nirantk/geneticsQA-train huggingface dataset:
Question: Does strenuous physical activity affect thyroid hormone metabolism?

Context:
The results of the present study in a unique experimental human model of maximal exposure to altitude and physical exercise demonstrate that extreme HA and strenuous physical exercise are coupled with specific endocrine adaptations. These include increased activity of the GH/IGF-I axis and a low T(3) syndrome
3,5,3'-triiodothyronine (T3) and T4 levels increase during strenuous exercise, and, at the end of the exercise bout, a decrease of T3 and T4 levels, with an increase in TSH during the following 4-5 days, is seen.
the obtained results indicate that in intense exercise, causing the rapid development of fatigue, rapid increases in serum levels of hormones of the pituitary-adrenocortical, pituitary-gonadal and pituitary-thyroid systems occur.
Mean levels of fasting plasma estradiol, luteinizing hormone, follicle-stimulating hormone, free thyroxine and triiodothyronine were significantly lower in AR compared to ER and SE.
Reductions in plasma T4, T3 and T3/T4 ratio are probably due to inhibition of T4 secretion and 5'-monodeiodination with possible conversion of T4 to reverse T3 (rT3). These processes may represent a mechanism for regulation of thyroid hormone metabolism during strenuous and extended flight.
Strenuous endurance training seems to have minor changes on the function of the thyroid gland. Depressed T4 levels in runners may rather be due to lowered TBG levels than due to direct effect of training.
brief strenuous swimming or moderate bicycle exercise had minor or no effect on thyroid hormone concentrations when consideration was given to the attendant hemoconcentration.
thyroxine were determined in 26 men participating in a 90-km cross-country ski race, before, immediately after, and on the following days
Total thyroxine and free thyroxine in serum were significantly increased at the end of the race, but had returned to the pre-raced levels during the rest of the observation period.
There are controversial results concerning thyroid hormone metabolism during strenuous exercise in adult athletes and only scant data concerning the impact of strenuous exercise on thyroid hormone metabolism in children and adolescents.

Answer: YES
Exact answer: yes
Question: Which is the mass-tag that reveal the ubiquitination of a lysine residue?

Context:
antibodies that recognize the Lys-ɛ-Gly-Gly (K-ɛ-GG) remnant produced by trypsin digestion of proteins having ubiquitinated lysine side chains have markedly improved the ability to enrich and detect endogenous ubiquitination sites by mass spectrometry (MS). 
Recent publications have also highlighted the use of peptide-level immunoaffinity enrichment of K-GG modified peptides from whole cell lysates for global characterization of ubiquitination sites. 
In this work, levels of lysine ubiquitination were quantitated using a structurally homologous label that is chemically similar to the diglycine (GlyGly) tag, which is left at the ubiquitination site upon trypsinolysis
Tandem mass spectrometry (LC-MS/MS) analysis of immunoprecipitated proteins resulted in the identification of five peptides containing ubiquitin (diglycine) modifications on eIF2Bε

Answer: Lys-ɛ-Gly-Gly (K-ɛ-GG) is the remnant produced by trypsin digestion of proteins having ubiquitinated lysine side chains.
Exact answer: Lys-ɛ-Gly-Gly (K-ɛ-GG) is the remnant produced by trypsin digestion of proteins having ubiquitinated lysine side chains.
Question: List components of the CRSP/Med complex.

Context:
 Here we describe a new human factor, CRSP, that is required together with the TAF(II)s for transcriptional activation by Sp1. Purification of CRSP identifies a complex of approximate relative molecular mass 700,000 (M(r) approximately 700K) that contains nine subunits with M(r) values ranging from 33K to 200K. Cloning of genes encoding CRSP subunits reveals that CRSP33 is a homologue of the yeast mediator subunit Med7, whereas CRSP150 contains a domain conserved in yeast mediator subunit Rgr1. CRSP p200 is identical to the nuclear hormone-receptor co-activator subunit TRIP2/PBP. CRSPs 34, 77 and 130 are new proteins, but the amino terminus of CRSP70 is homologous to elongation factor TFIIS.
CRSP contains unique subunits as well as polypeptides that are shared with other cofactor complexes.
The multi-subunit, human CRSP coactivator-also known as Mediator (Med)-regulates transcription by mediating signals between enhancer-bound factors (activators) and the core transcriptional machinery. Interestingly, different activators are known to bind distinct subunits within the CRSP/Med complex. We have isolated a stable, endogenous CRSP/Med complex (CRSP/Med2) that specifically lacks both the Med220 and the Med70 subunits. 

Answer: Mediator of RNA polymerase II transcription subunit 7
Mediator of RNA polymerase II transcription subunit 14
Mediator of RNA polymerase II transcription subunit 17
Mediator of RNA polymerase II transcription subunit 23
Mediator of RNA polymerase II transcription subunit 24
Mediator of RNA polymerase II transcription subunit 26
Mediator of RNA polymerase II transcription subunit 27
Exact answer: Mediator of RNA polymerase II transcription subunit 7, Mediator of RNA polymerase II transcription subunit 14, Mediator of RNA polymerase II transcription subunit 17, Mediator of RNA polymerase II transcription subunit 23, Mediator of RNA polymerase II transcription subunit 26, Mediator of RNA polymerase II transcription subunit 27, Mediator of RNA polymerase II transcription subunit 24
Question: Which is the molecular function of the protein CCDC40?

Context:
Primary ciliary dyskinesia (PCD) is a genetically heterogeneous, autosomal recessive disorder that results from functional and ultrastructural abnormalities of motile cilia.
Primary ciliary dyskinesia (PCD) is a rare genetic disorder leading to recurrent respiratory tract infections.
Ciliary beat pattern and frequency in genetic variants of primary ciliary dyskinesia.
Mutations in CCDC39 and CCDC40 are the major cause of primary ciliary dyskinesia with axonemal disorganization and absent inner dynein arms.
Human cilia were once thought merely to be important in respiratory mucociliary clearance, with primary ciliary dyskinesia (PCD) the sole manifestation of ciliary dysfunction. 
The coiled-coil domain containing protein CCDC40 is essential for motile cilia function and left-right axis formation.
CCDC39 and CCDC40 mutations represent the major cause of PCD with IDA defects and axonemal disorganisation.

Answer: The coiled-coil domain containing protein CCDC40 is essential for motile cilia function and left-right axis formation and mutations in CCDC39 and CCDC40 are the major cause of primary ciliary dyskinesia with axonemal disorganization and absent inner dynein arms.
Question: Do statins cause diabetes?

Context:
Statin use has been associated with increased risk of developing type 2 diabetes (T2DM), and with impaired glycemic control in T2DM patients
The relationship between T2DM and statins is further complicated since these drugs can cause new onset diabetes (NOD) although there is an overall benefit in terms of preventing vascular events 
It has been repeatedly reported that statins may cause new-onset diabetes mellitus (DM).
However, a small, but significant risk of new-onset diabetes has been reported in patients treated with statins.
The National Lipid Association (NLA) Statin Diabetes Safety Task Force concluded that the cardiovascular benefit of statin therapy outweighs the risk for developing diabetes
It has been repeatedly reported that statins may cause new-onset diabetes mellitus (DM)
It has been repeatedly reported that statins may cause new-onset diabetes mellitus (DM). However, limited evidence exists from direct head to head comparisons of statins on whether the risk of DM differs among statins.
Short-term statin exposure is associated with reduced all-cause mortality in persons with diabetes.
Despite the fact that higher statin doses are more likely to lead to new-onset diabetes, for every case of diabetes caused, there are approximately three cardiovascular events reduced with high dose versus moderate dose statin therapy.
It has been repeatedly reported that statins may cause new-onset diabetes mellitus (DM).
 Statins are evidence-based drugs to prevent cardiovascular (CV) disease. However, their benefits have been disputed by a statin-related increased risk of new onset diabetes
 Compared with pravastatin, treatment with higher potency statins, especially atorvastatin and simvastatin, might be associated with an increased risk of new onset diabetes
 statins are associated with a small increase in incidence of diabetes in patients predisposed to glycemic alteration
 Higher potency statin use is associated with a moderate increase in the risk of new onset diabetes compared with lower potency statins in patients treated for secondary prevention of cardiovascular disease
An increased risk of new onset treated diabetes was found in those treated with statins showing significant duration and dose effect
Although most of the clinical studies suggest a worsening of insulin resistance and secretion, the cardiovascular benefits of statin therapy outweigh the risk of developing insulin resistance, thus the data suggest the need to treat dyslipidemia and to make patients aware of the possible risk of developing type 2 diabetes or, if they already are diabetic, of worsening their metabolic control
Statin therapy can slightly increase risk of incident diabetes in subjects with hypercholesterolemia.

Answer: The relationship between T2DM and statins is further complicated since these drugs can cause new onset diabetes (NOD) although there is an overall benefit in terms of preventing vascular events.
Statin use has been associated with increased risk of developing type 2 diabetes (T2DM), and with impaired glycemic control in T2DM patients
Exact answer: yes
Question: What is the life expectancy of professional athletes in respect to the general population?

Context:
In conclusion, while regular physical activity increases life expectancy, it remains unclear if high-intensity sports activities further increase life expectancy.
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.
It appears that elite endurance (aerobic) athletes and mixed-sports (aerobic and anaerobic) athletes survive longer than the general population, as indicated by lower mortality and higher longevity. Lower cardiovascular disease mortality is likely the primary reason for their better survival rates. On the other hand, there are inconsistent results among studies of power (anaerobic) athletes.

Answer: Elite endurance (aerobic) athletes and mixed-sports (aerobic and anaerobic) athletes show higher longevity than the general population, but results  about power (anaerobic) athletes are inconsistent.
It remains unclear if high-intensity sports activities further increase life expectancy.
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
It appears that elite endurance (aerobic) athletes and mixed-sports (aerobic and anaerobic) athletes survive longer than the general population, as indicated by lower mortality and higher longevity.
Exact answer: longer than the general population, No clear results indicating improved life expectancy in professional athletes
Question: Does Jarid2 play a role in early embryo development?

Context:
Jarid2 Coordinates Nanog Expression and PCP/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development
Unlike other PRC2-deficient embryonic stem cells (ESCs), however, Jarid2-deficient ESCs show a severe differentiation block, altered colony morphology, and distinctive patterns of deregulated gene expression. Here, we show that Jarid2(-/-) ESCs express constitutively high levels of Nanog but reduced PCP signaling components Wnt9a, Prickle1, and Fzd2 and lowered β-catenin activity. Depletion of Wnt9a/Prickle1/Fzd2 from wild-type ESCs or overexpression of Nanog largely phenocopies these cellular defects. Co-culture of Jarid2(-/-) with wild-type ESCs restores variable Nanog expression and β-catenin activity and can partially rescue the differentiation block of mutant cells. In addition, we show that ESCs lacking Jarid2 or Wnt9a/Prickle1/Fzd2 or overexpressing Nanog induce multiple ICM formation when injected into normal E3.5 blastocysts. These data describe a previously unrecognized role for Jarid2 in regulating a core pluripotency and Wnt/PCP signaling circuit that is important for ESC differentiation and for pre-implantation development.
Jarid2 Coordinates Nanog Expression and PCP/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development.
Consistent with an essential role for PcG proteins in early development, we demonstrate that JARID2 is required for the differentiation of mouse embryonic stem cells.
Jumonij (JMJ)/Jarid2 plays important roles in embryonic development and functions as a transcriptional repressor.
Thus, these results demonstrate that JARID2 is essential for the binding of PcG proteins to target genes and, consistent with this, for the proper differentiation of embryonic stem cells and normal development.
JARID2 is an accessory component of Polycomb repressive complex-2 (PRC2) required for the differentiation of embryonic stem cells (ESCs).
Jarid2 Coordinates Nanog Expression and PCP/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development.
These data describe a previously unrecognized role for Jarid2 in regulating a core pluripotency and Wnt/PCP signaling circuit that is important for ESC differentiation and for pre-implantation development..

Answer: Yes. Jarid2 coordinates Nanog expression and PCP/Wnt signaling required for efficient ESC differentiation and early embryo development.
Exact answer: yes
Question: What is the incidence of Edwards syndrom in the european population?

Context:
dwards syndrome (trisomy 18) occurs in 1: 8000 live births and is closely related to the mother's age
Mean incidence was 390.06 (449.08 in boys and 327.93 in girls) per 10 000 live births
The incidence of Edwards syndrome is 1:5000 of live-born
The OR for Patau syndrome was 1.10 (95% CI 0.83 to 1.45); for Edwards syndrome, 1.15 (0.96 to 1.38); for Klinefelter syndrome, 1.35 (1.02 to 1.79); and for XYY syndrome, 1.99 (0.75 to 5.26)
The live birth prevalence in the absence of prenatal screening and selective termination in England and Wales from 1997 to 2004 was 1.4 (95% CI: 1.2-1.6) per 10 000 births for trisomy 13 and 2.3 (95% CI: 2.1-2.5) for trisomy 18
During the period under the study, following total numbers, mean relative incidences (per 10,000 live births, in brackets) and mean prenatal diagnostics efficiency (in %) were found in following chromosomal syndromes: Down syndrome 2,244 (16.58) and 63.37%, Edwards syndrome 521 (3.85) and 79.93%, Patau syndrome 201 (1.49) and 68.87%, Turner syndrome 380 (2.81) and 79.89%, 47,XXX syndrome 61 (0.45) and 59.74%, Klinefelter syndrome 163 (1.20) and 73.65% and 47,XYY syndrome 22 (0.16) and 54.76%
There was evidence of space-time clustering for Down syndrome (fixed threshold of close in space: P = 0.01, NN threshold: P = 0.02), but little or no clustering for Patau (P = 0.57, P = 0.19) or Edwards (P = 0.37, P = 0.06) syndromes. 
Of the 49,806 pregnant women between 15 and 23 weeks' gestational age who received prenatal serum screening with a cut-off value (a risk of 1:270 for Down and 1:100 for Edwards syndrome), 2,116 (4.2%) and 196 (0.4%) were screen positive for Down syndrome and for Edwards syndrome, respectively.
26,803 of the 27,313 women (98%) were screened. The average was 25.1, and 1.7% of them were over 35. Serum screening showed that 1,244 (5%) were Down syndrome positive and 105 (0.4%) were Edwards syndrome positive.
235 pregnancies of women delivered in units in the North West Thames region over a two-year period (1990-91) whose babies or fetuses were diagnosed as having Down, Edwards or Patau syndrome. RESULTS: 33% of Down syndrome, 68% of Edwards syndrome and 52% of Patau syndrome were diagnosed prenatally (before 28 weeks) in the region without the use of serum screening. 

Answer: Between 0.125 and 39 in every 1000 live births. Most probably 1:5000 of live-born.
Exact answer: 1:5000
Question: What is known about the effectiveness of electronic food diaries ?

Context:
Electronic dietary records were better than food diaries in terms of fat percentage reduction in our trials, indicating that teledietetics increases healthy-eating awareness.
Nutrition monitoring is a relevant method to gain an overview of factors influencing health. However, keeping a food diary often constitutes a challenge for a patient, and developing a user-friendly and useful electronic food diary is not straightforward
The analyzed apps reflected a variety of approaches to recording food intake and nutrition using different terminals--mostly mobile phones (35%), followed by PCs (29%) and PDAs (23%) for older studies, designed mainly for users with obesity (45%), diabetes mellitus (42%) and overweight (32%), or people who want to stay healthy (10%). The majority of the reviewed applications (67%) offered only input of food type and quantity. All approaches (n=31), except for two, relied on manual input of data, either by typing or by selecting a food type from a database. The exceptions (n=2) used a barcode scanning function. Users of mobile phone applications were not limited to data recording, but could view their data on the screen and send it via email. The tested web applications offered similar functionalities for recording food intake.
electronic food diary on a mobile phone that includes an energy balance visualization and computes and displays the difference between energy intake from food entries and energy expenditure from a multiple-sensor device that provides objective estimates of energy expenditure in real time

Answer: Electronic dietary records were better than food diaries in terms of fat percentage reduction in our trials, indicating that teledietetics increases healthy-eating awareness.
Question: List functions that are evaluated with the Full Outline of Unresponsiveness score?

Context:
The Full Outline of UnResponsiveness (FOUR) Score is a coma scale that consists of four components (eye and motor response, brainstem reflexes, and respiration). 
Recently, the full outline of unresponsiveness (FOUR) score was introduced, which is composed of four clinically distinct categories of evaluation: eye reaction, motor function, brainstem reflexes and respiratory pattern. 
The FOUR (Full Outline of UnResponsiveness) score, a new coma scale, evaluates 4 components: eye and motor responses, brainstem reflexes and respiration. 
The FOUR (Full Outline of UnResponsiveness) score, a new coma scale, evaluates 4 components: eye and motor responses, brainstem reflexes and respiration.
To evaluate the validity of the FOUR (Full Outline of UnResponsiveness) score (ranging from 0 to 16), a new coma scale consisting of 4 components (eye response, motor response, brainstem reflexes, and respiration pattern), when used by the staff members of a medical intensive care unit (ICU).
To evaluate the validity of the FOUR (Full Outline of UnResponsiveness) score (ranging from 0 to 16), a new coma scale consisting of 4 components (eye response, motor response, brainstem reflexes, and respiration pattern), when used by the staff members of a medical intensive care unit (ICU).
Recently, the full outline of unresponsiveness (FOUR) score was introduced, which is composed of four clinically distinct categories of evaluation: eye reaction, motor function, brainstem reflexes and respiratory pattern.
The FOUR (Full Outline of UnResponsiveness) score, a new coma scale, evaluates 4 components: eye and motor responses, brainstem reflexes and respiration.

Answer: The FOUR (Full Outline of UnResponsiveness) score, a new coma scale, evaluates 4 components: eye and motor responses, brainstem reflexes and respiration.
Exact answer: eye responses, motor responses, brainstem reflexes, respiration
Question: Which drugs are utilized to treat eosinophilic esophagitis?

Context:
Current therapeutic options include use of proton-pump inhibitors, immunosuppressive drugs, elimination diets, and esophageal dilatation.
Aerosolized, swallowed fluticasone leads to a histologic but not a symptomatic response in adults with EoE
OVB is an effective treatment of pan-esophageal disease in children with EoE. OVB improves symptoms and endoscopic and histologic features. Proton pump inhibitor single therapy did not significantly improve esophageal eosinophilia or symptoms of EoE.

Answer: Therapeutic options of eosinophilic esophagitis include use of proton-pump inhibitors, immunosuppressive drugs, elimination diets, and esophageal dilatation.
Oral viscous budesonide (OVB) is an effective treatment of pan-esophageal disease in children with EoE. OVB improves symptoms and endoscopic and histologic features.
Exact answer: proton pump inhibitors, immunosoppressive drugs, budesonide
Question: What is a mitochondrial nucleoid?

Context:
A naked mtDNA molecule is longer than a typical mitochondrion and is therefore compacted in vivo to form a nucleoprotein complex, denoted the mitochondrial nucleoid.
The packaging of mitochondrial DNA (mtDNA) into DNA-protein assemblies called nucleoids provides an efficient segregating unit of mtDNA,
Mitochondrial DNA (mtDNA) is organized in nucleoids in complex with accessory proteins, proteins of mtDNA replication and gene expression machinery.
The independent mitochondrial genetic information is organized in so-called mitochondrial nucleoids
 packaging of mitochondrial DNA (mtDNA) into protein-DNA assemblies called nucleoids confers higher-order organization to the mitochondrial genome.
mitochondrial DNA is packaged into macromolecular assemblies called nucleoids, composed of one or more copies of mitochondrial DNA and associated proteins. 
human mitochondrial DNA (mtDNA) had long been believed to be rather naked because mitochondria lack histone

Answer: A naked mtDNA molecule is longer than a typical mitochondrion and is therefore compacted in vivo to form a nucleoprotein complex, denoted the mitochondrial nucleoid.
Question: Is Mammaprint approved by the United States Food and Drug Administration?

Context:
an FDA-cleared 70-gene signature of MammaPrint panel 
on MammaPrint, the first and only assay for breast cancer management that has been cleared by the FDA.
The MammaPrint assay has the advantages of a 510(k) clearance by the US Food and Drug Administration, a larger gene number which may enhance further utility, and the potentially wider patient eligibility including lymph node-positive, ER-negative, 
The MammaPrint assay has the advantages of a 510(k) clearance by the U.S. Food and Drug Administration, a larger gene number, which may enhance further utility, and a potentially wider patient eligibility, including lymph node-positive, estrogen receptor (ER)-negative, and younger patients being accrued into the prospective trial (Microarray in Node-Negative Disease May Avoid Chemotherapy). 

Answer: Yes, Mammaprint has been approved by the US Food and Drug Administration.
Exact answer: yes