niryuu/sni-each-converted huggingface dataset:
Context: Drosophila melanogaster has a single Adar gene encoding a protein related to mammalian ADAR2 that edits transcripts encoding glutamate receptor subunits. We describe the structure of the Drosophila Adar locus and use ModENCODE information to supplement published data on Adar gene transcription, and splicing. We discuss the roles of ADAR in Drosophila in terms of the two main types of RNA molecules edited and roles of ADARs as RNA-binding proteins. Site-specific RNA editing events in transcripts encoding ion channel subunits were initially found serendipitously and subsequent directed searches for editing sites and transcriptome sequencing have now led to 972 edited sites being identified in 597 transcripts. Four percent of D. melanogaster transcripts are site-specifically edited and these encode a wide range of largely membrane-associated proteins expressed particularly in CNS. Electrophysiological studies on the effects of specific RNA editing events on ion channel subunits do not suggest that loss of RNA editing events in ion channels consistently produce a particular outcome such as making Adar mutant neurons more excitable. This possibility would have been consistent with neurodegeneration seen in Adar mutant fly brains. A further set of ADAR targets are dsRNA intermediates in siRNA generation, derived from transposons and from structured RNA loci. Transcripts with convergent overlapping 3' ends are also edited and the first discovered instance of RNA editing in Drosophila, in the Rnp4F transcript, is an example. There is no evidence yet to show that Adar antagonizes RNA interference in Drosophila. Evidence has been obtained that catalytically inactive ADAR proteins exert effects on microRNA generation and RNA interference. Whether all effects of inactive ADARs are due to RNA-binding or to even further roles of these proteins remains to be determined. 
 Question: Which is the major RNA editing enzyme in Drosophila melanogaster?
Output: adar
Context: Drosophila melanogaster has a single Adar gene encoding a protein related to mammalian ADAR2 that edits transcripts encoding glutamate receptor subunits. We describe the structure of the Drosophila Adar locus and use ModENCODE information to supplement published data on Adar gene transcription, and splicing. We discuss the roles of ADAR in Drosophila in terms of the two main types of RNA molecules edited and roles of ADARs as RNA-binding proteins. Site-specific RNA editing events in transcripts encoding ion channel subunits were initially found serendipitously and subsequent directed searches for editing sites and transcriptome sequencing have now led to 972 edited sites being identified in 597 transcripts. Four percent of D. melanogaster transcripts are site-specifically edited and these encode a wide range of largely membrane-associated proteins expressed particularly in CNS. Electrophysiological studies on the effects of specific RNA editing events on ion channel subunits do not suggest that loss of RNA editing events in ion channels consistently produce a particular outcome such as making Adar mutant neurons more excitable. This possibility would have been consistent with neurodegeneration seen in Adar mutant fly brains. A further set of ADAR targets are dsRNA intermediates in siRNA generation, derived from transposons and from structured RNA loci. Transcripts with convergent overlapping 3' ends are also edited and the first discovered instance of RNA editing in Drosophila, in the Rnp4F transcript, is an example. There is no evidence yet to show that Adar antagonizes RNA interference in Drosophila. Evidence has been obtained that catalytically inactive ADAR proteins exert effects on microRNA generation and RNA interference. Whether all effects of inactive ADARs are due to RNA-binding or to even further roles of these proteins remains to be determined. 
 Question: Which is the major RNA editing enzyme in Drosophila melanogaster?
Output: adenosine deaminase, rna-specific
Context: Chronic myelogenous leukemia (CML) results from the neoplastic transformation of primitive hematopoietic stem cells, and has been classified as a myeloproliferative disorder. The hallmark of CML is the presence of a balanced translocation between the long arms of chromosomes 9 and 22, t(9;22)(q34;q11.2), which is known as the Philadelphia (Ph) chromosome. This translocation results in the formation of the bcr-abl fusion gene, which, in turn, is translated into a chimeric Bcr-Abl protein with deregulated tyrosine kinase activity. Constitutive Bcr-Abl expression has been shown to be necessary and sufficient for the transformed phenotype of CML cells. CML is unique among human cancers in that a single genetic defect, the Ph chromosome, is responsible for the transformed phenotype. Since this discovery more than 40 years ago, our understanding of the clinical course, therapy, and prognosis of patients with CML has changed significantly. These changes have culminated in the emergence of imatinib, the first rationally designed, molecularly targeted therapy for human malignancy. In this review, the authors describe the molecular biology of CML and the development of imatinib as a therapeutic agent for the treatment of CML. 
 Question: What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?
Output: bcr-abl
Context: The 34th government of Turkey (11 December 1971 -- 22 May 1972) was a government in the history of Turkey. 
 Question: On what date did 34th government of Turkey end?
Output: 1972
Context: Most of the time, you breathe without thinking about it. Breathing is mostly an involuntary action that is controlled by a part of your brain that also controls your heart beat. If you swim, do yoga, or sing, you know you can control your breathing, however. Taking air into the body through the nose and mouth is called inhalation. Pushing air out of the body through the nose or mouth is called exhalation. The woman pictured below is exhaling before she surfaces from the pool water (Figure 1.1). How do lungs allow air in? Air moves into and out of the lungs by the movement of muscles. The most important muscle in the process of breathing is the diaphragm, a sheet of muscle that spreads across the bottom of the rib cage. The diaphragm and rib muscles contract and relax to move air into and out of the lungs. During inhalation, the diaphragm contracts and moves downward. The rib muscles contract and cause the ribs to move outward. This causes the chest volume to increase. Because the chest volume is larger, the air pressure inside the lungs is lower than the air pressure outside. This difference in air pressures causes air to be sucked into the lungs. When the diaphragm and rib muscles relax, air is pushed out of the lungs. Exhalation is similar to letting the air out of a balloon. How does the inhaled oxygen get into the bloodstream? The exchange of gasses between the lungs and the blood happens in tiny sacs called alveoli. The walls of the alveoli are very thin and allow gases to pass though them. The alveoli are lined with capillaries (Figure 1.2). Oxygen moves from the alveoli to the blood in the capillaries that surround the alveoli. At the same time, carbon dioxide moves in the opposite direction, from capillary blood to the alveoli. The gases move by simple diffusion, passing from an area of high concentration to an area of low concentration. For example, initially there is more oxygen in the alveoli than in the blood, so oxygen moves by diffusion from the alveoli into the blood. The process of getting oxygen into the body and releasing carbon dioxide is called respiration. Sometimes breathing is called respiration, but there is much more to respiration than just breathing. Breathing is only the movement of oxygen into the body and carbon dioxide out of the body. The process of respiration also includes the exchange of oxygen and carbon dioxide between the blood and the cells of the body. 
 Question: pushing air out of the body through the nose or mouth is
Output: exhalation.
Context: The generation of reactive oxygen species (ROS) is required for proper cell signaling, but must be tightly regulated to minimize deleterious oxidizing effects. Activation of the NADPH oxidases (Nox) triggers ROS production and, thus, regulatory mechanisms exist to properly control Nox activity. In this study, we report a novel mechanism in which Nox1 activity is regulated through the proteasomal degradation of Nox organizer 1 (NoxO1). We found that through the interaction between NoxO1 and growth receptor-bound protein 2 (Grb2), the Casitas B-lineage lymphoma (Cbl) E3 ligase was recruited, leading to decreased NoxO1 stability and a subsequent reduction in ROS generation upon epidermal growth factor (EGF) stimulation. Additionally, we show that EGF-mediated phosphorylation of NoxO1 induced its release from Grb2 and facilitated its association with Nox activator 1 (NoxA1) to stimulate ROS production. Consistently, overexpression of Grb2 resulted in decreased Nox1 activity, whereas knockdown of Grb2 led to increased Nox1 activity in response to EGF. CRISPR/Cas9-mediated NoxO1 knockout in human colon cancer cells abrogated anchorage-independent growth on soft agar and tumor-forming ability in athymic nude mice. Moreover, the expression and stability of NoxO1 were significantly increased in human colon cancer tissues compared with normal colon. Taken together, these results support a model whereby Nox1 activity and ROS generation are regulated by Grb2/Cbl-mediated proteolysis of NoxO1 in response to EGF, providing new insight into the processes by which excessive ROS production may promote oncogenic signaling to drive colorectal tumorigenesis. 
 Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nadph oxidase 1
Context: The generation of reactive oxygen species (ROS) is required for proper cell signaling, but must be tightly regulated to minimize deleterious oxidizing effects. Activation of the NADPH oxidases (Nox) triggers ROS production and, thus, regulatory mechanisms exist to properly control Nox activity. In this study, we report a novel mechanism in which Nox1 activity is regulated through the proteasomal degradation of Nox organizer 1 (NoxO1). We found that through the interaction between NoxO1 and growth receptor-bound protein 2 (Grb2), the Casitas B-lineage lymphoma (Cbl) E3 ligase was recruited, leading to decreased NoxO1 stability and a subsequent reduction in ROS generation upon epidermal growth factor (EGF) stimulation. Additionally, we show that EGF-mediated phosphorylation of NoxO1 induced its release from Grb2 and facilitated its association with Nox activator 1 (NoxA1) to stimulate ROS production. Consistently, overexpression of Grb2 resulted in decreased Nox1 activity, whereas knockdown of Grb2 led to increased Nox1 activity in response to EGF. CRISPR/Cas9-mediated NoxO1 knockout in human colon cancer cells abrogated anchorage-independent growth on soft agar and tumor-forming ability in athymic nude mice. Moreover, the expression and stability of NoxO1 were significantly increased in human colon cancer tissues compared with normal colon. Taken together, these results support a model whereby Nox1 activity and ROS generation are regulated by Grb2/Cbl-mediated proteolysis of NoxO1 in response to EGF, providing new insight into the processes by which excessive ROS production may promote oncogenic signaling to drive colorectal tumorigenesis. 
 Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nicotinamide adenine dinucleotide phosphate-oxidase 1
Context: The generation of reactive oxygen species (ROS) is required for proper cell signaling, but must be tightly regulated to minimize deleterious oxidizing effects. Activation of the NADPH oxidases (Nox) triggers ROS production and, thus, regulatory mechanisms exist to properly control Nox activity. In this study, we report a novel mechanism in which Nox1 activity is regulated through the proteasomal degradation of Nox organizer 1 (NoxO1). We found that through the interaction between NoxO1 and growth receptor-bound protein 2 (Grb2), the Casitas B-lineage lymphoma (Cbl) E3 ligase was recruited, leading to decreased NoxO1 stability and a subsequent reduction in ROS generation upon epidermal growth factor (EGF) stimulation. Additionally, we show that EGF-mediated phosphorylation of NoxO1 induced its release from Grb2 and facilitated its association with Nox activator 1 (NoxA1) to stimulate ROS production. Consistently, overexpression of Grb2 resulted in decreased Nox1 activity, whereas knockdown of Grb2 led to increased Nox1 activity in response to EGF. CRISPR/Cas9-mediated NoxO1 knockout in human colon cancer cells abrogated anchorage-independent growth on soft agar and tumor-forming ability in athymic nude mice. Moreover, the expression and stability of NoxO1 were significantly increased in human colon cancer tissues compared with normal colon. Taken together, these results support a model whereby Nox1 activity and ROS generation are regulated by Grb2/Cbl-mediated proteolysis of NoxO1 in response to EGF, providing new insight into the processes by which excessive ROS production may promote oncogenic signaling to drive colorectal tumorigenesis. 
 Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nox1
Context: Change in gene expression associated with pancreatic cancer could be attributed to the variation in histone posttranslational modifications leading to subsequent remodeling of the chromatin template during transcription. However, the interconnected network of molecules involved in regulating such processes remains elusive. hPaf1/PD2, a subunit of the human PAF-complex, involved in the regulation of transcriptional elongation has oncogenic potential. Our study explores the possibility that regulation of histone methylation by hPaf1 can contribute towards alteration in gene expression by nucleosomal rearrangement. Here, we show that knockdown of hPaf1/PD2 leads to decreased di- and tri-methylation at histone H3 lysine 4 residues in pancreatic cancer cells. Interestingly, hPaf1/PD2 colocalizes with MLL1 (Mixed Lineage Leukemia 1), a histone methyltransferase that methylates H3K4 residues. Also, a reduction in hPaf1 level resulted in reduced MLL1 expression and a corresponding decrease in the level of CHD1 (Chromohelicase DNA-binding protein 1), an ATPase dependent chromatin remodeling enzyme that specifically binds to H3K4 di and trimethyl marks. hPaf1/PD2 was also found to interact and colocalize with CHD1 in both cytoplasmic and nuclear extracts of pancreatic cancer cells. Further, reduced level of CHD1 localization in the nucleus in hPaf1/PD2 Knockdown cells could be rescued by ectopic expression of hPaf1/PD2. Micrococcal nuclease digestion showed an altered chromatin structure in hPaf1/PD2-KD cells. Overall, our results suggest that hPaf1/PD2 in association with MLL1 regulates methylation of H3K4 residues, as well as interacts and regulates nuclear shuttling of chromatin remodeling protein CHD1, facilitating its function in pancreatic cancer cells. 
 Question: Which is the histone residue methylated by MLL1?
Output: h3k4
Context: Yosemite Sam is on the hunt for a rabbit, and smells Bugs cooking carrots over a rotisserie. When an audience member attempts to leave, Yosemite Sam forces him back into his seat at gunpoint and breaks the fourth wall, threatening to kill anyone who tries to leave the theatre, fearing they could spoil his plan.Sam corners Bugs, and tells him he will be killed at the count of 10. During the countdown, Bugs takes out a piece of bubble gum, chews it, and jams Sam's rifle with it. When Sam fires, he is enveloped in a bubble gum bubble. The bubble is virtually weightless and highly durable; Bugs blows it away, and it falls over a cliff. Sam frantically blows upward, which causes the bubble to stop falling and drift up again. However, Bugs is waiting at the top of the cliff, and he uses a pin to burst the bubble. Sam is enveloped in the sticky remains of the bubble, and sticks to the ground when he falls, bouncing upward repeatedly.Sam chases after Bugs again, managing to get the bubble gum off his body. He forces Bugs out of his hole with a shovel, and marches him to his house at gunpoint.Sam prepares to cook Bugs in a wood stove. Bugs throws Sam's hat into the fire, but when Sam goes to retrieve it, he retrieves a piece of burning firewood by mistake. He quickly gets his hat again, and orders Bugs into the oven (again at gunpoint). While Sam sets the table, he is surprised to find Bugs calmly exiting the oven, retrieving a pitcher of water and a fan, and stepping inside again. Sam is not pleased, but Bugs opens the door again and asks for a bottle opener, which Sam gives to him. The sounds of a party can be heard inside the oven.Bugs exits the oven again to get some ice and chairs, then returns once more and empties two full ashtrays into Sam's hat. When Bugs emerges for the fifth time, he is covered with lipstick marks, and tells Sam plenty of girls are waiting for him inside. Sam quickly puts on a bowtie, and steps into the oven, prompting Bugs to slam the door. Bugs "warms the party up" by throwing some more firewood into the stove, but then decides he's gone too far with this prank.He opens the oven door to tell Sam about the prank, but is flabbergasted to find an actual party taking place inside the oven. He excitedly dives into the oven to join the party, emerging one more time to quip to the audience, "I don't ask questions, I just have fun!" Iris out. 
 Question: What quote does Bugs say in the end ?
Output: "i don't ask questions, i just have fun!"
Context: Sotos syndrome is an overgrowth syndrome with characteristic facial dysmorphism, variable severity of learning disabilities and macrocephaly with overgrowth. Haploinsufficiency of the nuclear receptor SET domain-containing protein 1 (NSD1) gene located on 5q35 has been implicated as the cause of Sotos syndrome. This study was performed to investigate the mutation spectrum of NSD1 abnormalities and meaningful genotype-phenotype correlations in Korean patients with Sotos syndrome. Eighteen unrelated Korean patients with Sotos syndrome were enrolled for clinical and molecular analyses. Cytogenetic studies were performed to confirm 5q35 microdeletion, and NSD1 sequencing analysis was performed to identify intragenic mutations. NSD1 abnormalities were identified in 15 (83%) patients. Among them, eight patients (53%) had 5q35 microdeletions and the other seven patients (47%) had seven different NSD1 intragenic mutations including four novel mutations. The mutation spectrum of Korean patients with Sotos syndrome was similar to that of previous studies for Japanese patients. Height was significantly shorter and age of walking alone was significantly older in the microdeletion group compared with those in the intragenic mutation group. No significant differences were observed for other clinical characteristics between the microdeletion and intragenic mutation groups. Further studies with a larger number of patients will be necessary to draw conclusive genotype-phenotype correlations. 
 Question: Which gene is responsible for the development of Sotos syndrome?
Output: nsd1 gene
Context: Ivan Grafenauer (7 March 1880 - 29 December 1964) was a Slovenian literary historian and ethnologist of Carinthian Slovene origin. 
 Question: What language did Ivan Grafenauer speak?
Output: slovene
Context: Superoxide production by Nox1, a member of the Nox family NAPDH oxidases, requires expression of its regulatory soluble proteins Noxo1 (Nox organizer 1) and Noxa1 (Nox activator 1) and is markedly enhanced upon cell stimulation with phorbol 12-myristate 13-acetate (PMA), a potent activator of protein kinase C (PKC). The mechanism underlying PMA-induced enhancement of Nox1 activity, however, remains to be elucidated. Here we show that, in response to PMA, Noxo1 undergoes phosphorylation at multiple sites, which is inhibited by the PKC inhibitor GF109203X. Among them, Thr341 in Noxo1 is directly phosphorylated by PKC invitro, and alanine substitution for this residue reduces not only PMA-induced Noxo1 phosphorylation but also PMA-dependent enhancement of Nox1-catalyzed superoxide production. Phosphorylation of Thr341 allows Noxo1 to sufficiently interact with Noxa1, an interaction that participates in Nox1 activation. Thus phosphorylation of Noxo1 at Thr341 appears to play a crucial role in PMA-elicited activation of Nox1, providing a molecular link between PKC-mediated signal transduction and Nox1-catalyzed superoxide production. Furthermore, Ser154 in Noxo1 is phosphorylated in both resting and PMA-stimulated cells, and the phosphorylation probably participates in a PMA-independent constitutive activity of Nox1. Ser154 may also be involved in protein kinase A (PKA) mediated regulation of Nox1; this serine is the major residue that is phosphorylated by PKA invitro. Thus phosphorylation of Noxo1 at Thr341 and at Ser154 appears to regulate Nox1 activity in different manners. Noxo1 binds to p22phox by pull down (1, 2, 3) Noxo1 binds to Noxo1 by pull down (View interaction) Noxa1 binds to Noxo1 by pull down (1, 2, 3, 4, 5). 
 Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nadph oxidase 1
Context: Superoxide production by Nox1, a member of the Nox family NAPDH oxidases, requires expression of its regulatory soluble proteins Noxo1 (Nox organizer 1) and Noxa1 (Nox activator 1) and is markedly enhanced upon cell stimulation with phorbol 12-myristate 13-acetate (PMA), a potent activator of protein kinase C (PKC). The mechanism underlying PMA-induced enhancement of Nox1 activity, however, remains to be elucidated. Here we show that, in response to PMA, Noxo1 undergoes phosphorylation at multiple sites, which is inhibited by the PKC inhibitor GF109203X. Among them, Thr341 in Noxo1 is directly phosphorylated by PKC invitro, and alanine substitution for this residue reduces not only PMA-induced Noxo1 phosphorylation but also PMA-dependent enhancement of Nox1-catalyzed superoxide production. Phosphorylation of Thr341 allows Noxo1 to sufficiently interact with Noxa1, an interaction that participates in Nox1 activation. Thus phosphorylation of Noxo1 at Thr341 appears to play a crucial role in PMA-elicited activation of Nox1, providing a molecular link between PKC-mediated signal transduction and Nox1-catalyzed superoxide production. Furthermore, Ser154 in Noxo1 is phosphorylated in both resting and PMA-stimulated cells, and the phosphorylation probably participates in a PMA-independent constitutive activity of Nox1. Ser154 may also be involved in protein kinase A (PKA) mediated regulation of Nox1; this serine is the major residue that is phosphorylated by PKA invitro. Thus phosphorylation of Noxo1 at Thr341 and at Ser154 appears to regulate Nox1 activity in different manners. Noxo1 binds to p22phox by pull down (1, 2, 3) Noxo1 binds to Noxo1 by pull down (View interaction) Noxa1 binds to Noxo1 by pull down (1, 2, 3, 4, 5). 
 Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nicotinamide adenine dinucleotide phosphate-oxidase 1
Context: Superoxide production by Nox1, a member of the Nox family NAPDH oxidases, requires expression of its regulatory soluble proteins Noxo1 (Nox organizer 1) and Noxa1 (Nox activator 1) and is markedly enhanced upon cell stimulation with phorbol 12-myristate 13-acetate (PMA), a potent activator of protein kinase C (PKC). The mechanism underlying PMA-induced enhancement of Nox1 activity, however, remains to be elucidated. Here we show that, in response to PMA, Noxo1 undergoes phosphorylation at multiple sites, which is inhibited by the PKC inhibitor GF109203X. Among them, Thr341 in Noxo1 is directly phosphorylated by PKC invitro, and alanine substitution for this residue reduces not only PMA-induced Noxo1 phosphorylation but also PMA-dependent enhancement of Nox1-catalyzed superoxide production. Phosphorylation of Thr341 allows Noxo1 to sufficiently interact with Noxa1, an interaction that participates in Nox1 activation. Thus phosphorylation of Noxo1 at Thr341 appears to play a crucial role in PMA-elicited activation of Nox1, providing a molecular link between PKC-mediated signal transduction and Nox1-catalyzed superoxide production. Furthermore, Ser154 in Noxo1 is phosphorylated in both resting and PMA-stimulated cells, and the phosphorylation probably participates in a PMA-independent constitutive activity of Nox1. Ser154 may also be involved in protein kinase A (PKA) mediated regulation of Nox1; this serine is the major residue that is phosphorylated by PKA invitro. Thus phosphorylation of Noxo1 at Thr341 and at Ser154 appears to regulate Nox1 activity in different manners. Noxo1 binds to p22phox by pull down (1, 2, 3) Noxo1 binds to Noxo1 by pull down (View interaction) Noxa1 binds to Noxo1 by pull down (1, 2, 3, 4, 5). 
 Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nox1
Context: The Besbre is a river in central France, left tributary of the river Loire. 
 Question: Which river system contains Besbre?
Output: loire
Context: Dough and Dynamite is a 1914 American comedy silent film made by Keystone Studios starring Charlie Chaplin. 
 Question: Which person directed Dough and Dynamite?
Output: charlie chaplin
Context: Transgenic mice over-expressing a mutated form of the human amyloid precursor protein (APP, 695 isoform) bearing a mutation associated with Alzheimer's disease (V642I, so-called London mutation, hereafter APPLd2) and wild-type controls were studied at age periods (3 and 10 months) prior to the overt development of neuritic amyloid plaques. Both 3- and 10-month-old APPLd2 mice had reflex eyelid responses like those of controls, but only younger mice were able to acquire a classical conditioning of eyelid responses in a trace paradigm. In vitro studies on hippocampal slices showed that 10-month-old APPLd2 mice also presented deficits in paired-pulse facilitation and long-term potentiation, but presented a normal synaptic activation of CA1 pyramidal cells by the stimulation of Schaffer collaterals. It is proposed that definite functional changes may appear well in advance of noticeable structural alterations in this animal model of Alzheimer's disease, and that specific learning tasks could have a relevant diagnostic value. 
 Question: Which disease the London mutation involved in?
Output: alzheimer's disease
Context: Transgenic mice over-expressing a mutated form of the human amyloid precursor protein (APP, 695 isoform) bearing a mutation associated with Alzheimer's disease (V642I, so-called London mutation, hereafter APPLd2) and wild-type controls were studied at age periods (3 and 10 months) prior to the overt development of neuritic amyloid plaques. Both 3- and 10-month-old APPLd2 mice had reflex eyelid responses like those of controls, but only younger mice were able to acquire a classical conditioning of eyelid responses in a trace paradigm. In vitro studies on hippocampal slices showed that 10-month-old APPLd2 mice also presented deficits in paired-pulse facilitation and long-term potentiation, but presented a normal synaptic activation of CA1 pyramidal cells by the stimulation of Schaffer collaterals. It is proposed that definite functional changes may appear well in advance of noticeable structural alterations in this animal model of Alzheimer's disease, and that specific learning tasks could have a relevant diagnostic value. 
 Question: Which disease the London mutation involved in?
Output: ad
Context: Singles' Day, also called Double Eleven, began as a day for unmarried or uncoupled people to celebrate their lives on November 11, 1993. In China, however, Singles' Day has become the biggest online shopping day in the world, which was created in 2009 by Alibaba's CEO Daniel Zhang to increase online sales. Since then, it has grown into a cultural phenomenon. China Singles' Day, as a shopping day, takes place on November 11 each year. There are sharp _ and other promotions designed by Alibaba to attract online customers. In 2015, E-commerce giant Alibaba broke records with sales of $14.3 billion on China Singles' Day, with online sales increasing 60 percent from last year, according to Alibaba. "Most people shop on mobile phones or ipads and online shopping has become a comfortable channel for most consumers", said Kitty Fok, China manager for market research. "China is a big market with close to one billion smart, connected device users. It is good news for both Alibaba and their competitors," she said. The company is focusing on international e-commerce for future Singles' Days, reported Reuters. "Within the next five years, we expect China will become the world's largest e-commerce market for imported products," President Michael Evans told reporters on Wednesday. Alibaba Chief Executive Daniel Zhang said in a statement that Singles' Day would mean that "the whole world will see the power of Chinese consumption." Over 130 million users visited Alibaba's marketplace app, Taobao, reported the BBC. 
 Question: What does Alibaba expect to do on Singles' Day?
Output: increase online sales
Context: In a phase I study, Gilead Sciences' PI3K- inhibitor idelalisib produced rapid tumor shrinkage-a response that lasted for 17 months on average-in about half of the 54 patients with chronic lymphocytic leukemia who participated. 
 Question: What is the target protein of the drug Idelalisib?
Output: phosphoinositol-3 kinase delta isoform
Context: In a phase I study, Gilead Sciences' PI3K- inhibitor idelalisib produced rapid tumor shrinkage-a response that lasted for 17 months on average-in about half of the 54 patients with chronic lymphocytic leukemia who participated. 
 Question: What is the target protein of the drug Idelalisib?
Output: pi3k-δ
Context: Song and Dance Man is a children's picture book written by Karen Ackerman and illustrated by Stephen Gammell. 
 Question: What person illustrated Song and Dance Man?
Output: stephen gammell
Context: Toni Young (born January 11, 1991) is an American professional basketball player who last played for the New York Liberty of the WNBA. 
 Question: What team did Toni Young play for?
Output: new york liberty
Context: In 1804, all of the Louisiana Purchase south of the 33rd parallel became the Orleans Territory, and the remainder became the District of Louisiana. The Organic Act of 1804, passed on March 26 for October 1 implementation, also created the United States District Court for the District of Orleansthe only time Congress has ever provided a territory with a United States district court equal in its authority and jurisdiction to those of the states. Congress also established the Superior Court for the Territory of Orleans whose three judges were the top territorial court. On April 10, 1805, the Territorial Legislature organized 12 counties : Orleans County, LaFourche County, German Coast, Acadia County, Iberville County, Attakapas County, Pointe Coupee County, Opelousas County, Rapides County, Concordia County, Natchitoches County, and Ouachita County. The Florida Parishes on the east side of the Mississippi River were not included in Orleans Territory at this time, as they were in the Spanish territory of West Florida until they were formally annexed on April 14, 1812. The western boundary with Spanish Texas was not fully defined until the Adams-Onis Treaty in 1819. A strip of land known as the Sabine Free State just east of the Sabine River served as a neutral ground buffer area from about 1807 until 1819. The Orleans Territory was the site of the largest slave revolt in American history, the 1811 German Coast Uprising. 
 Question: What was not included?
Output: parishes on the east side
Context: As of May, 2010, the California Secretary of State reports that San Benito County has 34,562 eligible voters. Of those 24,736 (71.57%) are registered voters. Of those, 11,959 (48.35%) are registered Democratic, 7,477 (30.23%) are registered Republican, 565 (2.28%)are registered American Independent, and 116 (0.47%) are Green Party. The two incorporated municipalities of Hollister and San Juan Bautista have Democratic majorities on their voter rolls, whereas the unincorporated areas of San Benito County have a small Republican plurality in voter registration. 
 Question: Are there more registered as Democratic or Republican?
Output: democratic
Context: You are on vacation at the beach. You take your flip-flops off so you can go swimming. The sand is so hot it hurts your feet. You have to run to the water. Now imagine if it were hot enough for the sand to melt. Some places inside Earth are so hot that rock melts. Melted rock inside the Earth is called magma. Magma can be hotter than 1,000C. When magma erupts onto Earths surface, it is known as lava, as Figure 3.17 shows. Minerals form when magma and lava cool. Most water on Earth, like the water in the oceans, contains elements. The elements are mixed evenly through the water. Water plus other substances makes a solution. The particles are so small that they will not come out when you filter the water. But the elements in water can form solid mineral deposits. Fresh water contains a small amount of dissolved elements. Salt water contains a lot more dissolved elements. Water can only hold a certain amount of dissolved substances. When the water evaporates, it leaves behind a solid layer of minerals, as Figure 3.18 shows. At this time, the particles come together to form minerals. These solids sink to the bottom. The amount of mineral formed is the same as the amount dissolved in the water. Seawater is salty enough for minerals to precipitate as solids. Some lakes, such as Mono Lake in California, or Utahs Great Salt Lake, can also precipitate salts. Salt easily precipitates out of water, as does calcite, as Figure 3.19 shows. The limestone towers in the figure are made mostly of the mineral calcite. The calcite was deposited in the salty and alkaline water of Mono Lake, in California. Calcium-rich spring water enters the bottom of the lake. The water bubbles up into the alkaline lake. The Underground water can be heated by magma. The hot water moves through cracks below Earths surface. Hot water can hold more dissolved particles than cold water. The hot, salty solution has chemical reactions with the rocks around it. The water picks up more dissolved particles. As it flows through open spaces in rocks, the water deposits solid minerals. When a mineral fills cracks in rocks, the deposits are called veins. Figure 3.20 shows a white quartz vein. When the minerals are deposited in open spaces, large crystals grow. These rocks are called geodes. Figure 3.20 shows a geode that was formed when amethyst crystals grew in an open space in a rock. 
 Question: to come out of a solution as a solid
Output: precipitate
Context: Diamond-Blackfan anemia (DBA) is a congenital bone marrow failure syndrome characterized by a specific deficiency in erythroid progenitors. Forty percent of the patients are blood transfusion-dependent. Recent reports show that the ribosomal protein S19 (RPS19) gene is mutated in 25% of all patients with DBA. We constructed oncoretroviral vectors containing the RPS19 gene to develop gene therapy for RPS19-deficient DBA. These vectors were used to introduce the RPS19 gene into CD34(+) bone marrow (BM) cells from 4 patients with DBA with RPS19 gene mutations. Overexpression of the RPS19 transgene increased the number of erythroid colonies by almost 3-fold. High expression levels of the RPS19 transgene improved erythroid colony-forming ability substantially whereas low expression levels had no effect. Overexpression of RPS19 had no detrimental effect on granulocyte-macrophage colony formation. Therefore, these findings suggest that gene therapy for RPS19-deficient patients with DBA using viral vectors that express the RPS19 gene is feasible. 
 Question: In which syndrome is the RPS19 gene most frequently mutated?
Output: dba
Context: Diamond-Blackfan anemia (DBA) is a congenital bone marrow failure syndrome characterized by a specific deficiency in erythroid progenitors. Forty percent of the patients are blood transfusion-dependent. Recent reports show that the ribosomal protein S19 (RPS19) gene is mutated in 25% of all patients with DBA. We constructed oncoretroviral vectors containing the RPS19 gene to develop gene therapy for RPS19-deficient DBA. These vectors were used to introduce the RPS19 gene into CD34(+) bone marrow (BM) cells from 4 patients with DBA with RPS19 gene mutations. Overexpression of the RPS19 transgene increased the number of erythroid colonies by almost 3-fold. High expression levels of the RPS19 transgene improved erythroid colony-forming ability substantially whereas low expression levels had no effect. Overexpression of RPS19 had no detrimental effect on granulocyte-macrophage colony formation. Therefore, these findings suggest that gene therapy for RPS19-deficient patients with DBA using viral vectors that express the RPS19 gene is feasible. 
 Question: In which syndrome is the RPS19 gene most frequently mutated?
Output: diamond-blackfan anemia
Context: As of the census of 2000, there were 218,590 people, 79,667 households, and 60,387 families residing in the county. The population density was 496 people per square mile (192/km). There were 83,146 housing units at an average density of 189 per square mile (73/km). The racial makeup of the county was 86.77% Race (United States Census), 9.27% Race (United States Census), 0.23% Race (United States Census), 1.52% Race (United States Census), 0.06% Race (United States Census), 0.69% from Race (United States Census), and 1.47% from two or more races. 1.91% of the population were Race (United States Census) or Race (United States Census) of any race. 22.5% were of German people, 13.1% Irish people, 9.8% Italian people, 9.2% English, 8.1% "American" and 6.0% Polish ancestry. 
 Question: Which group from the census is smaller: German or Italian?
Output: italian
Context: MicroRNAs (miRNAs) are a recently discovered group of small RNA molecules involved in the regulation of gene expression. Analogously to mRNAs, the non-protein-encoding pri-miRNAs are synthesized by RNA polymerase II and post-transcriptionally modified by addition of a 5'-cap and a 3'-poly (A) tail. Subsequently, the pri-miRNA undergoes a number of processing steps in the nucleus and cytoplasm, and ends up as a mature approximately 22 nt miRNA, which can exert its function by binding to the 3'-untranslated region of a subset of mRNAs. Binding of the miRNA to the mRNA results in a reduced translation rate and/or increased degradation of the mRNA. In this way a large number of cellular pathways, such as cellular proliferation, differentiation, and apoptosis, are regulated by mi-RNAs. As corruption of these pathways is the hallmark of many cancers, dysregulation of miRNA biogenesis or expression levels may lead to tumorigenesis. The mechanisms that alter the expression of miRNAs are similar to those that change the expression levels of mRNAs of tumor suppressor- and oncogenes, i.e. gross genomic aberrations, epigenetic changes, and minor mutations affecting the expression level, processing, or target-interaction potential of the miRNA. Furthermore, expression profiling of miRNAs has been found to be useful for classification of different tumor types. Taken together, miRNAs can be classified as onco-miRs or tumor suppressor-miRs, and may turn out to be potential targets for cancer therapy. 
 Question: Which polymerase transcribes pri-miRNAs?
Output: rnapii
Context: MicroRNAs (miRNAs) are a recently discovered group of small RNA molecules involved in the regulation of gene expression. Analogously to mRNAs, the non-protein-encoding pri-miRNAs are synthesized by RNA polymerase II and post-transcriptionally modified by addition of a 5'-cap and a 3'-poly (A) tail. Subsequently, the pri-miRNA undergoes a number of processing steps in the nucleus and cytoplasm, and ends up as a mature approximately 22 nt miRNA, which can exert its function by binding to the 3'-untranslated region of a subset of mRNAs. Binding of the miRNA to the mRNA results in a reduced translation rate and/or increased degradation of the mRNA. In this way a large number of cellular pathways, such as cellular proliferation, differentiation, and apoptosis, are regulated by mi-RNAs. As corruption of these pathways is the hallmark of many cancers, dysregulation of miRNA biogenesis or expression levels may lead to tumorigenesis. The mechanisms that alter the expression of miRNAs are similar to those that change the expression levels of mRNAs of tumor suppressor- and oncogenes, i.e. gross genomic aberrations, epigenetic changes, and minor mutations affecting the expression level, processing, or target-interaction potential of the miRNA. Furthermore, expression profiling of miRNAs has been found to be useful for classification of different tumor types. Taken together, miRNAs can be classified as onco-miRs or tumor suppressor-miRs, and may turn out to be potential targets for cancer therapy. 
 Question: Which polymerase transcribes pri-miRNAs?
Output: rna polymerase ii
Context: The People's Unity Assembly (Catalan: Assemblea d'Unitat Popular, AUP) was an independentist organization and movement active between 1993 and 1996. 
 Question: What year was People's Unity Assembly formed in?
Output: 1993
Context: ZFHX1B encodes Smad-interacting protein 1, a transcriptional corepressor involved in the transforming growth factors beta (TGFbeta) signaling pathway. ZFHX1B mutations cause a complex developmental phenotype characterized by severe mental retardation (MR) and multiple congenital defects. We compared the distribution of ZFHX1B transcripts during mouse and human embryogenesis as well as in adult mice and humans. This showed that this gene is strongly transcribed at an early stage in the developing peripheral and central nervous systems of both mice and humans, in all neuronal regions of the brains of 25-week human fetuses and adult mice, and at varying levels in numerous nonneural tissues. Northern blot analysis suggested that ZFHX1B undergoes tissue-specific alternative splicing in both species. These results strongly suggest that ZFHX1B determines the transcriptional levels of target genes in various tissues through the combinatorial interactions of its isoforms with different Smad proteins. Thus, as well as causing neural defects, ZFHX1B mutations may also cause other malformations. 
 Question: Which gene is responsible for the development of the Mowat-Wilson syndrome?
Output: zeb2
Context: ZFHX1B encodes Smad-interacting protein 1, a transcriptional corepressor involved in the transforming growth factors beta (TGFbeta) signaling pathway. ZFHX1B mutations cause a complex developmental phenotype characterized by severe mental retardation (MR) and multiple congenital defects. We compared the distribution of ZFHX1B transcripts during mouse and human embryogenesis as well as in adult mice and humans. This showed that this gene is strongly transcribed at an early stage in the developing peripheral and central nervous systems of both mice and humans, in all neuronal regions of the brains of 25-week human fetuses and adult mice, and at varying levels in numerous nonneural tissues. Northern blot analysis suggested that ZFHX1B undergoes tissue-specific alternative splicing in both species. These results strongly suggest that ZFHX1B determines the transcriptional levels of target genes in various tissues through the combinatorial interactions of its isoforms with different Smad proteins. Thus, as well as causing neural defects, ZFHX1B mutations may also cause other malformations. 
 Question: Which gene is responsible for the development of the Mowat-Wilson syndrome?
Output: zfhx1b
Context: ZFHX1B encodes Smad-interacting protein 1, a transcriptional corepressor involved in the transforming growth factors beta (TGFbeta) signaling pathway. ZFHX1B mutations cause a complex developmental phenotype characterized by severe mental retardation (MR) and multiple congenital defects. We compared the distribution of ZFHX1B transcripts during mouse and human embryogenesis as well as in adult mice and humans. This showed that this gene is strongly transcribed at an early stage in the developing peripheral and central nervous systems of both mice and humans, in all neuronal regions of the brains of 25-week human fetuses and adult mice, and at varying levels in numerous nonneural tissues. Northern blot analysis suggested that ZFHX1B undergoes tissue-specific alternative splicing in both species. These results strongly suggest that ZFHX1B determines the transcriptional levels of target genes in various tissues through the combinatorial interactions of its isoforms with different Smad proteins. Thus, as well as causing neural defects, ZFHX1B mutations may also cause other malformations. 
 Question: Which gene is responsible for the development of the Mowat-Wilson syndrome?
Output: sip-1
Context: Originating in Germany, the Danube flows southeast for 2,860 km (1,780 mi), passing through or touching the border of Austria, Slovakia, Hungary, Croatia, Serbia, Romania, Bulgaria, Moldova and Ukraine before emptying into the Black Sea. 
 Question: What body of water does Danube join?
Output: black sea
Context: Today, nearly 400 animals are listed as threatened or endangered animals in the United States. Many are at risk of becoming extinct or disappearing permanently. Unless efforts to save these vulnerable animals succeed, many of the country's greatest creatures will be lost forever. From the facts listed, guess which animals are endangered. Click on the picture to find out more about each of these animals in trouble. American Crocodile *American crocodiles are about 12 feet long. They live on land and in shallow water, swamps and marshes. *American crocodiles like to float in the water with only their eyes and noses above the water surface. *American crocodiles eat mostly small animals, which they grab with their strong jaws and sharp teeth. *American crocodiles lay eggs. They hide their eggs under twigs and leaves, or bury them in the sand. *Some crocodiles help their young hatch, and then carry them to the water in their mouth. Habitat Southern Florida, Mexico, Central and South American, Caribbean islands. Why It's Endangered Overhunted for its skin and habitat destruction. Peninsular Bighorn Sheep *Bighorn sheep can weigh as much as 280 pounds and stand about 3 feet tall. *They live in dry, desert mountain ranges, near rocky cliffs. *Bighorn sheep eat grass, twigs and leaves. *Male sheep are called rams and can be recognized by their huge, brown horns. The horns curl back over the ears, down,and up past the cheeks. *They live in herds or groups. The male sheep with the biggest horns are usually in charge. Male horns can weigh as much as 30 pounds. *Males will use their massive horns to fight. The fights can last as long as 24 hours. *Females are called ewes. They are smaller than rams and have shorter, smaller horns. Habitat Nevada and California to west Texas and south into Mexico. Why It's Endangered Loss of habitat, hunting illegally, drought and disease. 
 Question: Where can we find both American crocodiles and Bighorn sheep according to the passage?
Output: mexico.
Context: Coming off their Sunday night road win over the Packers, the Cowboys went home for a Week 4 NFC East showdown with the Washington Redskins. In the first quarter, the 'Boys shot first as QB Tony Romo completed a 21-yard TD pass to TE Jason Witten. In the second quarter, the Redskins took the lead as QB Jason Campbell completed a 3-yard TD pass to WR James Thrash and a 2-yard TD pass to WR Antwaan Randle El, along with kicker Shaun Suisham getting a 20-yard field goal. Dallas closed out the half with kicker Nick Folk getting a 36-yard field goal. In the third quarter, the Cowboys tied the game with Romo completing a 10-yard TD pass to WR Terrell Owens. Washington would respond with Suisham kicking a 33-yard field goal. In the fourth quarter, the Redskins increased their lead with Suisham nailing a 33-yard and a 29-yard field goal. The 'Boys tried to rally as Romo completed an 11-yard TD pass to WR Miles Austin. However, Dallas' onside kick attempt failed, preserving the Redskins' win. 
 Question: Which player threw the first touchdown pass of the game?
Output: tony romo