nirantk/geneticsQA-train huggingface dataset:
Question: List symptoms of Gradenigo's syndrome.

Context:
INTRODUCTION: Gradenigo's syndrome is nowadays a rare condition characterized by a triad of otorrhea, facial pain with trigeminal nerve involvement and abducens nerve palsy.
Gradenigo's syndrome is a rare but life threatening complication of acute otitis media (AOM), which includes a classic triad of otitis media, deep facial pain and ipsilateral abducens nerve paralysis. 
We report a case of typical Gradenigo's syndrome, including left abducens nerve palsy, left facial pain and paresthesia in V1 and V2 distribution of trigeminal nerve caused by solitary osseous plasmacytoma of the left petrous apex.
BACKGROUND: Gradenigo's syndrome is a rare disease, which is characterized by the triad of the following conditions: suppurative otitis media, pain in the distribution of the first and the second division of trigeminal nerve, and abducens nerve palsy.
RESULTS: It was after Gradenigo that the well-known syndrome consisting of diplopia and facial pain due to a middle ear infection was named.
Gradenigo's syndrome, the triad of suppurative otitis media, abducens nerve palsy and pain in the ophthalmic division of the trigeminal nerve, remains a rare complication of otitis media.
In 1904, Giuseppe Gradenigo published his case series on the triad of ipsilateral abducens nerve palsy, facial pain in the trigeminal nerve distribution, and suppurative otitis media, which would subsequently be referred to as Gradenigo syndrome

Answer: Gradenigo's syndrome is a rare but life threatening complication of acute otitis media, which includes a classic triad of otitis media, deep facial pain and ipsilateral abducens nerve paralysis.
Exact answer: otitis media, deep facial pain, abducens nerve paralysis
Question: What is targeted by Palbociclib?

Context:
BACKGROUND: Necitumumab is a second-generation, recombinant, human immunoglobulin G1 EGFR antibody. 
Epidermal growth factor receptor-directed monoclonal antibodies in nonsmall cell lung cancer: an update.
 A Southwest Oncology Group study currently prospectively evaluates the predictive biomarkers for cetuximab. In the SQUIRE phase III trial, necitumumab added to cisplatin and gemcitabine increased the survival in patients with advanced squamous cell NSCLC. 
BACKGROUND: Necitumumab is a second-generation recombinant human immunoglobulin G1 EGFR monoclonal antibody that competitively inhibits ligand binding. 
Numerous other drugs are in earlier stages of development for HNSCC treatment, including novel anti-EGFR mAbs (MEHD7945A, necitumumab, and RO5083945), small-molecule TKIs (vandetanib, icotinib, and CUDC-101), EGFR antisense, various add-on therapies to radiation and chemotherapy (bevacizumab, interleukin-12, lenalidomide, alisertib, and VTX-2337), and drugs (temsirolimus, everolimus, OSI-906, dasatinib, and PX-866) intended to overcome resistance to anti-EGFR agents. 
Necitumumab, a fully human monoclonal antibody, is currently evaluated in combination with chemotherapy in two phase III trials in patients with advanced NSCLC. 
Necitumumab is currently evaluated in combination with chemotherapy in two randomized phase III trials.
Joining cetuximab, sorafenib, afatinib, intedanib, and crizotinib in phase III development for non-small cell lung cancer (NSCLC) are ramucirumab (developed by ImClone, a subsidiary of Lilly), necitumumab (developed by ImClone and Bristol-Myers Squibb), and tivantinib (ARQ 197, developed by ArQule and Daiichi Sankyo). Necitumumab is a second-generation anti-EGFR monoclonal antibody (mAb) similar to cetuximab.
Necitumunab is a fully human IgG1 monoclonal antibody targeting EGFR, having the potential benefit of lower hypersensitivity reaction risk as compared with cetuximab and also equivalent antibody-dependent cell-mediated cytotoxicity.
Necitumumab, a monoclonal antibody directed against EGFR, is currently under development as a treatment for advanced NSCLC.
A phase I pharmacologic study of necitumumab (IMC-11F8), a fully human IgG1 monoclonal antibody directed against EGFR in patients with advanced solid malignancies.
PURPOSE: This study aimed to determine a maximum tolerated dose (MTD) and recommended dose for disease-directed studies of necitumumab (IMC-11F8), a fully human IgG(1) monoclonal antibody directed at the epidermal growth factor receptor, and to characterize the safety profile, pharmacokinetics, preliminary antitumor activity, and immunogenicity of necitumumab.

Answer: Necitumumab is a fully human IgG(1) monoclonal antibody directed at the epidermal growth factor receptor (EGFR). It is used for treatment of nonsmall cell lung cancer.
Exact answer: epidermal growth factor receptor
Question: Which computational frameworks are available for predicting enhancers?

Context:
In this study we developed DEEP, a novel ensemble prediction framework. DEEP integrates three components with diverse characteristics that streamline the analysis of enhancer's properties in a great variety of cellular conditions. In our method we train many individual classification models that we combine to classify DNA regions as enhancers or non-enhancers. DEEP uses features derived from histone modification marks or attributes coming from sequence characteristics. Experimental results indicate that DEEP performs better than four state-of-the-art methods on the ENCODE data. We report the first computational enhancer prediction results on FANTOM5 data where DEEP achieves 90.2% accuracy and 90% geometric mean (GM) of specificity and sensitivity across 36 different tissues. We further present results derived using in vivo-derived enhancer data from VISTA database. DEEP-VISTA, when tested on an independent test set, achieved GM of 80.1% and accuracy of 89.64%.
Our novel PRISM (predicting regulatory information from single motifs) approach obtains 2543 TF function predictions in a large variety of contexts, at a false discovery rate of 16%. The predictions are highly enriched for validated TF roles, and 45 of 67 (67%) tested binding site regions in five different contexts act as enhancers in functionally matched cells.
DEEP: a general computational framework for predicting enhancers
We report the first computational enhancer prediction results on FANTOM5 data where DEEP achieves 90.2% accuracy and 90% geometric mean (GM) of specificity and sensitivity across 36 different tissues
DEEP: a general computational framework for predicting enhancers.

Answer: DEEP integrates three components with diverse characteristics that streamline the analysis of enhancer's properties in a great variety of cellular conditions. DEEP uses features derived from histone modification marks or attributes coming from sequence characteristics. Experimental results indicate that DEEP performs better than four state-of-the-art methods on the ENCODE data. The PRISM (predicting regulatory information from single motifs) approach obtains 2543 TF function predictions in a large variety of contexts, at a false discovery rate of 16%. The predictions are highly enriched for validated TF roles, and 45 of 67 (67%) tested binding site regions in five different contexts act as enhancers in functionally matched cells.
Exact answer: DEEP, PRISM
Question: Is delayed enhancement documented in patients with non-ischemic dilated cardiomyopathy?

Context:
Myocardial fibrosis was present in 30% of patients, the majority of which was mid-myocardial (63%). 
 DCM patients frequently have myocardial fibrosis detected on CE-CMR, the majority of which is mid-myocardial.
Fifty (40%) patients showed myocardial DE, representing 12±7% of LV mass.
one case was dilated cardiomyopathy, in which the delayed enhancement was diffuse small midwall spots 
In the dilated cardiomyopathy group, only seven (29%) patients showed delayed enhancement and its pattern was characterized by mid-wall, patchy or diffuse location.
Patterns of delayed enhancement are different in dilated cardiomyopathy and ischemic cardiomyopathy, reflecting the presence of scarring or various degrees of fibrosis in left ventricular myocardium. The presence of subendocardial or transmural delayed enhancement at contrast-enhanced cardiovascular magnetic resonance allowed distinction between dilated cardiomyopathy and ischemic cardiomyopathy with high sensitivity (88%) and specificity (100%).

Answer: Delayed enhancement is documented in almost 30% of patients with non-ischemic dilated cardiomyopathy and  its pattern is characterized by mid-wall, patchy or diffuse location.
Exact answer: yes
Question: Does PU.1 (SPI1) affect NF-kB binding?

Context:
Recent data demonstrate that developmental transcription factors like the macrophage fate-determining Pu.1 set the stage for the activity of ubiquitous transcription factors activated by inflammatory stimuli, like NF-kB, AP-1, and interferon regulatory factors (IRFs).
Within 1217 bp of upstream sequence, 3 sites for NF-kB, 10 sites for NF-IL6, 15 sites for AP1, 6 sites for AP4, 2 sites for CHOP/CEBP alpha and 1 site for SP1 and PU.1 were identified.
As little as 82 bp of upstream sequence gave relatively strong luciferase activity, a region containing both a PU.1 and NF-kB site.
Potential transcription regulatory elements, AP1, AP2, AP3, NF-kB and GATA recognition sequences, are located within 523 bp upstream of the p35 gene; however, no TATA box was identified. The p40 subunit gene consists of eight exons. A TATA box is located 30 bp upstream from the transcription start site, and AP1, AP3, GATA, and Pu.1 recognition sequences are located within 690 bp upstream of the p40 gene.
Several putative binding sequences for ubiquitous (Sp1, AP-1, AP-2, and NF-kB) and leukocyte-specific (PU.1) transcription factors have been identified in the proximal region of the CD11c promoter which may participate in the regulation of the expression of p150,95.
PU.1 is regulated by NF-kappaB through a novel binding site in a 17 kb upstream enhancer element.

Answer: Recent data demonstrate that developmental transcription factors like the macrophage fate-determining Pu.1 set the stage for the activity of ubiquitous transcription factors activated by inflammatory stimuli, like NF-kB, AP-1, and interferon regulatory factors (IRFs). Within 1217 bp of upstream sequence, 3 sites for NF-kB, 10 sites for NF-IL6, 15 sites for AP1, 6 sites for AP4, 2 sites for CHOP/CEBP alpha and 1 site for SP1 and PU.1 were identified.
Recent data demonstrate that developmental transcription factors like the macrophage fate-determining Pu.1 set the stage for the activity of ubiquitous transcription factors activated by inflammatory stimuli, like NF-kB, AP-1, and interferon regulatory factors (IRFs).
Exact answer: yes
Question: What is known about the role of mHealth in the prevention of disease?

Context:
mHealth approaches to child obesity prevention
Daily text messaging for weight control among racial and ethnic minority women
text messaging intervention for weight loss among predominantly black women. 
Given the increasing penetration of mobile devices, text messaging may be a useful self-monitoring tool for weight control, particularly among populations most in need of intervention
The review revealed evidence that mHealth tools support HIV programmatic priorities, including: linkage to care, retention in care, and adherence to antiretroviral treatment. In terms of technical features, mHealth tools facilitate alerts and reminders, data collection, direct voice communication, educational messaging, information on demand, and more
Mobile health messages help sustain recent weight loss.
 A clinically significant decrease in mean weight, higher rate of sustained weight loss, and medium-to-large effects on sustained weight loss occurred in the promotion and prevention interventions
A mobile health intervention for weight management among young adults:
HIV prevalence in Uganda has leveled off, however trends indicate that incidence is on the rise and disproportionately affects certain vulnerable groups, such as women. There is growing support for using mobile health (mHealth) programs to reach vulnerable populations. 
We successully designed and implemented a mobile phone SMS-based system to track pregnancy and maternal and child outcomes in limited resources setting.
The purpose of the study, Project ACTION (Adult smoking Cessation Treatment through Innovative Outreach to Neighborhoods), is to utilize a mobile clinic model, a network of community sites (i.e., community centers and churches) and an interactive mobile messaging system to reach and deliver smoking cessation treatment to underserved, low-income communities.
Participants were randomized to usual prenatal care plus text messaging or usual care alone. The evaluation has a theoretical model of behavior change and measures mediators as well as behavioral outcomes. Results will inform how behavioral theory works within mobile health programs.

Answer: Most reported uses of mHealth are for treatment, we identified report on approaches to child obesity prevention.
Question: Does Apolipoprotein E (ApoE) have anti-inflammatory activity?

Context:
 have previously reported that apolipoprotein E (apoE), a protein component of very-low-density lipoproteins (VLDL) and high-density lipoproteins and a potent plasma-borne atheroprotective factor, exerts anti-inflammatory activity in macrophages by switching the activation profile from M1 ("classic") to M2 ("alternative") in a process involving signaling via low-density lipoprotein receptor 
anti-inflammatory activity in macrophages 
Small peptides corresponding to the receptor-binding region of apoE mimic the anti-inflammatory activity of the apoE 
Apolipoprotein (apo) E-containing high-density lipoprotein (HDL) has antioxidant, anti-inflammatory and anti-atherogenic properties

Answer: Yes. ApoE has anti-inflammatory activity
Exact answer: yes
Question: List fluorescent reporter proteins.

Context:
Fluorescent Timer, or DsRed1-E5, is a mutant of the red fluorescent protein, dsRed, in which fluorescence shifts over time from green to red as the protein matures.
green fluorescent protein (Gfp)
Characterization of flavin-based fluorescent proteins: an emerging class of fluorescent reporters.
Flavin-based fluorescent proteins (FbFPs)
mCherry was employed as a reporter protein 
yellow fluorescent protein
red cytoplasmic fluorescent reporter protein. 
red fluorescent reporter protein
 enhanced green fluorescent reporter protein
Fluorescent and luminescent reporter genes have become popular tools for the real-time monitoring of gene expression in living cells. 
 fluorescent reporter protein [green fluorescent protein (GFP) and DsRed2]
coral fluorescent reporter protein 
driving a cassette for the enhanced green "live" fluorescent reporter protein (eGFP) 
GFP as a fluorescent reporter protein
 protein
red fluorescent reporter protein (RFP) gene. 
The red fluorescent protein eqFP611
the green fluorescent reporter protein gene 
 red fluorescent reporter protein
beta-phycoerythrin, a fluorescent reporter protein derived from algae
 live-cell fluorescent reporter protein, Timer
red fluorescent reporter protein

Answer: Fluorescent and luminescent reporter genes have become popular tools for the real-time monitoring of gene expression in living cells:
green fluorescent protein
Timer
red fluorescent protein
yellow fluorescent protein
beta-phycoerythrin
coral fluorescent reporter protein
enhanced green fluorescent reporter protein
mCherry
Exact answer: green fluorescent protein, Gfp, Timer, DsRed1-E5, red fluorescent protein, dsRed, yellow fluorescent protein, beta-phycoerythrin, coral fluorescent reporter protein, enhanced green fluorescent reporter protein, mCherry
Question: Which hormone receptor function is altered in patients with Donohue syndrome?

Context:
This disease is caused by a defective insulin receptor and features abnormal glucose metabolism and retarded intrauterine and postnatal growth.
Biallelic insulin receptor (INSR) gene mutations cause congenital syndromes of severe insulin resistance (SIR) known as Donohue syndrome (DS) and Rabson-Mendenhall syndrome (RMS). 
Severe progressive obstructive cardiomyopathy and renal tubular dysfunction in Donohue syndrome with decreased insulin receptor autophosphorylation due to a novel INSR mutation.
Donohue syndrome (leprechaunism; OMIM *246200) is a rare, recessively inherited disorder of extreme insulin resistance due to mutations in the insulin receptor gene (INSR) causing either defects in insulin binding or receptor autophosphorylation and tyrosine kinase activity.
Leprechaunism (Donohue syndrome): a case bearing novel compound heterozygous mutations in the insulin receptor gene.
Leprechaunism (Donohue syndrome) is the most severe type of insulin receptor (INSR) gene anomaly with the majority of patients surviving for only 2 years.
A novel mutation of the insulin receptor gene in a preterm infant with Donohue syndrome and heart failure.
Donohue syndrome (DS) is a rare autosomal recessive condition caused by mutations in the gene encoding the insulin receptor.
Any dysfunction of insulin signalling pathway as a result of insulin receptor gene mutations is linked with various forms of insulin resistance, including insulin resistance type A, Donohue or Rabson-Mendenhall syndrome, which differ in the level of severity. 
Donohue syndrome in a neonate with homozygous deletion of exon 3 of the insulin receptor gene.
Donohue syndrome describes the clinical consequences of the most severe genetic loss of insulin receptor function.
Homozygous or compound heterozygous mutations within the insulin binding domain of the human insulin receptor (INSR) are usually associated with severe impairment of insulin binding leading to Donohue syndrome ("Leprechaunism"), which is characterized by excessive hyperglycemia with hyperinsulinism, pre- and postnatal growth retardation, distinct dysmorphism and early death. 
The former mutation has been described in homozygous form in Donohue syndrome, while the latter is novel. 

Answer: Donohue syndrome (leprechaunism) is a rare, recessively inherited disorder of extreme insulin resistance due to mutations in the insulin receptor gene causing either defects in insulin binding or receptor autophosphorylation and tyrosine kinase activity. This syndrome is characterized by excessive hyperglycemia with hyperinsulinism, pre- and postnatal growth retardation, distinct dysmorphism and early death. Progressive obstructive cardiomyopathy and renal tubular dysfunction have been described in patients with Donohue syndrome. Milder form of insulin resistance due to insulin receptor gene mutation is coined as Rabson-Mendenhall syndrome.
Exact answer: insulin receptor
Question: Is airplane stroke syndrome a common disease.

Context:
Only 37 cases of stroke during or soon after long-haul flights have been published to our knowledge. 
Our centre admitted 5727 stroke patients, of whom 42 (0.73%) had flight-related strokes.
The authors report three cases of ischemic stroke in young adults that occurred during or after an airplane flight.

Answer: No. Only 37 cases of stroke during or soon after long-haul flights have been published. A single center study reported that 42 out of 5727 stroke admissions (0.73%) were flight-related strokes.
Exact answer: no
Question: Have thyronamines  effects on fat tissue?

Context:
In conclusion, trace amines and thyronamines are negative inotropic agents.
Their in vivo administration induces effects opposite to those induced by thyroid hormone, including lowering of body temperature.

Answer: There is not clear evidence that thyronamines have direct effect on adipose tissue
Exact answer: no
Question: What is the mode of inheritance of Facioscapulohumeral muscular dystrophy (FSHD)?

Context:
autosomal dominant FSHD1
Facioscapulohumeral muscular dystrophy (FSHD) is a neuromuscular disease, characterized by an autosomal dominant mode of inheritance, facial involvement, and selectivity and asymmetry of muscle involvement.
Facioscapulohumeral dystrophy (FSHD) is an autosomal-dominant disorder characterized by weakness of the face, upper arm, shoulder, and lower limb musculature, with an onset between the first and third decades. 
Clinical diagnosis is made from the distinctive pattern of weakness, autosomal-dominant inheritance, and confirmed by genetic testing.
 In one family together with prenatal diagnosis founder mutation in FSHD A1 gene was detected, according to the autosomal dominant (AD) inheritance.
Facioscapulohumeral muscular dystrophy (FSHD) is a primary muscle disorder with autosomal dominant inheritance.
Facioscapulohumeral muscular dystrophy (FSHD) is a slowly progressive myopathy with autosomal dominant inheritance remarkable for its early involvement of facial musculature.
Consensual diagnostic criteria for facioscapulohumeral dystrophy (FSHD) include onset of the disease in facial or shoulder girdle muscles, facial weakness in more than 50% of affected family members, autosomal dominant inheritance in familial cases, and evidence of myopathic disease in at least one affected member without biopsy features specific to alternative diagnoses
Facioscapulohumeral dystrophy (FSHD) is an autosomal-dominant muscular disorder associated with a short (<35 kb) EcoRI/BlnI fragment resulting from deletion of an integral number of units of a 3.3-kb repeat located at 4q35.
In 139 families, dominant inheritance was observed in 97, a pattern compatible with germline mosaicism in 6, while sporadic cases were found in 36 families. 
In 139 families, dominant inheritance was observed in 97, a pattern compatible with germline mosaicism in 6, while sporadic cases were found in 36 families.

Answer: Facioscapulohumeral muscular dystrophy has an autosomal dominant inheritance pattern.
Exact answer: autosomal dominant
Question: Which tool is available for predicting regulatory interactions from ChIP-seq data?

Context:
CisMapper: predicting regulatory interactions from transcription factor ChIP-seq data
We present CisMapper, which predicts the regulatory targets of a TF using the correlation between a histone mark at the TF's bound sites and the expression of each gene across a panel of tissues.
Using both chromatin conformation capture and differential expression data, we show that CisMapper is more accurate at predicting the target genes of a TF than the distance-based approaches currently used, and is particularly advantageous for predicting the long-range regulatory interactions typical of tissue-specific gene expression
 CisMapper also predicts which TF binding sites regulate a given gene more accurately than using genomic distance. Unlike distance-based methods, CisMapper can predict which transcription start site of a gene is regulated by a particular binding site of the TF
CisMapper: predicting regulatory interactions from transcription factor ChIP-seq data.
CisMapper: predicting regulatory interactions from transcription factor ChIP-seq data.
Using both chromatin conformation capture and differential expression data, we show that CisMapper is more accurate at predicting the target genes of a TF than the distance-based approaches currently used, and is particularly advantageous for predicting the long-range regulatory interactions typical of tissue-specific gene expression.

Answer: CisMapper predicts the regulatory targets of a TF using the correlation between a histone mark at the TF's bound sites and the expression of each gene across a panel of tissues. CisMapper is more accurate at predicting the target genes of a TF than the distance-based approaches currently used, and is particularly advantageous for predicting the long-range regulatory interactions typical of tissue-specific gene expression. CisMapper also predicts which TF binding sites regulate a given gene more accurately than using genomic distance. Unlike distance-based methods, CisMapper can predict which transcription start site of a gene is regulated by a particular binding site of the TF.
Exact answer: CisMapper