niryuu/sni-each-converted huggingface dataset:
Context: The War of the Spanish Succession was a European conflict of the early 18th century, triggered by the death of the childless Charles II of Spain in November 1700. His closest heirs were members of the Austrian Habsburg and French Bourbon families; acquisition of an undivided Spanish Empire or Monarchy by either threatened the European balance of power. Charles left his throne to Louis XIV's grandson Philip who was proclaimed King of Spain on 16 November 1700. Disputes over the separation of the Spanish and French crowns, division of territories and commercial rights led to war in 1701 between the Bourbons of France and Spain and the Grand Alliance, whose candidate was Archduke Charles, younger son of Habsburg Emperor Leopold. By 1710, fighting was deadlocked; Allied victories in Italy and the Low Countries had driven the French back to their borders but they could not achieve a decisive breakthrough while Philip was secure in Spain. When Archduke Charles succeeded his brother Joseph I as Emperor in 1711, Britain effectively withdrew, forcing its Allies to make peace and leading to the 1713 Treaty of Utrecht, followed in 1714 with Rastatt and Baden. Philip was confirmed as King of Spain and renounced the French throne; Spain retained the bulk of its pre-war territories outside Europe with their European territories divided between Austria, Britain and Savoy. Longer term impacts included Britain's emergence as the leading maritime and commercial power, the beginning of the decline of the Dutch Republic, the creation of a centralised Spanish state and the acceleration of the break-up of the Holy Roman Empire. 
 Question: How was Charles related to Joseph I?
Output: brother
Context: According to 2011 census of India, Kumbakonam had a population of 140,156 with a sex-ratio of 1,021 females for every 1,000 males, much above the national average of 929. A total of 12,791 were under the age of six, constituting 6,495 males and 6,296 females.The average literacy of the city was 83.21%, compared to the national average of 72.99%. There were a total of 9,519 workers, comprising 32 cultivators, 83 main agricultural labourers, 1,206 in house hold industries, 7,169 other workers, 1,029 marginal workers, 24 marginal cultivators, 45 marginal agricultural labourers, 212 marginal workers in household industries and 0 other marginal workers. 
 Question: Which group of workers were the least in the population?
Output: other marginal workers
Context: Polycystic kidney disease (PKD) includes a group of disorders that are characterized by the presence of cysts in the kidney and other organs, including the pancreas. Here we show that in orpk mice, a model system for PKD that harbors a mutation in the gene that encodes the polaris protein, pancreatic defects start to occur at the end of gestation, with an initial expansion of the developing pancreatic ducts. Ductal dilation continues rapidly after birth and results in the formation of large, interconnected cysts. Expansion of pancreatic ducts is accompanied by apoptosis of neighboring acinar cells, whereas endocrine cell differentiation and islet formation appears to be unaffected. Polaris has been shown to co-localize with primary cilia, and these structures have been implicated in the formation of renal cysts. In the orpk pancreas, cilia numbers are reduced and cilia length is decreased. Expression of polycystin-2, a protein involved in PKD, is mislocalized in orpk mice. Furthermore, the cellular localization of beta-catenin, a protein involved in cell adhesion and Wnt signaling, is altered. Thus, polaris and primary cilia function are required for the maturation and maintenance of proper tissue organization in the pancreas. 
 Question: Which is the most common disease attributed to malfunction or absence of primary cilia?
Output: polycystic kidney disease (pkd)
Context: Although chronic stress is known to be linked with memory and other neurological disorders, little is known about the relationship between chronic stress and the onset or development of Alzheimer's disease (AD). In this study, we investigated the effects of long-term stress on the onset and severity of cognitive deficits and pathological changes in APPV717I-CT100 mice overexpressing human APP-CT100 containing the London mutation (V717I) after exposure to immobilization stress. We found that chronic immobilization stress accelerated cognitive impairments, as accessed by the Passive avoidance and the Social Transfer of Food Preference (STFP) tests. Moreover, the numbers and densities of vascular and extracellular deposits containing amyloid beta peptide (Abeta) and carboxyl-terminal fragments of amyloid precursor protein (APP-CTFs), which are pathologic markers of AD, were significantly elevated in stressed animals, especially in the hippocampus. Moreover, stressed animals, also showed highly elevated levels of neurodegeneration and tau phosphorylation and increased intraneuronal Abeta and APP-CTFs immunoreactivities in the hippocampus and in the entorhinal and piriform cortex. This study provides the first evidence that chronic stress accelerates the onset and severity of cognitive deficits and that these are highly correlated with pathological changes, which thus indicates that chronic stress may be an important contributor to the onset and development of AD. 
 Question: Which disease the London mutation involved in?
Output: alzheimer's disease
Context: Although chronic stress is known to be linked with memory and other neurological disorders, little is known about the relationship between chronic stress and the onset or development of Alzheimer's disease (AD). In this study, we investigated the effects of long-term stress on the onset and severity of cognitive deficits and pathological changes in APPV717I-CT100 mice overexpressing human APP-CT100 containing the London mutation (V717I) after exposure to immobilization stress. We found that chronic immobilization stress accelerated cognitive impairments, as accessed by the Passive avoidance and the Social Transfer of Food Preference (STFP) tests. Moreover, the numbers and densities of vascular and extracellular deposits containing amyloid beta peptide (Abeta) and carboxyl-terminal fragments of amyloid precursor protein (APP-CTFs), which are pathologic markers of AD, were significantly elevated in stressed animals, especially in the hippocampus. Moreover, stressed animals, also showed highly elevated levels of neurodegeneration and tau phosphorylation and increased intraneuronal Abeta and APP-CTFs immunoreactivities in the hippocampus and in the entorhinal and piriform cortex. This study provides the first evidence that chronic stress accelerates the onset and severity of cognitive deficits and that these are highly correlated with pathological changes, which thus indicates that chronic stress may be an important contributor to the onset and development of AD. 
 Question: Which disease the London mutation involved in?
Output: ad
Context: Ra Patera is an extraterrestrial volcano located on Io. 
 Question: On what celestial body is Ra Patera located?
Output: io
Context: Health care workers (HCW) are particularly at risk of acquiring tuberculosis (TB), even in countries with low TB incidence. Therefore, TB screening in HCW is a useful prevention strategy in countries with both low and high TB incidence. Tuberculin skin test (TST) is widely used although it suffers of low specificity; on the contrary, the in vitro enzyme immunoassay tests (IGRA) show superior specificity and sensitivity but are more expensive. The present study reports the results of a three-year TB surveillance among HCW in a large teaching hospital in Rome, using TST (by standard Mantoux technique) and IGRA (by QuantiFERON-TB) as first- and second-level screening tests, respectively. Out of 2290 HCW enrolled, 141 (6.1%) had a positive TST; among them, 99 (70.2%) underwent the IGRA and 16 tested positive (16.1%). The frequency of HCW tested positive for TB seems not far from other experiences in low incidence countries. Our results confirm the higher specificity of IGRA, but, due to its higher cost, TST can be considered a good first level screening test, whose positive results should be further confirmed by IGRA before the patients undergo X-ray diagnosis and/or chemotherapy. 
 Question: The Mantoux test detects what latent infection/disease?
Output: tuberculosis
Context: Coming off their last-second victory over the Bengals, the Broncos would play their Week 2 home opener against the Cleveland Browns. In the first quarter, Denver would trail early as Browns kicker Phil Dawson got a 22-yard field goal. Afterwards, the Broncos took the lead as quarterback Kyle Orton completed a 2-yard touchdown pass to tight end Tony Scheffler. Cleveland would creep close as Dawson made a 47-yard field goal, but Denver would answer as kicker Matt Prater got a 23-yard field goal in the second quarter and a 38-yard field goal in the third quarter. In the fourth, the Broncos pulled away as fullback Peyton Hillis got a 2-yard touchdown run and running back Correll Buckhalter got a 45-yard touchdown run. 
 Question: Who had the longest rushing touchdown
Output: correll buckhalter
Context: Reprimo (RPRM), is a gene located at human chromosome 2q23 whose expression in conjunction with p53, along with other genes which are p53-induced, is associated with the arrest of the cell cycle at the G2 phase.Reprimo's protein product is a highly glycosylated polypeptide which, upon its expression, is localized to the cytoplasm where it is primarily active. 
 Question: What species is Reprimo specific to?
Output: human
Context: Neuroacanthocytosis syndromes are mainly comprised of two diseases: chorea-acanthocytosis (ChAc) and McLeod syndrome (MLS). There is a high incidence of psychiatric disorders such as mood disorder and schizophrenia among neuroacanthocytosis patients. We hypothesized that neuroacanthocytosis-related-genes might be associated with susceptibility to these psychiatric disorders. We performed a comprehensive mutation screen of VPS13A and XK, the gene responsible for ChAc and MLS, respectively, in 85 mood disorder subjects and XK in 86 schizophrenia subjects and compared the variants to 100 or more control alleles. We also performed copy number variation (CNV) analysis in 72 mood disorder subjects and 86 schizophrenia subjects. We identified three non-synonymous, two synonymous and six intron variants in mood disorder subjects and a novel GAT triplet repeat polymorphism in VPS13A. By CNV analysis, we identified a heterozygous exon 60-61 deletion in VPS13A in one mood disorder subject. We identified one non-synonymous and one intron variant in mood disorder and schizophrenia subjects, respectively, in XK. The presence of a pathogenic mutation or a potentially functional variant in mood disorder or schizophrenia subjects suggests that neuroacanthocytosis-related-genes might be involved in the pathogenesis of these psychiatric disorders. 
 Question: Mutation of which gene is associated with McLeod syndrome?
Output: xk
Context: Imatinib is an inhibitor of the Bcr-Abl tyrosine kinase; however, resistance is common. Flavopiridol, a cyclin-dependent kinase (CDK) inhibitor, down-regulates short-lived anti-apoptotic proteins via inhibition of transcription. In preclinical studies, flavopiridol synergizes with imatinib to induce apoptosis. We investigated this novel combination regimen in patients with Bcr-Abl(+) malignancies. In a phase I dose-escalation study, imatinib was administered orally daily, and flavopiridol by 1h intravenous infusion weekly for 3weeks every 4weeks. Adults with chronic myelogenous leukemia or Philadelphia chromosome-positive acute leukemia were eligible. Patients were divided into two strata based on peripheral blood and bone marrow blast counts. The primary objective was to identify the recommended phase II doses for the combination. Correlative pharmacokinetic and pharmacodynamic studies were also performed. A total of 21 patients received study treatment. Four dose levels were evaluated before the study was closed following the approval of the second-generation Bcr-Abl tyrosine kinase inhibitors (TKIs). Five patients responded, including four sustained responses. Four patients had stable disease. All but one responder, and all patients with stable disease had previously been treated with imatinib. One patient had a complete response sustained for 30months. Changes in expression of phospho-Bcr/Abl, -Stat5, and Mcl-1 were monitored. No major pharmacokinetic interaction was observed. This is the first study to evaluate the combination of a CDK inhibitor and a TKI in humans. The combination of flavopiridol and imatinib is tolerable and produces encouraging responses, including in some patients with imatinib-resistant disease. 
 Question: What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?
Output: bcr-abl
Context: Pearl Django is a jazz group established in 1994 in Tacoma, Washington by guitarists Neil Andersson and Dudley Hill, and bassist David ''Pope'' Firman. 
 Question: What city was Pearl Django formed in?
Output: tacoma
Context: Founded in Paris by Marco Tinelli in 1998 under the name Grey Interactive, over the past 15 years the digital agency has become an integrated communications group composed of 20 agencies around Europe and in 8 different countries (France, Spain, Portugal, Italy, United Kingdom, Germany, U.S. and China) FullSIX Group has 10 agency networks: 
 Question: In what city is FullSIX based?
Output: paris
Context: Biological products have proven its high efficacy on autoimmune disease such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Meanwhile, small molecular drugs have attracted attention over the years because of its availability of oral administration and cost effectiveness. Spleen tyrosine kinase (Syk) is a 72 kDa protein tyrosine kinase widely expressed on cells that are involved in the immune system and inflammation such as B cells, T cells, macrophages and synovial fibroblast. Syk is involved in intracellular signaling of the multi-chain immune receptors, including B cell receptor (BCR), chain of T-cell receptor (TCR), FcR and integrins, which contains the immune-receptor tyrosine-based activation motif (ITAM). Recently, Syk inhibitor fostamatinib has exerted potent therapeutic efficacy against autoimmune and allergic diseases such as rheumatoid arthritis (RA), bronchial asthma and thrombocytopenic purpura (ITP). Moreover, Syk blockade prevented the development of skin and kidney lesions in lupus-prone mice, however the mechanism of action is unclear. We have revealed that Syk-mediated BCR-signaling is prerequisite for optimal induction of toll-like receptor (TLR)-9, thereby allowing efficient propagation of CD40- and TLR9- signaling in human B cells. These results indicate that inhibition of Syk have a potential to regulate B-cell mediated inflammatory diseases such as SLE. We here document the in vitro and in vivo effects of a Syk inhibitor for the treatment of autoimmune diseases, mainly in RA and SLE. 
 Question: Which enzyme is inhibited by a drug fostamatinib?
Output: spleen tyrosine kinase
Context: To investigate the effect of global cerebral ischemia on brain cell proliferation in young adult macaques, we infused 5-bromo-2'-deoxyuridine (BrdU), a DNA replication indicator, into monkeys subjected to ischemia or sham-operated. Subsequent quantification by BrdU immunohistochemistry revealed a significant postischemic increase in the number of BrdU-labeled cells in the hippocampal dentate gyrus, subventricular zone of the temporal horn of the lateral ventricle, and temporal neocortex. In all animals, 20-40% of the newly generated cells in the dentate gyrus and subventricular zone expressed the neural progenitor cell markers Musashi1 or Nestin. A few BrdU-positive cells in postischemic monkeys were double-stained for markers of neuronal progenitors (class III beta-tubulin, TUC4, doublecortin, or Hu), neurons (NeuN), or glia (S100beta or GFAP). Our results suggest that ischemia activates endogenous neuronal and glial precursors residing in diverse locations of the adult primate central nervous system. 
 Question: Which intermediate filament (IF) protein can be used as a non-specific marker of the neuronal precursor cells of the subventricular zone?
Output: nestin
Context: Halo 4 was the first title released by 343 Industries in which they played a lead development role. 
 Question: What is the product of 343 Industries?
Output: halo 4
Context: Stella Crawford is a fictional character from the BBC soap opera EastEnders, played by Sophie Thompson from 7 September 2006 to 23 July 2007. 
 Question: To which fictional work does Stella Crawford appear in?
Output: eastenders
Context: In the mean time, Maha Nawrahta opened the southern front on 23 October 1765 in three directions. He had 20,000 to 30,000 under his command. A small army invaded by the Three Pagodas Pass towards Suphanburi. Another small army invaded down the Tenasserim coast towards Mergui and Tenasserim town. However, the main thrust of his attack was at Kanchanaburi. His 20,000-strong main southern army invaded via the Myitta Pass. Kanchanaburi fell with little resistance. The main reason for the quick fall of Kanchanaburi could be that the Burmese were more battle-hardened. But it could also be that the Siamese command miscalculated where the Burmese main attack would come from, and had not sufficiently reinforced the fort to withstand a major attack. Judging by the Siamese chronicles' reporting of the main attack route, the Siamese command appeared to have believed that the main Burmese attack would come from the Gulf of Siam coastline, instead of the most obvious and shortest route via Kanchanaburi. The Siamese sources say that Maha Nawrahta's main invasion route came from southern Tenasserim, crossing the Tenasserim range at Chumphon and Phetburi. The path is totally different from the Kanchanaburi route reported by the Burmese chronicles. Historian Kyaw Thet specifically adds that the main attack route was via the Myitta Pass. 
 Question: How many Maha Nawrahta opened the southern front?
Output: three directions
Context: Coming off their bye week, the Jets stayed at home for a Week 10 duel with the Jacksonville Jaguars. New York would trail early in the first quarter with running back Maurice Jones-Drew's 33-yard touchdown run. The Jets would respond with kicker Jay Feely getting a 32-yard field goal, followed by rookie quarterback Mark Sanchez completing a 7-yard touchdown pass to wide receiver Jerricho Cotchery. In the second quarter, Jacksonville would take the lead as quarterback David Garrard got an 11-yard touchdown run and completed a 26-yard touchdown pass to wide receiver Mike Sims-Walker. New York would close out the half as Feely made a 37-yard field goal. After a scoreless third quarter, the Jets would regain the lead in the fourth quarter with a 40-yard field goal from Feely and a 1-yard touchdown run from running back Thomas Jones (with a failed 2-point conversion). However, the Jaguars got the last laugh as kicker Josh Scobee booted the game-winning 21-yard field goal. 
 Question: Who made the shortest touchdown run?
Output: thomas jones
Context: This study aimed to explore retrospective childhood ADHD symptomatology, psychiatric comorbidity, rates of substance-use disorders (SUD), as well as their association with high-risk health behaviors in prison and adverse health outcomes. A randomly selected representative sample of inmates in the Puerto Rico correctional system (N = 1,179) was assessed with the Spanish-language Wender Utah Rating Scale (WURS); the Composite International Diagnostic Interview (CIDI) modules for lifetime/current major depression disorder (MDD), generalized anxiety disorder (GAD), and SUD; the Davidson Trauma Scale (DTS; posttraumatic stress disorder [PTSD]); and self-reports of in-site high-risk behaviors. Wald (2) tests revealed significant associations of ADHD with MDD and PTSD, as well as increased risk for overdosing and intravenous drug use in prison. A logistic regression model adjusted for mood and anxiety comorbidity predicted lifetime SUD diagnosis (odds ratio = 2.38; 95% confidence interval = [1.15, 4.94]). Our results provide further evidence on the association of drug dependence and ADHD symptoms, and their overrepresentation among prison inmates. 
 Question: Symptoms of which disorder are evaluated with the Davidson Trauma Scale?
Output: ptsd
Context: This study aimed to explore retrospective childhood ADHD symptomatology, psychiatric comorbidity, rates of substance-use disorders (SUD), as well as their association with high-risk health behaviors in prison and adverse health outcomes. A randomly selected representative sample of inmates in the Puerto Rico correctional system (N = 1,179) was assessed with the Spanish-language Wender Utah Rating Scale (WURS); the Composite International Diagnostic Interview (CIDI) modules for lifetime/current major depression disorder (MDD), generalized anxiety disorder (GAD), and SUD; the Davidson Trauma Scale (DTS; posttraumatic stress disorder [PTSD]); and self-reports of in-site high-risk behaviors. Wald (2) tests revealed significant associations of ADHD with MDD and PTSD, as well as increased risk for overdosing and intravenous drug use in prison. A logistic regression model adjusted for mood and anxiety comorbidity predicted lifetime SUD diagnosis (odds ratio = 2.38; 95% confidence interval = [1.15, 4.94]). Our results provide further evidence on the association of drug dependence and ADHD symptoms, and their overrepresentation among prison inmates. 
 Question: Symptoms of which disorder are evaluated with the Davidson Trauma Scale?
Output: post-traumatic stress disorder
Context: Alphonse Milne-Edwards (Paris, 13 October 1835 -- Paris, 21 April 1900) was a French mammalologist, ornithologist and carcinologist. 
 Question: Where did Alphonse Milne-Edwards live when he died?
Output: paris
Context: New research shows how kids' brains reorganize as they learn math. All the time you spent memorizing multiplication tables may have made you a better mathematician, according to a new study. A team of scientists from Stanford University, in California, have shown how the brain reorganizes itself as kids learn math. After a certain amount of time spent practicing math, kids can put away the calculator . They don't even need to count on their fingers. They simply know the answers to subtraction , addition, and multiplication facts. The quicker kids can recall basic math facts, the easier it is for them to solve more complicated math problems. The Stanford University researchers observed the brain activity of 28 students aged 7to 9 for the study. They took scans of the students' brains as the students solved math calculations without the help of a calculator, pen or paper. A calculation--three plus four equals seven, for example--flashed on a screen. The students pushed a button to say if the answer was right or wrong. The scientists also recorded the response speed, and what parts of the brain became active as the kids pushed the button. These observations showed a process called fact retrieval . Rather than using their fingers to count, or writing out answers on a piece of paper, the students pulled the answers from memory. It's as if the answers to basic math problems are kept in a long-term storage area in the brain, which was built from repetition. "Experience really does matter," said Dr. Kathy Mann Koepeke. Children make the shift from counting to fact retrieval when they are 8 to 9 years old, the study shows. This is the time when most students are learning basic addition and subtraction. When kids have basic math facts memorized, the brain has more free space to learn more complicated math. This process has benefits for the future. The study shows as kids grow older, their answers rely more on memory and become quicker and more accurate. Less brain activity is devoted to counting. Some children make this shift quicker than others. 
 Question: What plays a key role in solving a math problem?
Output: experience
Context: Haploinsufficiency of the NSD1 gene due to 5q35 microdeletions or intragenic mutations is the major cause of Sotos syndrome characterized by generalized overgrowth, large hands and feet with advanced bone age, craniofacial dysmorphic features, learning disability, and possible susceptibility to tumors. Here, we report on a 14-month-old boy with a reverse phenotype of Sotos syndrome due to the reciprocal duplication of the 5q35.3 region, including the NSD1 gene, detected by array CGH. The phenotype includes delayed bone age, microcephaly, seizures, and failure to thrive. Our case suggests that the gene dosage effect of the NSD1 gene is the likely cause for the reversed phenotype of Sotos syndrome in this patient. 
 Question: Which gene is responsible for the development of Sotos syndrome?
Output: nsd1 gene
Context: Ginger Pye is a book by Eleanor Estes about a dog named Ginger Pye. 
 Question: What person illustrated Ginger Pye?
Output: eleanor estes
Context: Tissue injury following ischemia-reperfusion (I/R) occurs as a consequence of actions of soluble factors and immune cells. Growing evidence supports a role for platelets in the manifestation of tissue damage following I/R. Spleen tyrosine kinase has been well documented to be important in lymphocyte activation and more recently in platelet activation. We performed experiments to evaluate whether inhibition of platelet activation through inhibition of spleen tyrosine kinase prevents tissue damage after mesenteric I/R injury. Platelets isolated from C57BL/6J mice fed with R788 for 10 days were transfused into C57BL/6J mice depleted of platelets 2 days before mesenteric I/R injury. Platelet-depleted mice transfused with platelets from R788-treated mice before mesenteric I/R displayed a significant reduction in the degree of remote lung damage, but with little change in the degree of local intestinal damage compared with control I/R mice. Transfusion of R788-treated platelets also decreased platelet sequestration, C3 deposition, and immunoglobulin deposition in lung, but not in the intestine, compared with control groups. These findings demonstrate that platelet activation is a requisite for sequestration in the pulmonary vasculature to mediate remote tissue injury after mesenteric I/R. The use of small-molecule inhibitors may be valuable to prevent tissue damage in remote organs following I/R injury. 
 Question: Which enzyme is inhibited by a drug fostamatinib?
Output: spleen tyrosine kinase
Context: at the Georgia Dome, Atlanta, Georgia Trying to end a three-game skid, the Falcons returned home for an NFC South rematch with the New Orleans Saints. From the get-go, the Falcons trailed as in the first quarter, QB Drew Brees completed a 76-yard TD pass to WR Devery Henderson, while RB Deuce McAllister got a 1-yard TD run. Atlanta would respond with kicker Morten Andersen kicking a 22-yard field goal. In the second quarter, Andersen gave the Falcons a 30-yard field goal, yet New Orleans continued dominating with Brees completing an incredible 48-yard TD pass to WR Terrance Copper on the very last offensive play of the half. In the third quarter, RB Warrick Dunn gave Atlanta some room to operate, as he a 1-yard TD run for the only score of the half. However, in the fourth quarter, the Saints wrapped up the game with kicker John Carney getting a 25-yard field goal, while McAllister got a 9-yard TD run. After the game, as QB Michael Vick was leaving the field, he flicked off an insulting fan with both hands. He was fined $10,000 from the NFL and had to donate another $10,000 to charity. With their fourth-straight loss, the Falcons fell to 5-6. 
 Question: Which player had the shortest TD pass?
Output: terrance copper
Context: Speech and language disorders are some of the most common referral reasons to child development centers accounting for approximately 40% of cases. Stuttering is a disorder in which involuntary repetition, prolongation, or cessation of the sound precludes the flow of speech. About 5% of individuals in the general population have a stuttering problem, and about 80% of the affected children recover naturally. The causal factors of stuttering remain uncertain in most cases; studies suggest that genetic factors are responsible for 70% of the variance in liability for stuttering, whereas the remaining 30% is due to environmental effects supporting a complex cause of the disorder. The use of high-resolution genome wide array comparative genomic hybridization has proven to be a powerful strategy to narrow down candidate regions for complex disorders. We report on a case with a complex set of speech and language difficulties including stuttering who presented with a 10Mb deletion of chromosome region 7q33-35 causing the deletion of several genes and the disruption of CNTNAP2 by deleting the first three exons of the gene. CNTNAP2 is known to be involved in the cause of language and speech disorders and autism spectrum disorder and is in the same pathway as FOXP2, another important language gene, which makes it a candidate gene for causal studies speech and language disorders such as stuttering. 
 Question: Which gene is responsible for proper speech development?
Output: foxp2
Context: Spinocerebellar ataxia type 3 is caused by a polyglutamine expansion in the ataxin-3 protein, resulting in gain of toxic function of the mutant protein. The expanded glutamine stretch in the protein is the result of a CAG triplet repeat expansion in the penultimate exon of the ATXN3 gene. Several gene silencing approaches to reduce mutant ataxin-3 toxicity in this disease aim to lower ataxin-3 protein levels, but since this protein is involved in deubiquitination and proteasomal protein degradation, its long-term silencing might not be desirable. Here, we propose a novel protein modification approach to reduce mutant ataxin-3 toxicity by removing the toxic polyglutamine repeat from the ataxin-3 protein through antisense oligonucleotide-mediated exon skipping while maintaining important wild type functions of the protein. In vitro studies showed that exon skipping did not negatively impact the ubiquitin binding capacity of ataxin-3. Our in vivo studies showed no toxic properties of the novel truncated ataxin-3 protein. These results suggest that exon skipping may be a novel therapeutic approach to reduce polyglutamine-induced toxicity in spinocerebellar ataxia type 3. 
 Question: Which is the protein implicated in Spinocerebellar ataxia type 3?
Output: ataxin-3
Context: Parkinson's disease (PD) is the second most common neurodegenerative disorder, defined by the presence of resting tremor, muscular rigidity, bradykinesia, and postural instability. PD is characterized by the progressive loss of dopaminergic neurons within the substantia nigra pars compacta of the midbrain. The neuropathological hallmark of the disease is the presence of intracytoplasmic inclusions, called Lewy bodies (LBs) and Lewy neurites (LNs), containing -synuclein, a small protein which is widely expressed in the brain. The -synuclein gene, SNCA, is located on chromosome 4q22.1; SNCA-linked PD shows an autosomal dominant inheritance pattern with a relatively early onset age, and it usually progresses rapidly. Three missense mutations, A53T, A30P, and E46K, in addition to gene multiplications of the SNCA have been described so far. Although it is clear that LBs and LNs contain mainly the -synuclein protein, the mechanism(s) which leads -synuclein to accumulate needs to be elucidated. The primary question in the molecular pathology of PD is how wild-type -synuclein aggregates in PD, and which interacting partner(s) plays role(s) in the aggregation process. It is known that dopamine synthesis is a stressfull event, and -synuclein expression somehow affects the dopamine synthesis. The aberrant interactions of -synuclein with the proteins in the dopamine synthesis pathway may cause disturbances in cellular mechanisms. The normal physiological folding state of -synuclein is also important for the understanding of pathological aggregates. Recent studies on the -synuclein protein and genome-wide association studies of the -synuclein gene show that PD has a strong genetic component, and both familial and idiopathic PD have a common denominator, -synuclein, at the molecular level. It is clear that the disease process in Parkinson's disease, as in other neurodegenerative disorders, is very complicated; there can be several different molecular pathways which are responsible for diverse and possibly also unrelated functions inside the neuron, playing roles in PD pathogenesis. 
 Question: Which is the primary protein component of Lewy bodies?
Output: αsyn
Context: Parkinson's disease (PD) is the second most common neurodegenerative disorder, defined by the presence of resting tremor, muscular rigidity, bradykinesia, and postural instability. PD is characterized by the progressive loss of dopaminergic neurons within the substantia nigra pars compacta of the midbrain. The neuropathological hallmark of the disease is the presence of intracytoplasmic inclusions, called Lewy bodies (LBs) and Lewy neurites (LNs), containing -synuclein, a small protein which is widely expressed in the brain. The -synuclein gene, SNCA, is located on chromosome 4q22.1; SNCA-linked PD shows an autosomal dominant inheritance pattern with a relatively early onset age, and it usually progresses rapidly. Three missense mutations, A53T, A30P, and E46K, in addition to gene multiplications of the SNCA have been described so far. Although it is clear that LBs and LNs contain mainly the -synuclein protein, the mechanism(s) which leads -synuclein to accumulate needs to be elucidated. The primary question in the molecular pathology of PD is how wild-type -synuclein aggregates in PD, and which interacting partner(s) plays role(s) in the aggregation process. It is known that dopamine synthesis is a stressfull event, and -synuclein expression somehow affects the dopamine synthesis. The aberrant interactions of -synuclein with the proteins in the dopamine synthesis pathway may cause disturbances in cellular mechanisms. The normal physiological folding state of -synuclein is also important for the understanding of pathological aggregates. Recent studies on the -synuclein protein and genome-wide association studies of the -synuclein gene show that PD has a strong genetic component, and both familial and idiopathic PD have a common denominator, -synuclein, at the molecular level. It is clear that the disease process in Parkinson's disease, as in other neurodegenerative disorders, is very complicated; there can be several different molecular pathways which are responsible for diverse and possibly also unrelated functions inside the neuron, playing roles in PD pathogenesis. 
 Question: Which is the primary protein component of Lewy bodies?
Output: α-synuclein
Context: Parkinson's disease (PD) is the second most common neurodegenerative disorder, defined by the presence of resting tremor, muscular rigidity, bradykinesia, and postural instability. PD is characterized by the progressive loss of dopaminergic neurons within the substantia nigra pars compacta of the midbrain. The neuropathological hallmark of the disease is the presence of intracytoplasmic inclusions, called Lewy bodies (LBs) and Lewy neurites (LNs), containing -synuclein, a small protein which is widely expressed in the brain. The -synuclein gene, SNCA, is located on chromosome 4q22.1; SNCA-linked PD shows an autosomal dominant inheritance pattern with a relatively early onset age, and it usually progresses rapidly. Three missense mutations, A53T, A30P, and E46K, in addition to gene multiplications of the SNCA have been described so far. Although it is clear that LBs and LNs contain mainly the -synuclein protein, the mechanism(s) which leads -synuclein to accumulate needs to be elucidated. The primary question in the molecular pathology of PD is how wild-type -synuclein aggregates in PD, and which interacting partner(s) plays role(s) in the aggregation process. It is known that dopamine synthesis is a stressfull event, and -synuclein expression somehow affects the dopamine synthesis. The aberrant interactions of -synuclein with the proteins in the dopamine synthesis pathway may cause disturbances in cellular mechanisms. The normal physiological folding state of -synuclein is also important for the understanding of pathological aggregates. Recent studies on the -synuclein protein and genome-wide association studies of the -synuclein gene show that PD has a strong genetic component, and both familial and idiopathic PD have a common denominator, -synuclein, at the molecular level. It is clear that the disease process in Parkinson's disease, as in other neurodegenerative disorders, is very complicated; there can be several different molecular pathways which are responsible for diverse and possibly also unrelated functions inside the neuron, playing roles in PD pathogenesis. 
 Question: Which is the primary protein component of Lewy bodies?
Output: alpha-synuclein
Context: Selenocysteine (Sec, U) insertion into proteins is directed by translational recoding of specific UGA codons located upstream of a stem-loop structure known as Sec insertion sequence (SECIS) element. Selenoproteins with known functions are oxidoreductases containing a single redox-active Sec in their active sites. In this work, we identified a family of selenoproteins, designated SelL, containing two Sec separated by two other residues to form a UxxU motif. SelL proteins show an unusual occurrence, being present in diverse aquatic organisms, including fish, invertebrates, and marine bacteria. Both eukaryotic and bacterial SelL genes use single SECIS elements for insertion of two Sec. In eukaryotes, the SECIS is located in the 3' UTR, whereas the bacterial SelL SECIS is within a coding region and positioned at a distance that supports the insertion of either of the two Sec or both of these residues. SelL proteins possess a thioredoxin-like fold wherein the UxxU motif corresponds to the catalytic CxxC motif in thioredoxins, suggesting a redox function of SelL proteins. Distantly related SelL-like proteins were also identified in a variety of organisms that had either one or both Sec replaced with Cys. Danio rerio SelL, transiently expressed in mammalian cells, incorporated two Sec and localized to the cytosol. In these cells, it occurred in an oxidized form and was not reducible by DTT. In a bacterial expression system, we directly demonstrated the formation of a diselenide bond between the two Sec, establishing it as the first diselenide bond found in a natural protein. 
 Question: What is the name of the stem loop present in the 3' end of genes encoding for selenoproteins?
Output: secis
Context: Progress M-10M (Russian: -10), identified by NASA as Progress 42 or 42P, is a Progress spacecraft which was launched on 27 April 2011 to resupply the International Space Station. 
 Question: On what date was Progress M-10M launched?
Output: 27 april 2011
Context: In Beverly Hills, California, wealthy heiress Vivian "Viv" Ashe leaves her richly pampered pet chihuahua, Chloe, with her irresponsible niece, Rachel, while she embarks on a business trip for ten days. Papi, the gardener Sam's pet Chihuahua of Mexican descent, has an unrequited crush on Chloe, by which she is disgusted. Rachel decides to go to Mexico with her friends and stay at a hotel by the beach. When Rachel leaves Chloe alone in the hotel room to go dancing at a club, Chloe goes looking for her. Chloe gets dog-napped as she tries to find Rachel and is sent to the dog fights in Mexico City. There, she meets a street-smart German Shepherd named Delgado. Rachel comes back to the hotel and is frantic when she finds Chloe missing. Chloe is picked to fight in the pit against El Diablo, a fierce Argentinean-Bolivian Doberman Pinscher. Delgado helps her escape the dog fights, unleashing the other dogs from their cages and unlocking the ring to allow both Chloe and himself to flee. After several arguments, he then decides to return her to Beverly Hills safely. Meanwhile, Rachel and Sam go to the Mexican police and offer rewards in an effort to find Chloe. El Diablo is sent by the dog fight ringleader, Vasquez, to capture Chloe and obtain the reward from Rachel. Delgado and Chloe arrive at Puerto Vallarta, where Chloe is caught by El Diablo but rescued. She then waits for Delgado to find help but is tricked into handing over her diamond-studded necklace to con artists Chico, an iguana, and Manuel, a pack rat who claims to be from the Yucutan. Chloe and Delgado sneak onto a train heading towards the border, but they are caught and are forced to jump out, eventually arriving in the barren deserts of Chihuahua, where Delgado explains that he was a former police dog; he was retired after he lost his sense of smell during a raid and a sneak attack from El Diablo. Rachel and Sam are in Puerto Vallarta and find that Chloe was spotted in the state of Chihuahua. After tracking Chloe and Delgado from Mexico City, El Diablo arrives in Chihuahua and attempts to capture Chloe, but Papi saves her and ends getting captured in a cage inside an abandoned Aztec temple, but Delgado comes to rescue the two and is briefly defeated. Chloe then rescues Papi, but Delgado discovers that El Diablo had vanished. Rachel finds Chloe, and Vasquez get arrested by the police. Chloe returns safely to Beverly Hills without Vivian finding out what happened and accepts a romantic relationship with Papi, as well as Rachel with Sam. The characters' fates are later revealed: Delgado returns to being a police dog in Mexico. El Diablo is recaptured by Delgado and is adopted by a rich lady who "had a passion for fashion". Chico and Manuel move to Beverly Hills and become rich. Papi and Chloe have their first date. 
 Question: Who is the male chihuahua in love with Chloe?
Output: papi
Context: In the county, the population was spread out with 23.20% under the age of 18, 7.70% from 18 to 24, 27.00% from 25 to 44, 28.00% from 45 to 64, and 14.10% who were 65 years of age or older. The median age was 40 years. For every 100 females, there were 97.00 males. For every 100 females age 18 and over, there were 96.40 males. 
 Question: Which age group is larger: 25 to 44 or 45 to 64?
Output: 45 to 64
Context: In recent years, we have seen remarkable progress in our understanding of the disease mechanism underlying facioscapulohumeral muscular dystrophy (FSHD). The purpose of this review is to provide a comprehensive overview of our current understanding of the disease mechanism and to discuss the observations supporting the possibility of a developmental defect in this disorder. In the majority of cases, FSHD is caused by contraction of the D4Z4 repeat array (FSHD1). This results in local chromatin relaxation and stable expression of the DUX4 retrogene in skeletal muscle, but only when a polymorphic DUX4 polyadenylation signal is present. In some cases (FSHD2), D4Z4 chromatin relaxation and stable DUX4 expression occur in the absence of D4Z4 array contraction. DUX4 is a germline transcription factor and its expression in skeletal muscle leads to activation of early stem cell and germline programs and transcriptional activation of retroelements. Recent studies have provided a plausible disease mechanism for FSHD in which FSHD results from inappropriate expression of the germline transcription factor DUX4. The genes regulated by DUX4 suggest several mechanisms of muscle damage, and provide potential biomarkers and therapeutic targets that should be investigated in future studies. 
 Question: Which disease is associated with the ectopic expression of the protein encoded by the gene DUX4?
Output: fshd
Context: In recent years, we have seen remarkable progress in our understanding of the disease mechanism underlying facioscapulohumeral muscular dystrophy (FSHD). The purpose of this review is to provide a comprehensive overview of our current understanding of the disease mechanism and to discuss the observations supporting the possibility of a developmental defect in this disorder. In the majority of cases, FSHD is caused by contraction of the D4Z4 repeat array (FSHD1). This results in local chromatin relaxation and stable expression of the DUX4 retrogene in skeletal muscle, but only when a polymorphic DUX4 polyadenylation signal is present. In some cases (FSHD2), D4Z4 chromatin relaxation and stable DUX4 expression occur in the absence of D4Z4 array contraction. DUX4 is a germline transcription factor and its expression in skeletal muscle leads to activation of early stem cell and germline programs and transcriptional activation of retroelements. Recent studies have provided a plausible disease mechanism for FSHD in which FSHD results from inappropriate expression of the germline transcription factor DUX4. The genes regulated by DUX4 suggest several mechanisms of muscle damage, and provide potential biomarkers and therapeutic targets that should be investigated in future studies. 
 Question: Which disease is associated with the ectopic expression of the protein encoded by the gene DUX4?
Output: facioscapulohumeral dystrophy
Context: The Institute on the Arts and Civic Dialogue (IACD) was founded in 1997 by actress, playwright, and professor Anna Deavere Smith. 
 Question: In what year did Institute on the Arts and Civic Dialogue originate?
Output: 1997
Context: Looking to stop a three-game losing streak, the Raiders welcomed Derek Carr back after missing one week due to injury to face the Los Angeles Chargers. However, things did not start well for Carr as he threw an interception on his first pass of the day and the Chargers took over at the Raider 30-yard line. the defense held the Chargers to a field goal attempt from 48 yards out which was no good. The Raiders took advantage and moved the ball down the field before Carr hit Michael Crabtree from 23 yards out to give the Raiders a 7-0 lead. Neither team could muster much offense until midway through the second quarter when the Chargers moved 82 yards and scored on a Melvin Gordon touchdown run from one yard out to tie the game. With, 1:34 remaining in the half, the Raiders moved into Charger territory and connected on a Giorgio Tavecchio 44-yard field goal as time expired to give the Raiders a 10-7 lead at the half. On their first possession of the second half, the Raiders moved deep into Charger territory, but managed no points as Carr was intercepted for the second time in the game. The teams exchanged punts and fumbles as the game moved into the fourth quarter. The Chargers finally managed some offense as Philip Rivers hit Melvin Gordon for a six-yard touchdown pass to give the Charger at 14-10 lead. On their ensuing possession, Cordarrelle Patterson took the ball on an end around and scampered 47 yards for a touchdown. Giorgio Tavecchio would, however, miss the ensuing point after to leave the Raider lead at two points, 16-14. After exchanging punts, the Chargers took over with 4:09 remaining in the game. Rivers hit Hunter Henry for a 23-yard pass play to move the ball into Raider territory. with less than two minutes remaining, the Chargers moved the ball to the Raider 10 yard line and lined up for the game-winning field goal with three second left in the game. The field goal was good and the Raiders suffered their fourth straight loss, falling to 2-4 on the season. The four losses through six gamed equaled the number of losses they suffered the entire season the prior year. The Raider defense again struggled, giving up 343 total yards while the offense struggled as well, managing only 274 yards. Carr's two interceptions proved costly in his return. After the game, the team said his poor play was not due to his injury. 
 Question: Who is the Raiders field goal kicker?
Output: giorgio tavecchio
Context: The Ghost Dance War was an armed conflict in the United States between the Lakota Sioux and the United States government from 1890 until 1891. 
 Question: What year did Ghost Dance War start?
Output: 1890