumab are encouraging but must also be interpreted with caution. Such medicines could potentially delay the onset of dementia and would therefore markedly reduce its prevalence.
Aducanumab is an anti-Aβ antibody being developed for the treatment of AD, and interim analyses of a phase 1b clinical trial have suggested potential beneficial effects on the amyloid pathology and the cognitive status in patients treated with aducanumab
The antibody aducanumab reduces Aβ plaques in Alzheimer's disease.

Answer: Aducanumab is an anti-Aβ antibody being developed for the treatment of Alzheimer's disease (AD).
Exact answer: Alzheimer's disease
Question: Which drugs acting via bradykinin system are effective for treatment of ACE-inhibitor-induced angioedema?

Context:
Medications recently developed, primarily icatibant and ecallantide, to control hereditary angioedema, a disorder also associated with kallikrein-kinin activation, have been used to treat ACEI angioedema with some success. 
A patient with acute ACE inhibitor-induced angioedema was treated with icatibant, a specific bradykinin B2 receptor antagonist approved for the treatment of hereditary angioedema. 
A patient with acute ACE inhibitor-induced angioedema was treated with icatibant, a specific bradykinin B2 receptor antagonist approved for the treatment of hereditary angioedema.

Answer: Icatibant and ecallantide are medication acting via bradykinin system that are used for treatment of ACE-inhibitor-induced angioedema.
Exact answer: icatibant, ecallantide
Question: Does Serca2a bind PLN in the heart?

Context:
The human phospholamban Arg14-deletion mutant localizes to plasma membrane and interacts with the Na/K-ATPase.
Moreover, PLN-R14Del did not co-immunoprecipitate with SERCA2a (as did WT-PLN),
n this review, we attempted to highlight the functional significance of PLN in vertebrate cardiac physiology. We will refer to the huge literature on mammals in order to describe the molecular characteristics of this protein, its interaction with SERCA2a
There is clear evidence for direct regulatory protein-protein interactions between phospholamban (PLN) and the Ca2+-ATPase of cardiac sarcoplasmic reticulum (SERCA2a) in cytoplasmic domains
These results suggest that PLN modulates the apparent Ca2+ affinity of SERCA2a through intramembrane interactions, which are disrupted at long range and in concert with disruption of the well characterized cytoplasmic interactions.
Phospholamban (PLN), a homopentameric, integral membrane protein, reversibly inhibits cardiac sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) activity through intramembrane interactions.
The concentration of this inhibited complex is determined by the dissociation constant for the PLN pentamer (which is mutation-sensitive) and by the dissociation constant for the PLN/SERCA2a heterodimer (which is likely to be mutation-sensitive).
These results support the proposal that PLN inhibition of SERCA2a involves, first, depolymerization of PLN and, second, the formation of inhibitory interactions between monomeric PLN and SERCA2a.
SLN and PLN appear to bind to the same regulatory site in SERCA. However, in a ternary complex, PLN occupies the regulatory site and SLN binds to the exposed side of PLN and to SERCA.
Cellular and biochemical studies revealed that, unlike wild-type PLN, PLN(R9C) did not directly inhibit SERCA2a.
. Conversely, using anti-SERCA2a antibody, both PLN and acylphosphatase were co-immunoprecipitated with SERCA2a, and the PLN amount in the precipitate decreased with increasing acylphosphatase concentrations.
Reconstitution of the cytoplasmic interaction between phospholamban and Ca(2+)-ATPase of cardiac sarcoplasmic reticulum.
Phospholamban (PLN) reversibly inhibits the Ca(2+)-ATPase of cardiac sarcoplasmic reticulum (SERCA2a) through a direct protein-protein interaction, playing a pivotal role in the regulation of intracellular Ca(2+) in heart muscle cells.
Phospholamban (PLN) is a key regulator of Ca(2+) homeostasis and contractility in the heart. Its regulatory effects are mediated through its interaction with the sarcoplasmic reticulum Ca(2+)-ATPase, (SERCA2a), resulting in alterations of its Ca(2+)-affinity
In a co-immunoprecipitation of PLN with SERCA2a, the physical interaction between the two proteins was increased in PUGNAc-treated cardiomyocytes.

Answer: Yes, Serca2a bind PLN in the heart.
Exact answer: yes
Question: Is the Dictyostelium discoideum proteome known?

Context:
The Negative Proteome Database (NPD) is populated with pair-wise protein sequence comparisons between each of the following proteomes: Homo sapiens, Mus musculus, Drosophila melanogaster, Caenorhabditis elegans, Saccharomyces cerevisiae, Dictyostelium discoideum, Chlamydomonus reinhardti, Escherichia coli K12, Arabidopsis thaliana and Methanoscarcina acetivorans.
The Dictyostelium discoideum proteome--the SWISS-2DPAGE database of the multicellular aggregate (slug).
Consequently, this genomic sequence information can now be exploited to realize D. discoideum proteomics projects. 
The Dictyostelium discoideum genome has been sequenced, assembled and annotated to a high degree of reliability. The parts-list of proteins and RNA encoded by the six chromosomes can now be accessed and analyzed. 
The 34 Mb genome of Dictyostelium discoideum is carried on 6 chromosomes and has been fully sequenced by an international consortium. The sequence was assembled on the classical and physical maps that had been built up over the years and refined by HAPPY mapping. Annotation of the sequence predicted about 12,000 genes for proteins of at least 50 amino acids in length.
In this study, a quantitative comparative proteomics approach has been used to analyze the Dictyostelium discoideum mitochondrial proteome variations during vegetative growth, starvation and the early stages of development. 
The secreted proteome profile of developing Dictyostelium discoideum cells.
The present repertoire validates our purification method and paves the way for a future proteomics approach to study the dynamics of macropinocytosis.
Proteomic analysis of a developmentally regulated secretory vesicle.

Answer: Yes, The Dictyostelium discoideum genome has been sequenced, assembled and annotated to a high degree of reliability. The parts-list of proteins and RNA encoded by the six chromosomes can now be accessed and analyzed. Consequently, this genomic sequence information can now be exploited to realize D. discoideum proteomics projects.
Exact answer: yes
Question: What is the role of thyroid hormone receptor alpha1 in insulin secretion?

Context:
loss of Thra protects mice from high-fat diet-induced hepatic steatosis and hepatic and peripheral insulin resistance.
liganded TR(alpha) plays a critical role in beta-cell replication and in expansion of the beta-cell mass during postnatal development. Thus, liganded TR(alpha) may be a target for therapeutic strategies that can induce the expansion and regeneration of beta-cells.
the TRalpha P398H mutation is associated with visceral adiposity and insulin resistance

Answer: Liganded TR(alpha) plays a critical role in beta-cell replication and in expansion of the beta-cell mass. the TRalpha P398H mutation which cannot bind T3, is associated with  insulin resistance. Loss of Thra protects mice from high-fat diet-induced hepatic and peripheral insulin resistance.
Question: Do U6-associated proteins Lsm4 and Lsm6 interact with SMN?

Context:
SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6. 
Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6
Furthermore, we present evidence for two separate binding sites in SMN for Sm/Lsm proteins.
Interestingly, SMN also interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6. 
Symmetrical dimethylation of arginine residues in spliceosomal Sm protein B/B' and the Sm-like protein LSm4, and their interaction with the SMN protein.
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.
This entity promotes the binding of a set of factors, termed LSm/Sm proteins, onto snRNA to form the core structure of these particles. 
Toward an assembly line for U7 snRNPs: interactions of U7-specific Lsm proteins with PRMT5 and SMN complexes.
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.
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.
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.
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. 

Answer: SMN interacts with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6.
yes
SMN was found to interact with at least two of the U6-associated Sm-like (Lsm) proteins, Lsm4 and Lsm6.
Exact answer: yes