nirantk/geneticsQA-train huggingface dataset:
Question: What is the term for synapsin as a conserved presynaptic phosphoprotein?

Context:
Synapsin is an evolutionarily conserved presynaptic phosphoprotein.
Synapsins as a family of presynaptic terminal phosphoprotein participates in neuronal development
Synapsin III (SynIII) is a phosphoprotein
The neuronal phosphoprotein synapsin III
Synapsin II is a member of the neuronal phosphoprotein family.
phosphoprotein synapsin
Synapsin is an evolutionarily conserved presynaptic phosphoprotein.
Synapsins as a family of presynaptic terminal phosphoprotein participates in neuronal development
Synapsin III (SynIII) is a phosphoprotein
The neuronal phosphoprotein synapsin III
Synapsin II is a member of the neuronal phosphoprotein family.
phosphoprotein synapsin

Answer: Synapsin
Question: What are the symptoms of abacavir hypersensitivity?

Context:
patients receiving abacavir develop a hypersensitivity reaction, characterized by rash, fever and, occasionally, multisystemic involvement
The predictors included any one of several specific symptoms commonly found with this reaction, a claims diagnosis of adverse effect of drug, anaphylactic shock or unspecified allergy, and a discontinuation in abacavir prior to completing a 90-day course of therapy.
patients who receive abacavir develop an idiosyncratic hypersensitivity reaction. The most common symptoms are fever, skin rash and gastrointestinal disorders. Respiratory symptoms occurred in approximately 20% of patients who have hypersensitivity reaction. We describe the first case, to our knowledge, of hypesensitivity reaction characterized by enanthema and fever without skin rash promptly resolved after discontinuation of abacavir
Abacavir is associated with an infrequent but potentially serious hypersensitivity reaction (HSR) that can include a wide range of signs and symptoms.
Rash was associated with hypersensitivity (odds ratio [OR] = 13.1, P = 0.02) as was the presence of nausea (OR = 30, P < 0.001), vomiting (OR = 17.1, P = 0.001) or diarrhoea (OR = 22, P < 0.001). The number of gastrointestinal symptoms was also predictive of hypersensitivity reaction (
the number of gastrointestinal symptoms (OR = 8.6, P = 0.0032), cough (OR = 0.039, P = 0.02) and rash (OR = 16.9, P = 0.07). Abacavir hypersensitivity is strongly associated with gastrointestinal (GI) symptoms.

Answer: Patients receiving abacavir develop an idiosyncratic hypersensitivity reaction that can include a wide range of symptoms. The most common are: fever, enathema, skin rash, nausea, vomiting, diarrhoea, cough, gastrointestinal disorders, anaphylactic shock, respiratory symptoms.
Exact answer: fever, enathema, skin rash, nausea, vomiting, diarrhea, cough, gastrointestinal disorders, anaphylactic shock, respiratory symptoms
Question: Are there currently applications of deep learning in genomics?

Context:
Deep learning of the tissue-regulated splicing code.
Using a deep neural network, we developed a model inferred from mouse RNA-Seq data that can predict splicing patterns in individual tissues and differences in splicing patterns across tissues. Our architecture uses hidden variables that jointly represent features in genomic sequences and tissue types when making predictions. A graphics processing unit was used to greatly reduce the training time of our models with millions of parameters.
We show that the deep architecture surpasses the performance of the previous Bayesian method for predicting AS patterns. With the proper optimization procedure and selection of hyperparameters, we demonstrate that deep architectures can be beneficial, even with a moderately sparse dataset. An analysis of what the model has learned in terms of the genomic features is presented.
Machine learning applications in genetics and genomics

Answer: Yes. Deep learning has been used so far in genomics for predicting splicing patterns in individual tissues and differences in splicing patterns across tissues. The deep architecture surpasses the performance of the previous Bayesian method for predicting alternative splicing (AS) patterns.
Exact answer: yes
Question: is intense physical activity associated with longevity ?

Context:
We found a very significant increase in average longevity (17%) of the cyclists when compared with the general population. The age at which 50% of the general population died was 73.5 vs. 81.5 years in Tour de France participants. Our major finding is that repeated very intense exercise prolongs life span in well trained practitioners.
Competitive exercise does not induce cardiac damage in individuals with healthy hearts, but does induce physiological functional and structural cardiac adaptations which have positive effects on life expectancy.
Medallists lived an average of 2.8 years longer than controls. Medallists in eight of the nine country groups had a significant survival advantage compared with controls. Gold, silver, and bronze medallists each enjoyed similar sized survival advantages. Medallists in endurance sports and mixed sports had a larger survival advantage over controls at 30 years (1.13, 1.09 to 1.17; 1.11, 1.09 to 1.13) than that of medallists in power sports (1.05, 1.01 to 1.08). CONCLUSIONS: Olympic medallists live longer than the general population, irrespective of country, medal, or sport. This study was not designed to explain this effect, but possible explanations include genetic factors, physical activity, healthy lifestyle, and the wealth and status that come with international sporting glory.
Long-term endurance training induces in elderly subjects an increased HRV and a higher exercise working capacity, which are well-established predictors of cardiovascular and overall mortality.
Sports activity in adolescents and young adults was associated with an increased risk of SD, both in males and females. Sports, per se, was not a cause of the enhanced mortality, but it triggered SD in those athletes who were affected by cardiovascular conditions predisposing to life-threatening ventricular arrhythmias during physical exercise.

Answer: Several survival studies showed that professional athletes has higher longevity than general population. These epidemiological data matches the evidences that long-term endurance training induces in elderly subjects an increased HRV and a higher exercise working capacity, which are well-established predictors of cardiovascular and overall mortality, and also telomere length.
Exact answer: yes
Question: Are seizures among the neurological symptoms of incontinentia pigmenti?

Context:
High-dose glucocorticoid therapy in the management of seizures in neonatal incontinentia pigmenti
Incontinentia pigmenti is an X-linked dominant disorder resulting from a mutation of IKBKG. This disorder has a classic dermatologic presentation, but neurologic involvement, with seizures and cortical infarction, can arise shortly after birth
Some children with incontinentia pigmenti exhibit encephalopathic features with severe seizures and disturbed consciousness, from the neonatal through the early infantile period
Incontinentia pigmenti (IP) is a rare X-linked dominant neurocutaneous disorder affecting ectodermal tissue: skin, eyes, central nervous system, hair, nails, and teeth. It is usually lethal for males in utero. The involved gene is NEMO, an essential component of the nuclear factor-kappa B (NF-κB) signaling pathway. Skin lesions are highly diagnostic, occurring in neonates, with a particular distribution on Blaschko lines. The severity of the disease is related to ocular and neurological impairment. The hallmark of ocular IP is retinal vasculopathy including peripheral retinal vascular nonperfusion, macular infarction and neovascularization, and preretinal neovascularization. CNS involvement consists of seizures, mental retardation, hemiparesis, spasticity, microcephaly, cerebellar ataxia, and coma
Incontinentia Pigmenti is a rare X-linked multisystem disorder with well described and pathognomonic skin manifestations. Neurological manifestations are found in 30% of IP patients, forming one of the major causes of morbidity and mortality of the condition. In this review, clinical and brain imaging data of 45 IP patients with a neurological phenotype are reviewed. Several clinical presentations could be identified, comprising seizures, infantile encephalopathy, acute disseminated encephalomyelitis and ischemic stroke
Incontinentia pigmenti presenting as seizures.
Neonatal seizures in two sisters with incontinentia pigmenti.
High-dose glucocorticoid therapy in the management of seizures in neonatal incontinentia pigmenti: a case report.
Incontinentia Pigmenti is an X-linked dominant neurocutaneous disorder with central nervous system manifestations in 30% of cases, including seizures and mental retardation.
Neonatal seizures in two sisters with incontinentia pigmenti
A rare cause of neonatal seizure: incontinentia pigmenti.
Here, we describe the clinical, electrographic, and neuroradiologic effect of systemic glucocorticoid therapy in a neonate with incontinentia pigmenti manifesting an epileptic encephalopathy.
Incontinentia pigmenti presenting as seizures.
Neonatal seizures in two sisters with incontinentia pigmenti.

Answer: Incontinentia pigmenti is an X-linked dominant disorder resulting from a mutation of IKBKG. This disorder has a classic dermatologic presentation, but neurologic involvement, with seizures and cortical infarction, can arise shortly after birth.
Exact answer: yes
Question: List bacterial species identified in the iceman tissues.

Context:
Here, we report the molecular detection of the oral spirochete Treponema denticola in ancient human tissue biopsies of the Iceman, a 5,300-year-old Copper Age natural ice mummy. 
The colon, on the other hand, contains several members of the fecal flora of humans, such as Clostridium perfringens, C. ghonii, C. sordellii, Eubacterium tenue, and Bacteroides sp. The Iceman's colon, however, was found to contain, rather unexpectedly, also some members of the genus Vibrio. 
 while the untreated skin still bears the remains of large numbers of bacteria belonging to the genera Sphingomonas, Afipia, Curtobacterium, Microbacterium, Agromyces, and others.

Answer: Spirochete Treponema denticola
Clostridium perfringens
Clostridium ghonii
Clostridium sordellii
Eubacterium tenue
Bacteroides sp
Vibrio
Sphingomonas
Afipia
Curtobacterium
Microbacterium
Agromyces
Exact answer: Spirochete Treponema denticola, Clostridium perfringens, Clostridium ghonii, Clostridium sordellii, Eubacterium tenue, Bacteroides sp, Vibrio, Sphingomonas, Afipia, Curtobacterium, Microbacterium, Agromyces
Question: What is known about telomere length shortening and stress?

Context:
A significant relationship between more perceived stress and shorter telomere length is consistent with theoretical frameworks positing that stress induces physiological changes that result in shortened telomeres. 
Psychological stress contributes to numerous diseases and may do so in part through damage to telomeres, protective non-coding segments on the ends of chromosomes.
Our results support the hypothesis that depression is associated with accelerated cell aging. Future studies are required to clarify whether the association is mediated through environmental stress, and whether effective treatment can halt cell aging.
Telomere length, a reliable predictor of disease pathogenesis, can be affected by genetics, chronic stress and health behaviors. Cross-sectionally, highly stressed postmenopausal women have shorter telomeres, but only if they are inactive. 

Answer: A significant relationship between more perceived stress and shorter telomere length is consistent with theoretical frameworks positing that stress induces physiological changes that result in shortened telomeres.
Question: What is a "chemobrain"?

Context:
Frequency of chemotherapy-related cognitive impairment or "chemobrain" is mentioned to be significant in literature, although very little is known about the chemotherapy-caused chemobrain and its connection with metal homeostasis alteration.
Cognitive decline or dementia is a debilitating problem of neurological disorders such as Alzheimer's and Parkinson's disease, including special conditions like chemobrain. 
Most cancer patients treated with systemic adjuvant chemotherapy endure long-lasting side effects including decrease in concentration, forgetfulness and slower thinking, which are globally termed "chemobrain." 
The frequent use of chemotherapy to combat a range of malignancies can elicit severe cognitive dysfunction often referred to as "chemobrain," a condition that can persist long after the cessation of treatment in as many as 75% of survivors.
The term "chemobrain" is sometimes used to denote deficits in neuropsychological functioning that may occur as a result of cancer treatment. 

Answer: The term "chemobrain" is sometimes used to denote deficits in neuropsychological functioning that may occur as a result of cancer treatment.
Exact answer: The term "chemobrain" is sometimes used to denote deficits in neuropsychological functioning that may occur as a result of cancer treatment.
Question: What is clathrin?

Context:
Clathrin-mediated endocytosis is a central and well-studied trafficking process in eukaryotic cells.
We reported the first small molecule inhibitors of the interaction between the clathrin N-terminal domain (TD) and endocyctic accessory proteins (i.e., clathrin inhibition1).
Tubulobulbar complexes are elaborate clathrin/actin related structures that form at sites of intercellular attachment in the seminiferous epithelium of the mammalian testis.
 Clathrin-coated vesicles (CCVs) are formed at the plasma membrane and act as vectors for endocytosis. They also assemble at the trans-Golgi network (TGN), but their exact function at this organelle is unclear. 
 Clathrin immunohistochemistry and immunoblotting showed increased immunoreactivity of clathrin protein in the placental tissues of mice treated with 20- and 50-nm gold nanoparticles; clathrin immunopositivity was observed in syncytiotrophoblasts and fetal endothelial cells.

Answer: Clathrin helps build small vesicles in order to safely transport molecules within and between cells.
Question: How does stress affect telomere length?

Context:
A significant relationship between more perceived stress and shorter telomere length is consistent with theoretical frameworks positing that stress induces physiological changes that result in shortened telomeres. 
Psychological stress contributes to numerous diseases and may do so in part through damage to telomeres, protective non-coding segments on the ends of chromosomes.
Our results support the hypothesis that depression is associated with accelerated cell aging. Future studies are required to clarify whether the association is mediated through environmental stress, and whether effective treatment can halt cell aging.
Telomere length, a reliable predictor of disease pathogenesis, can be affected by genetics, chronic stress and health behaviors. Cross-sectionally, highly stressed postmenopausal women have shorter telomeres, but only if they are inactive. 

Answer: Stress can lead to physiological changes that result in shortened telomeres. Psychological stress may contribute to diseases by damaging telomeres, which are protective segments on the ends of chromosomes. Highly stressed postmenopausal women have shorter telomeres, particularly if they are inactive.
Question: Which protein is causing Netherton syndrome?

Context:
Netherton syndrome (NTS) is a rare genetic skin disease caused by mutations in the serine protease inhibitor Kazal-type 5 gene, which encodes the lympho-epithelial Kazal-type-related inhibitor.
Netherton syndrome is caused by loss-of-function mutations in SPINK5 encoding the Kazal-type inhibitor LEKTI-1 
Netherton syndrome (NS) is a serious inherited skin disorder caused by mutations in the gene SPINK5 (serine protease inhibitor Kazal type 5) which encodes for a serine protease inhibitor LEKTI (lymphoepithelial Kazal type-related inhibitor)
Mutations in the serine protease inhibitor Kazal type 5 (SPINK5) gene leading to lymphoepithelial Kazal-type-related inhibitor (LEKTI) deficiency cause NS.
NS is due to loss-of-function mutations in the SPINK5 gene and to the consequent lack of expression of its encoded protein LEKTI in the skin and all stratified epithelial tissues.
syndrome and caused by a genetic mutation in SPINK5, may be a facilitating factor for the infection.
NS is caused by loss-of-function mutations in SPINK5 (serine protease inhibitor of kazal type 5) encoding LEKTI-1 (lympho-epithelial kazal type related inhibitor type 5) expressed in stratified epithelia. 
Netherton syndrome, which arises due to mutations in serine protease inhibitor Kazal-type 5 (SPINK5)
Lympho-epithelial Kazal-type-related inhibitor (LEKTI) is the defective protein of the ichthyosiform condition Netherton syndrome (NS).
Deficiency in the serine protease inhibitor LEKTI is the etiological origin of Netherton syndrome, which causes detachment of the stratum corneum and chronic inflammation. 

Answer: Netherton syndrome (NS) is a serious inherited skin disorder caused by mutations in the gene SPINK5 (serine protease inhibitor Kazal type 5) which encodes for a serine protease inhibitor LEKTI (lymphoepithelial Kazal type-related inhibitor)
Exact answer: LEKTI, lymphoepithelial Kazal type-related inhibitor
Question: Is Stat4 a transcription factor?

Context:
transcription factors T-bet and STAT4
STAT4 is a member of the signal transducer and activator of transcription (STAT) family of molecules that localizes to the cytoplasm. STAT4 regulates various genes expression as a transcription factor after it is phosphorylated, dimerizes and translocates to the nucleus. 
STAT4 is a latent cytosolic factor that encodes a transcription factor transmitting signals stimulated by cytokines. 
 To investigate the role of signal transduction and activation of transcription 4 (STAT4) in the development and progression of human hepatocellular carcinoma (HCC)

Answer: Yes, Stat4 is a transcription factor.
Stat4 is a member of the signal transducer and activator of transcription (STAT) family of molecules that localizes to the cytoplasm. STAT4 regulates various genes expression as a transcription factor after it is phosphorylated, dimerizes and translocates to the nucleus.
Exact answer: yes
Question: What is the target of the drug Olaparib?

Context:
We show that targeting PARP by the small molecule inhibitors, Olaparib 
Following treatment with the PARP1 inhibitor olaparib, 
the PARP inhibitor olaparib
Olaparib (AZD-2281, Ku-0059436) is an orally bioavailable and well-tolerated poly(ADP-ribose) polymerase (PARP) inhibitor currently under investigation in patients with solid tumors.
The poly(ADP-ribose) polymerase inhibitor olaparib
olaparib (poly(ADP ribose)polymerase inhibitor)
 olaparib, a PARP inhibitor, 
Olaparib is an oral poly (ADP-ribose) polymerase inhibitor
olaparib, a small molecule inhibitor of the repair enzymes PARP1/2. 
he poly (ADP-ribose) polymerase inhibitor olaparib 
 PARP-inhibitor, Olaparib
Olaparib is a poly(ADP-ribose) polymerase inhibitor
olaparib, a specific PARP1 inhibitor.
PARP inhibitor olaparib 
We used two PARP inhibitors in clinical development, olaparib and rucaparib
 the PARPi, olaparib, 

Answer: The drug Olaparib target the protein poly(ADP-ribose) polymerase.
Exact answer: poly(ADP-ribose) polymerase
PARP
Question: Which is the E3 ubiquitin ligase of Hsp90?

Context:
C-terminal Hsp-interacting protein (CHIP) is an HSP70 and HSP90 interacting co-chaperone and an E3 ubiquitin ligase. Previous studies have reported the role of CHIP in cancer progression by targeting protein degradation.
The U-box E3 ubiquitin ligase CHIP (C terminus of Hsc70-interacting protein) binds Hsp90 and/or Hsp70 via its tetratricopeptide repeat (TPR), facilitating ubiquitination of the chaperone-bound client proteins.
In vitro ubiquitination assays indicated that Ca(2+)/S100A2 and S100P are efficient and specific inhibitors of CHIP-mediated ubiquitination of Hsp70, Hsp90, HSF1, and Smad1.
The E3 ubiquitin ligase CHIP (C-terminus of Hsc70-interacting protein) is believed to be a central player in the cellular triage decision, as it links the molecular chaperones Hsp70/Hsc70 and Hsp90 to the ubiquitin proteasomal degradation pathway.
We found that CHIP has a sixfold higher affinity for Hsp90 compared with Hsc70.
Carboxyl terminus of hsc70-interacting protein (CHIP) can remodel mature aryl hydrocarbon receptor (AhR) complexes and mediate ubiquitination of both the AhR and the 90 kDa heat-shock protein (hsp90) in vitro
The analysis of the sucrose-gradient-fractionated in vitro translated AhR complexes revealed that CHIP can mediate hsp90 ubiquitination while cooperating with unidentified factors to promote the ubiquitination of mature unliganded AhR complexes.

Answer: Carboxyl terminus of hsc70-interacting protein (CHIP) can mediate ubiquitination of the 90 kDa heat-shock protein (hsp90) in vitro, with subsequent proteasomal degradation of the chaperone.
Exact answer: Carboxyl terminus of hsc70-interacting protein (CHIP)
Question: List human proteins that are subject to a dimer-to-tetramer transition.

Context:
 the ability of GAC to undergo the dimer-to-tetramer transition necessary for enzyme activation.
while SHMT2 undergoes a dimer-to-tetramer transition upon PLP binding.
AMPARs that is required for the critical dimer-to-tetramer transition.
We conclude that the human Orai1 and Orai3 channels undergo a dimer-to-tetramer transition to form a Ca(2+)-selective pore during store-operated activation and that Orai3 forms a dimeric nonselective cation pore upon activation by 2-APB.
the conformational requirement for the dimer-to-tetramer transition during the maturation of AMPA-Rs. 

Answer: GAC
SHMT2
AMPAR
Orai1
Orai3
Exact answer: GAC, SHMT2, AMPAR, Orai1, Orai3