nirantk/geneticsQA-train huggingface dataset:
Question: What memory problems are reported in the " Gulf war syndrome"?

Context:
The strongest associations were for mood swings (OR 20.9, 95%CI 16.2-27.0), memory loss/lack of concentration (OR 19.6, 95% CI 15.5-24.8), night sweats (OR 9.9, 95% CI 6.5-15.2), general fatigue (OR 9.6, 95% CI 8.3-11.1) and sexual dysfunction (OR 4.6, 95%CI 3.2-6.6).
The symptoms include incapacitating fatigue, musculoskeletel and joint pains, headaches, neuropsychiatric disorders, affect changes, confusion, visual problems, changes of gait, loss of memory, lymphadenopathies, respiratory impairment, impotence, and urinary tract morphological and functional alterations. 
In early 1992, U.S. troops returning from the Gulf War began reporting a variety of nonspecific symptoms such as fatigue, skin rash, headache, muscle and joint pain, and loss of memory. These reports marked the beginning of what was to be identified as the Gulf War Syndrome (GWS). 
We report on a 29-year-old man who suffered from dysmnesia, disturbance of orientation, cognitive impairment, and double vision. His history revealed several front-line operations in 1990 and 1991 during the Gulf War. 
Neuropsychological tests disclosed severe cognitive impairment especially concerning memory.
A cluster of common health problems included: skin rash, cough, depression, unintentional weight loss, insomnia, and memory problems.
Syndromes 1 ("impaired cognition," characterized by problems with attention, memory, and reasoning, as well as insomnia, depression, daytime sleepiness, and headaches), 2 ("confusion-ataxia," characterized by problems with thinking, disorientation, balance disturbances, vertigo, and impotence), and 3 ("arthro-myo-neuropathy," characterized by joint and muscle pains, muscle fatigue, difficulty lifting, and extremity paresthesias) represented strongly clustered symptoms; whereas, syndromes 4 ("phobia-apraxia"), 5 ("fever-adenopathy"), and 6 ("weakness-incontinence") involved weaker clustering and mostly overlapped syndromes 2 and 3. 

Answer: Loss of memory and dysmnesia are memory problems reported in the " Gulf war syndrome". Patients suffering from this syndrome often have other
nonspecific symptoms such as fatigue, skin rash, headache, muscle and joint pain and sexual dysfunction.
Exact answer: loss of memory, dysmnesia
Question: Which drugs have been found effective for the treatment of chordoma?

Context:
The combination treatment of bortezomib with topoisomerase I and II inhibitors increased the therapeutic potency in U-CH2 and patient-derived primary cultures.
Vincristine, doxorubicin, etoposide, cisplatin, and fludarabine, each at a concentration of 10 μM, decreased the number of chordoma cells when given alone down to 11%, 0%, 30%, 67%, and 3%, respectively. Etoposide and cisplatin, each at a concentration of 10 μM, reduced the percentage of viable chordoma cells in a more effective way when given with 1 μM ATRA simultaneously, reducing the number of viable cells to 14% and 9%, respectively.
Percutaneous intratumoral injection with pingyangmycin lipiodol emulsion for the treatment of recurrent sacrococcygeal chordomas
Preliminary results showed that PIIT with pingyangmycin lipiodol emulsion under fluoroscopic guidance is effective and safe and may be considered as a treatment option.
Percutaneous intratumoral injection with pingyangmycin lipiodol emulsion for treatment of recurrent sacrococcygeal chordomas
During the follow-up (median time of 21.7 months, range 10-26 months), all the patients showed obviously reduced tumor size and VAS, and partial remission was achieved in 6 patients and stable disease (SD) in 1 patient.
Fluoroscopy-guided percutaneous intratumoral injection of PLE can be effective and safe and may serve as a alternative for treatment of recurrent sacrococcygeal chordomas.
The expression of Stat3 signaling cascade was inhibited in all chordoma cell lines after treatment with SD-1029. The cytotoxicity of the combination of SD-1029 and chemotherapeutic drugs is significantly better than either agent alone. Phosphorylation of Stat3 in chordoma cells in vitro and cellular proliferation in three-dimensional culture were inhibited by SD-1029.
In conclusion, the Stat3 pathway is constitutively activated in chordomas and the level of expression may serve as a predictor for prognosis. Blockade of the Stat3 pathway represents a potential strategy for future treatment.

Answer: Established chordoma cell lines, and patient-derived primary cell cultures, as well as chordoma tumors in vivo were found to be sensitive to treatment with bortezomib, vincristine, doxorubicin, etoposide, cisplatin, fludarabine and SD-1029 Stat3 inhibitor. Moreover, percutaneous intratumoral injection with pingyangmycin lipiodol emulsion was shown to be effective against chordoma. It should be stressed that combination treatment with the use of the above drugs was always able to increase the therapeutic potency.
Exact answer: bortezomib, vincristine, doxorubicin, etoposide, cisplatin, fludarabine, SD-1029 Stat3 inhibitor, pingyangmycin lipiodol emulsion
Question: What is the mode of inheritance of  long QT  Jervell and Lange-Nielsen syndrome?

Context:
Homozygous or compound heterozygous mutations in KCNQ1 cause Jervell and Lange-Nielsen syndrome, a rare, autosomal-recessive form of long-QT syndrome characterized by deafness, marked QT prolongation, and a high risk of sudden death.
KCNQ1 is associated with two different entities of LQTS, the autosomal-dominant Romano-Ward syndrome (RWS), and the autosomal-recessive Jervell and Lange-Nielsen syndrome (JLNS) characterized by bilateral deafness
Jervell and Lange-Nielsen syndrome (JLNS) is characterized by sensorineural deafness, QT prolongation, abnormal T waves, ventricular tachyarrhythmias, and autosomal recessive inheritance.
Jervell and Lange-Nielsen syndrome (JLNS) is an autosomal recessive syndrome characterised by profound congenital sensorineural deafness and prolongation of the QT interval on the electrocardiogram, representing abnormal ventricular repolarisation.
Jervell and Lange-Nielsen syndrome (MIM 220400; JLNS), is a rare form of profound congenital deafness combined with syncopal attacks and sudden death due to prolonged QTc; it is an autosomal recessive trait. 
Different mutations in KVLQT1 cause the dominant Romano-Ward (RW) syndrome and the recessive Jervell and Lange-Nielsen (JLN) syndrome, which, in addition to cardiac abnormalities, includes congenital deafness. 
The Jervell and Lange-Nielsen syndrome (JLNS) is characterized by prolongation of the QT interval, deafness, and autosomal-recessive inheritance, and the Romano-Ward syndrome is characterized by a prolonged QT interval, autosomal-dominant inheritance, and no deafness. 

Answer: Jervell and Lange-Nielsen long QT syndrome (JLNS) is characterized by autosomal recessive mode of inheritance
Exact answer: autosomal recessive
Question: Is there any genetic determinant of hair pigmentation that could be useful in forensic analyses?

Context:
a recent paper has reported the genetic determination of eye and hair color in samples up to 800 years old. 
 Here, we demonstrate that human hair color is predictable from DNA variants with similarly high accuracies.
12 genes previously associated with human hair color variation
 several key pigmentation genes have been characterised, in particular the melanocortin 1 receptor gene (MC1R). Here, the function and known mutations of MC1R and other human pigmentation genes including ASIP, MATP, SLC24A5, TYR, TYRP1 and OCA2 are outlined, and a forensic test based on MC1R SNPs presented.
Recent studies have proved that there is a significant association between some genetic variants of the melanocortin 1 receptor (MC1R) gene and red hair color.
We describe a minisequencing protocol for screening DNA samples for the presence of 12 mutations in the human melanocortin 1 receptor gene (MC1R), eight of which are associated with the red hair phenotype. 
Interactions between HERC2, OCA2 and MC1R may influence human pigmentation phenotype.
Several genome-wide association studies for pigmentation have now been conducted and identified single nucleotide polymorphism (SNP) markers in known, TYR, TYRP1, OCA2, SLC45A2, SLC24A5, MC1R, ASIP, KITLG and previously unknown SLC24A4, IRF4, TPCN2, candidate genes. 
 five red hair colour (RHC) MC1R alleles, 
Naturally blond hair is rare in humans and found almost exclusively in Europe and Oceania. Here, we identify an arginine-to-cysteine change at a highly conserved residue in tyrosinase-related protein 1 (TYRP1) as a major determinant of blond hair in Solomon Islanders.

Answer: Yes, there are at least 12 genes associated with human hair color variation such as: TYR, TYRP1, OCA2, SLC45A2, SLC24A5, MC1R, ASIP and KITLG.
Exact answer: Yes, there are at least 12 genes associated with human hair color variation such as: TYR, TYRP1, OCA2, SLC45A2, SLC24A5, MC1R, ASIP and KITLG.
Question: What is the influence of patent expiry on  ACE inhibitor prescribing.

Context:
Generic switch after ramipril patent expiry is not associated with decreased pharmacy refill compliance: a retrospective study using the DAPI database.
The costs per DDD decreased for all three drugs and, as expected, these costs decrease more rapidly after patent expiry. Significant differences in the trend lines were found for enalapril and fluoxetine

Answer: Patent expiry has different effects on prescribing in different systems. It leads to decreased cost but no decreased refill compliance in countries like Sweden, Germany etc. In countries like Taiwan, where doctors profit directly from dispensing, patients are switched to ARBs which are more costly.
Question: What is the effect of ivabradine in heart failure with preserved ejection fraction?

Context:
Traditional agents with strong evidence in HFrEF have proved unsuccessful in HFpEF. Newer agents such as angiotensin receptor neprilysin inhibitor, sildenafil, and ivabradine have demonstrated benefits without improving mortality.
In db/db, a model of HFPEF, selective HR reduction by If-inhibition improved vascular stiffness, LV contractility, and diastolic function. Therefore, If-inhibition might be a therapeutic concept for HFPEF, if confirmed in humans.
Selective HR reduction with IVA reduces DD and cardiac fibrosis in hypercholesterolemic rabbits. These beneficial effects of IVA support testing pure HR reduction in patients with diastolic heart failure.
Beside its use in therapy of coronary artery disease, I(f)-channel inhibition potentially exhibits beneficial effects in systolic and diastolic heart failure as well.
In patients with HFpEF, short-term treatment with ivabradine increased exercise capacity, with a contribution from improved left ventricular filling pressure response to exercise as reflected by the ratio of peak early diastolic mitral flow velocity to peak early diastolic mitral annular velocity.

Answer: I(f)-channel inhibition potentially exhibits beneficial effects in diastolic heart failure.  In patients with heart failure with preserved ejection fraction (HFpEF), short-term treatment with ivabradine increased exercise capacity, with a contribution from improved left ventricular filling pressure response to exercise as reflected by the ratio of peak early diastolic mitral flow velocity to peak early diastolic mitral annular velocity.  Ivabradine has demonstrated benefits in HFpEF without improving mortality.	In db/db, a model of HFpEF, ivabradine improved vascular stiffness, left ventricular contractility, and diastolic function. Furthermore, ivabradine reduces cardiac fibrosis in hypercholesterolemic rabbits.
Question: Which drugs are utilized to treat amiodarone-induced thyroitoxicosis?

Context:
good response to anti-thyroid drugs and steroid therapy
The disease course of amiodarone-induced thyrotoxicosis is usually benign and remits with timely administration of anti-thyroid medications, with or without corticosteroids.
RIT may be a safe and useful method of AIT therapy in patients with low RAIU, in whom other treatment methods are contraindicated.
Treatment consists in the use of a high dose of anti-thyroid drugs and steroids in an isolated form or in combination.
the addition of lithium carbonate to the two other drugs resulted in a successful and safety therapy in controlling amiodarone-induced thyrotoxicosis.
lithium is a useful and safe medication for treatment of iodine-induced thyrotoxicosis caused by amiodarone.
Two patients with amiodarone-induced thyrotoxicosis were treated successfully with potassium perchlorate and carbimazole while treatment with amiodarone was continued.
Amiodarone-induced thyrotoxicosis seems to be a transient condition that can be treated successfully with a short course of antithyroid drugs without stopping amiodarone treatment.
Both patients were successfully treated with propylthiouracil (PTU) and dexamethasone (DXT).

Answer: Amiodarone-induced thyrotoxicosis treatment includes anti-thyroid drugs and steroid therapy
Radio Iodine Treatment (RIT) may be a safe and useful method of AIT therapy in patients with low RAIU, in whom other treatment methods are contraindicated.
Lithium is a useful and safe medication for treatment of iodine-induced thyrotoxicosis caused by amiodarone.
Thyrodectomy may be necessary in presence of unresponsiveness to standard medical treatments
Exact answer: Antithyroid drugs, Corticosteroids, Lithium, Radioiodine
Question: What is the role of LIMT lncRNA?

Context:
LIMT is a novel metastasis inhibiting lncRNA suppressed by EGF and downregulated in aggressive breast cancer.
This led to the identification of 11 prognostic lncRNAs. Functional analyses of this group uncovered LINC01089 (here renamed LncRNA Inhibiting Metastasis; LIMT), a highly conserved lncRNA, which is depleted in basal-like and in HER2-positive tumors, and the low expression of which predicts poor patient prognosis. Interestingly, EGF rapidly downregulates LIMT expression by enhancing histone deacetylation at the respective promoter. We also find that LIMT inhibits extracellular matrix invasion of mammary cells in vitro and tumor metastasis in vivo In conclusion, lncRNAs dynamically regulated by growth factors might act as novel drivers of cancer progression and serve as prognostic biomarkers.
Functional analyses of this group uncovered LINC01089 (here renamed LncRNA Inhibiting Metastasis; LIMT), a highly conserved lncRNA, which is depleted in basal-like and in HER2-positive tumors, and the low expression of which predicts poor patient prognosis.
Interestingly, EGF rapidly downregulates LIMT expression by enhancing histone deacetylation at the respective promoter.
We also find that LIMT inhibits extracellular matrix invasion of mammary cells in vitro and tumor metastasis in vivo In conclusion, lncRNAs dynamically regulated by growth factors might act as novel drivers of cancer progression and serve as prognostic biomarkers.
Functional analyses of this group uncovered LINC01089 (here renamed LncRNA Inhibiting Metastasis; LIMT), a highly conserved lncRNA, which is depleted in basal-like and in HER2-positive tumors, and the low expression of which predicts poor patient prognosis.
LIMT is a novel metastasis inhibiting lncRNA suppressed by EGF and downregulated in aggressive breast cancer.
We also find that LIMT inhibits extracellular matrix invasion of mammary cells in vitro and tumor metastasis in vivo In conclusion, lncRNAs dynamically regulated by growth factors might act as novel drivers of cancer progression and serve as prognostic biomarkers.

Answer: LINC01089 (LncRNA Inhibiting Metastasis; LIMT) is a highly conserved lncRNA, which is depleted in basal-like and in HER2-positive tumors, and the low expression of which predicts poor patient prognosis. Interestingly, EGF rapidly downregulates LIMT expression by enhancing histone deacetylation at the respective promoter. LIMT inhibits extracellular matrix invasion of mammary cells in vitro and tumor metastasis in vivo.
LIMT is a novel metastasis inhibiting lncRNA suppressed by EGF and downregulated in aggressive breast cancer.
Question: Does SCRIB deregulation promote cancer?

Context:
human homologs of Drosophila dlg, scrib, and lgl are cancer-associated genes.
Aberrant overexpression of the cell polarity module scribble in human cancer.
we show that Scrib is nearly universally overexpressed in cultured tumor cell lines and genetically disparate cancer patient series compared with matched normal tissues in vivo. 
These data uncover a previously unrecognized exploitation of Scrib for aberrant tumor cell motility and invasion, thus potentially contributing to disease progression in humans.
oss of miR-296 causes aberrantly increased and mislocalized Scrib in human tumors, resulting in exaggerated random cell migration and tumor cell invasiveness. 
Scrib levels predict tumor relapse in hepatocellular carcinoma patients.
Scrib heterozygosity predisposes to lung cancer
loss of Scrib and activated oncogenic KRas cooperate in vivo, resulting in more aggressive lung tumors, l
Scribble, a product of a well-known tumor suppressor gene
CD74-dependent deregulation of the tumor suppressor scribble in human epithelial and breast cancer cells.
 scribble (SCRIB) complexes) is intricately related to advanced stages of tumour progression and invasiveness. 
SCRIB expression is deregulated in human prostate cancer,
Scrib heterozygosity initiated prostate hyperplasia
The clinical significance of the work in mice was highlighted by our observation that SCRIB deregulation strongly correlated with poor survival in human prostate cancer.
we demonstrate that scribble inhibits breast cancer formation and that deregulation of polarity pathways promotes dysplastic and neoplastic growth in mammals by disrupting morphogenesis and inhibiting cell death.
Deregulation of scribble promotes mammary tumorigenesis and reveals a role for cell polarity in carcinoma.
loss of Scribble promotes invasion of cells through extracellular matrix in an organotypic culture system.
Scribble expression is decreased in many invasive human cancers.
Loss of human Scribble cooperates with H-Ras to promote cell invasion through deregulation of MAPK signalling.

Answer: Yes, deregulation of scribble promotes cancer.
Exact answer: yes
Question: What is trichotillomania?

Context:
Trichotillomania (hair pulling disorder, HPD) is characterized by significant psychological distress, childhood-onset, and, in adults, certain cognitive deficits such as inhibitory control. 
TRICHOTILLOMANIA (HAIR PULLING DISORDER)
Hair pulling disorder (HPD; trichotillomania) is thought to be associated with significant psychiatric comorbidity and functional impairment. 

Answer: Trichotillomania is a hair pulling disorder.
Exact answer: Trichotillomania is a hair pulling disorder.
Question: List features of the Perry syndrome.

Context:
BACKGROUND: Depression, parkinsonism, and hypoventilation (Perry syndrome) or familial motor neuron disease have been linked to mutations in dynactin P150(Glued) (DCTN1).
BACKGROUND: Perry syndrome (PS) caused by DCTN1 gene mutation is clinically characterized by autosomal dominant parkinsonism, depression, severe weight loss, and hypoventilation.
CONCLUSIONS AND RELEVANCE: Mutations of the DCTN1 gene have been previously associated with amyotrophic lateral sclerosis and with Perry syndrome, a rare autosomal dominant disorder characterized by weight loss, parkinsonism, central hypoventilation, and psychiatric disturbances. 
OBJECTIVES: Perry syndrome consists of autosomal dominant Parkinsonism, depression, weight loss, and central hypoventilation.
A patient with a mood disorder and a Parkinsonian syndrome with frontal cognitive impairment thought to resemble progressive supranuclear palsy defied precise diagnosis until the development of respiratory compromise, prompting consideration of the diagnosis of Perry syndrome.
Perry syndrome is a familial parkinsonism associated with central hypoventilation, mental depression, and weight loss. 
Perry syndrome (PS) caused by DCTN1 gene mutation is clinically characterized by autosomal dominant parkinsonism, depression, severe weight loss, and hypoventilation
Perry syndrome is a familial parkinsonism associated with central hypoventilation, mental depression, and weight loss
Perry syndrome due to the DCTN1 G71R mutation: a distinctive levodopa responsive disorder with behavioral syndrome, vertical gaze palsy, and respiratory failure
Perry syndrome consists of early-onset parkinsonism, depression, severe weight loss and hypoventilation, with brain pathology characterized by TDP-43 immunostaining. We carried out genome-wide linkage analysis and identified five disease-segregating mutations affecting the CAP-Gly domain of dynactin (encoded by DCTN1) in eight families with Perry syndrome; these mutations diminish microtubule binding and lead to intracytoplasmic inclusions. 

Answer: Perry syndrome is a familial parkinsonism associated with central hypoventilation, mental depression, and weight loss.
Exact answer: parkinsonism, central hypoventilation, depression, weight loss
Question: How is MicroRNA let-7a potentially useful as a marker for selection of paclitaxel in ovarian cancer management?

Context:
           in the carcinogenesis of ovarian cancer through deregulation of cell proliferation.             They may be novel biomarkers for early detection or therapeutic targets of ovarian             cancer", "MicroRNA let-7a: a potential marker for selection of paclitaxel in ovarian cancer management", " The study suggests that the beneficial impact of the addition of paclitaxel on EOC survival was significantly linked to let-7a levels, and that miRNAs such as let-7a may be a useful marker for selection of chemotherapeutic agents in EOC management", "miR-200c has potential as a predictor of survival, and is a biomarker of relapse, in stage I EOC", "MicroRNA microarray identifies Let-7i as a novel biomarker and therapeutic target in human epithelial ovarian cancer", " our results strongly suggest that let-7i might be used as a therapeutic target to modulate platinum-based chemotherapy and as a biomarker to predict chemotherapy response and survival in patients with ovarian cancer", "miRNAs-21, 92 and 93 are known oncogenes with therapeutic and biomarker potential", "Serum miR-132, miR-26a, let-7b, and miR-145 could be considered as potential candidates as novel biomarkers in serous ovarian cancer"]

Answer: The study suggests that the beneficial impact of the addition of paclitaxel on EOC survival was significantly linked to let-7a levels, and that miRNAs such as let-7a may be a useful marker for selection of chemotherapeutic agents in EOC management
Question: Which is the protein (antigen) targeted by anti-Vel antibodies in the Vel blood group?

Context:
Anti-Vel is an uncommon antibody to a high-prevalence antigen. Its clinical significance and management in the prenatal setting are not well characterized.
Haemolytic disease of the newborn because of rare anti-Vel.
A haemolytic anti-Vel was detected in the tube test. In contrast, the particular commercial gel test kit used did not reveal the haemolytic property or specificity of the antibody.

Answer: Disruption of SMIM1 causes the Vel- blood type. The protein carrying the Vel blood group antigen was biochemically purified from red blood cell membranes. Mass spectrometry-based de novo peptide sequencing identified this protein to be small integral membrane protein 1 (SMIM1), a previously uncharacterized single-pass membrane protein. Expression of SMIM1 cDNA in Vel- cultured cells generated anti-Vel cell surface reactivity, confirming that SMIM1 encoded the Vel blood group antigen. (PMID: 23505126)
SMIM1
Exact answer: SMIM1