niryuu/sni-each-converted huggingface dataset:
Context: Most sedimentary rocks form from sediments. Sediments are small pieces of other rocks, like pebbles, sand, silt, and clay. Sedimentary rocks may include fossils. Fossils are materials left behind by once-living organisms. Fossils can be pieces of the organism, like bones. They can also be traces of the organism, like footprints. Most often, sediments settle out of water (Figure 4.13). For example, rivers carry lots of sediment. Where the water slows, it dumps these sediments along its banks, into lakes and the ocean. When sediments settle out of water, they form horizontal layers. A layer of sediment is deposited. Then the next layer is deposited on top of that layer. So each layer in a sedimentary rock is younger than the layer under it. It is older than the layer over it. Sediments are deposited in many different types of environments. Beaches and deserts collect large deposits of sand. Sediments also continuously wind up at the bottom of the ocean and in lakes, ponds, rivers, marshes, and swamps. Avalanches produce large piles of sediment. The environment where the sediments are deposited determines the type of sedimentary rock that can form. Sedimentary rocks form in two ways. Particles may be cemented together. Chemicals may precipitate. Over time, deposited sediments may harden into rock. First, the sediments are compacted. That is, they are squeezed together by the weight of sediments on top of them. Next, the sediments are cemented together. Minerals fill in the spaces between the loose sediment particles. These cementing minerals come from the water that moves through the sediments. These types of sedimentary rocks are called clastic rocks. Clastic rocks are rock fragments that are compacted and cemented together. Clastic sedimentary rocks are grouped by the size of the sediment they contain. Conglomerate and breccia are made of individual stones that have been cemented together. In conglomerate, the stones are rounded. In breccia, the stones are angular. Sandstone is made of sand-sized particles. Siltstone is made of smaller particles. Silt is smaller than sand but larger than clay. Shale has the smallest grain size. Shale is made mostly of clay-sized particles and hardened mud. Chemical sedimentary rocks form when crystals precipitate out from a liquid. The mineral halite, also called rock salt, forms this way. You can make halite! Leave a shallow dish of salt water out in the Sun. As the water evaporates, salt crystals form in the dish. There are other chemical sedimentary rocks, like gypsum. Table 4.1 shows some common types of sedimentary rocks and the types of sediments that make them up. Picture Rock Name Conglomerate Type of Sedimentary Rock Clastic Breccia Clastic Sandstone Clastic Siltstone Clastic Limestone Bioclastic Coal Organic Picture Rock Name Rock Salt Type of Sedimentary Rock Chemical precipitate 
 Question: Which sedimentary rock is formed of rounded stones that have been cemented together?
Output: conglomerate
Context: Many factors influence the climate of a region. The most important factor is latitude because different latitudes receive different amounts of solar radiation. The Equator receives the most solar radiation. Days are equally long year-round and the Sun is just about directly overhead at midday. The polar regions receive the least solar radiation. The night lasts six months during the winter. Even in summer, the Sun never rises very high in the sky. Sunlight filters through a thick wedge of atmosphere, making the sunlight much less intense. The high albedo, because of ice and snow, reflects a good portion of the Suns light. Its easy to see the difference in temperature at different latitudes in the Figure 1.1. But temperature is not completely correlated with latitude. There are many exceptions. For example, notice that the western portion of South America The maximum annual temperature of the Earth, showing a roughly gradual temperature gradient from the low to the high latitudes. has relatively low temperatures due to the Andes Mountains. The Rocky Mountains in the United States also have lower temperatures due to high altitudes. Western Europe is warmer than it should be due to the Gulf Stream. Click image to the left or use the URL below. URL: 
 Question: what causes western europe to be warmer than the rest of europe?
Output: the gulf stream
Context: The U.S. Census for 2010 reported 332,199 households in Indianapolis, with an average household size of 2.42 and an average family size of 3.08. Of the total households, 59.3% were family households, with 28.2% of these including the familys own children under the age of 18; 36.5% were husband-wife families; 17.2% had a female householder (with no husband present) and 5.6% had a male householder (with no wife present). The remaining 40.7% were non-family households. , 32% of the non-family households included individuals living alone, 8.3% of these households included individuals age 65 years of age or older. 
 Question: Which group from the census is smaller: non-family households or husband-wife families?
Output: husband-wife families
Context: As of the 2010 United States Census, there were 1,951,269 people, 715,365 households, and 467,916 families residing in the county. The population density was . There were 840,343 housing units at an average density of . The racial makeup of the county was 60.9% white, 10.5% black or African American, 8.7% Asian, 0.7% Pacific islander, 0.7% American Indian, 13.5% from other races, and 5.1% from two or more races. Those of Hispanic or Latino origin made up 29.1% of the population. In terms of ancestry, 11.7% were Germans, 9.1% were Irish people, 7.6% were English people, 6.3% were Italians, and 2.7% were Americans. 
 Question: Where there fewer Germans or Irish?
Output: irish
Context: Selenoproteins are an elite group of proteins containing a rare amino acid, selenocysteine (Sec), encoded by the codon, UGA. In eukaryotes, incorporation of Sec requires a Sec insertion sequence (SECIS) element, a stem-loop structure located in the 3'-untranslated regions of selenoprotein mRNAs. Here we report identification of a noncanonical form of SECIS element in Toxoplasma gondii and Neospora canine, single-celled apicomplexan parasites of humans and domestic animals. This SECIS has a GGGA sequence in the SBP2-binding site in place of AUGA previously considered invariant. Using a combination of computational and molecular techniques, we show that Toxoplasma and Neospora possess both canonical and noncanonical SECIS elements. The GGGA-type SECIS element supported Sec insertion in mammalian HEK 293 and NIH 3T3 cells and did so more efficiently than the natural mammalian SECIS elements tested. In addition, mammalian type I and type II SECIS elements mutated into the GGGA forms were functional but manifested decreased Sec insertion efficiency. We carried out computational searches for both AUGA and GGGA forms of SECIS elements in Toxoplasma and detected five selenoprotein genes, including one coding for a previously undescribed selenoprotein, designated SelQ, and two containing the GGGA form of the SECIS element. In contrast, the GGGA-type SECIS elements were not detected in mammals and nematodes. As a practical outcome of the study, we developed pSelExpress1, a vector for convenient expression of selenoproteins in mammalian cells. It contains an SBP2 gene and the most efficient tested SECIS element: an AUGA mutant of the GGGA-type Toxoplasma SelT structure. 
 Question: What is the name of the stem loop present in the 3' end of genes encoding for selenoproteins?
Output: secis
Context: The Patriots clinched their fourth straight AFC East title with a close road win. After a scoreless first quarter, the Jaguars responded to a Gostkowski field goal with a Maurice Jones-Drew touchdown run. The Patriots challenged the play, as Jones-Drew appeared to fall down at the line of scrimmage, but the ruling on the field was upheld. New England came back before the halftime to retake the lead at 10-7 on a Dillon one-yard touchdown run. The Patriots maintained their lead as the teams traded touchdowns in the second half, including another touchdown by Jones-Drew. A David Garrard fumble with 1:55 left in the fourth quarter, recovered by safety Rodney Harrison, sealed the Patriots' 11th win of the season. 
 Question: Which player scored the first points of the game?
Output: gostkowski
Context: Viroids, subviral pathogens of plants, are composed of a single-stranded circular RNA of 246-399 nucleotides. Within the 27 viroids sequenced, avocado sunblotch, peach latent mosaic and chrysanthemum chlorotic mottle viroids (ASBVd, PLMVd and CChMVd, respectively) can form hammerhead structures in both of their polarity strands. These ribozymes mediate self-cleavage of the oligomeric RNAs generated in the replication through a rolling circle mechanism, whose two other steps are catalyzed by an RNA polymerase and an RNA ligase. ASBVd, and presumably PLMVd and CChMVd, replicate and accumulate in the chloroplast, whereas typical viroids replicate and accumulate in the nucleus. PLMVd and CChMVd do not adopt a rod-like or quasi rod-like secondary structure as typical viroids do but have a highly branched conformation. A pathogenicity determinant has been mapped in a defined region of the CChMVd molecule. 
 Question: Which are the smallest known subviral pathogens of plants?
Output: viroids
Context: The gene encoding the small subunit ribosomal protein 19 (RPS19) is mutated in about 25% of cases of the bone marrow failure syndrome Diamond Blackfan Anemia (DBA), a childhood disease characterized by failure of red cell production. In these cases DBA is inherited as an autosomal dominant trait and RPS19 haploinsufficiency is thought to cause the disease. To study the molecular pathogenesis of DBA we used siRNA to decrease the level of RPS19 in two human cell lines, HeLa cells and U-2 OS osteosarcoma cells. Cells with reduced RPS19 levels showed a dramatic reduction in the amounts of small 40S ribosome subunits and mature 80S ribosomes and an excess of large 60S subunits. These cells were defective in 18S rRNA production and accumulated 21S and 20S nuclear pre-rRNA molecules, suggesting that RPS19 is required for specific steps in rRNA processing. RPS19 depletion produced a reduction in steady-state levels of RPS6 and RPS16 via a post-transcriptional mechanism while the levels of RPL7 and RPL26 were unaltered, indicating that levels of ribosomal proteins are determined by subunit assembly. This has interesting implications for the pathogenesis of DBA suggesting that deficiency of any of the RPS proteins might have a similar effect and thus may be responsible for causing DBA. Finally in cell lines from DBA patients with mutations we find increased levels of 21S rRNA precursors but no abnormality in the ribosome profile on sucrose gradients or in the steady-state levels of RPS19 suggesting that some cells can partially compensate for the loss of one allele of RPS19. We conclude that defects in ribosome biogenesis may underlie the pathology of Diamond Blackfan Anemia. 
 Question: In which syndrome is the RPS19 gene most frequently mutated?
Output: dba
Context: The gene encoding the small subunit ribosomal protein 19 (RPS19) is mutated in about 25% of cases of the bone marrow failure syndrome Diamond Blackfan Anemia (DBA), a childhood disease characterized by failure of red cell production. In these cases DBA is inherited as an autosomal dominant trait and RPS19 haploinsufficiency is thought to cause the disease. To study the molecular pathogenesis of DBA we used siRNA to decrease the level of RPS19 in two human cell lines, HeLa cells and U-2 OS osteosarcoma cells. Cells with reduced RPS19 levels showed a dramatic reduction in the amounts of small 40S ribosome subunits and mature 80S ribosomes and an excess of large 60S subunits. These cells were defective in 18S rRNA production and accumulated 21S and 20S nuclear pre-rRNA molecules, suggesting that RPS19 is required for specific steps in rRNA processing. RPS19 depletion produced a reduction in steady-state levels of RPS6 and RPS16 via a post-transcriptional mechanism while the levels of RPL7 and RPL26 were unaltered, indicating that levels of ribosomal proteins are determined by subunit assembly. This has interesting implications for the pathogenesis of DBA suggesting that deficiency of any of the RPS proteins might have a similar effect and thus may be responsible for causing DBA. Finally in cell lines from DBA patients with mutations we find increased levels of 21S rRNA precursors but no abnormality in the ribosome profile on sucrose gradients or in the steady-state levels of RPS19 suggesting that some cells can partially compensate for the loss of one allele of RPS19. We conclude that defects in ribosome biogenesis may underlie the pathology of Diamond Blackfan Anemia. 
 Question: In which syndrome is the RPS19 gene most frequently mutated?
Output: diamond blackfan anemia
Context: The gene encoding the small subunit ribosomal protein 19 (RPS19) is mutated in about 25% of cases of the bone marrow failure syndrome Diamond Blackfan Anemia (DBA), a childhood disease characterized by failure of red cell production. In these cases DBA is inherited as an autosomal dominant trait and RPS19 haploinsufficiency is thought to cause the disease. To study the molecular pathogenesis of DBA we used siRNA to decrease the level of RPS19 in two human cell lines, HeLa cells and U-2 OS osteosarcoma cells. Cells with reduced RPS19 levels showed a dramatic reduction in the amounts of small 40S ribosome subunits and mature 80S ribosomes and an excess of large 60S subunits. These cells were defective in 18S rRNA production and accumulated 21S and 20S nuclear pre-rRNA molecules, suggesting that RPS19 is required for specific steps in rRNA processing. RPS19 depletion produced a reduction in steady-state levels of RPS6 and RPS16 via a post-transcriptional mechanism while the levels of RPL7 and RPL26 were unaltered, indicating that levels of ribosomal proteins are determined by subunit assembly. This has interesting implications for the pathogenesis of DBA suggesting that deficiency of any of the RPS proteins might have a similar effect and thus may be responsible for causing DBA. Finally in cell lines from DBA patients with mutations we find increased levels of 21S rRNA precursors but no abnormality in the ribosome profile on sucrose gradients or in the steady-state levels of RPS19 suggesting that some cells can partially compensate for the loss of one allele of RPS19. We conclude that defects in ribosome biogenesis may underlie the pathology of Diamond Blackfan Anemia. 
 Question: In which syndrome is the RPS19 gene most frequently mutated?
Output: diamond-blackfan anemia
Context: The Web site for the Anxiety Disorders Association of America (ADAA) receives more than 5 million visits per month and thus represents a unique medium for the study of anxiety disorders. ADAA Web site users from October 2002 to January 2003 were invited to complete a survey oriented toward trauma history and psychiatric sequelae. A diagnostic approximation of posttraumatic stress disorder (PTSD) was based on responses to the Trauma Questionnaire, the Davidson Trauma Scale, and questions about impairment. The Connor-Davidson Resilience Scale was also used. Variables were tested for their association with PTSD. Among 1558 participants, 87% had a history of trauma, and 38% had current PTSD. The population was comprised predominantly of white middle-class women, half of whom were married. More than 90% were first-time users of the site. Factors associated with PTSD included death of, or harm to, a loved one; personal history of incest, rape, or physical abuse; lower age; lower income; unemployment; missed work; increased medical care; dissatisfaction with psychotropic medication; depressive symptoms; and lower resilience. In this selective convenience sample, there were high rates of traumatization and PTSD. The demographics of this group are similar to those seen in previously studied populations that had contacted the ADAA. Furthermore, the factors associated with PTSD were like those in many community surveys. The ADAA Web site has the opportunity to benefit large numbers of highly distressed individuals. 
 Question: Symptoms of which disorder are evaluated with the Davidson Trauma Scale?
Output: ptsd
Context: The Web site for the Anxiety Disorders Association of America (ADAA) receives more than 5 million visits per month and thus represents a unique medium for the study of anxiety disorders. ADAA Web site users from October 2002 to January 2003 were invited to complete a survey oriented toward trauma history and psychiatric sequelae. A diagnostic approximation of posttraumatic stress disorder (PTSD) was based on responses to the Trauma Questionnaire, the Davidson Trauma Scale, and questions about impairment. The Connor-Davidson Resilience Scale was also used. Variables were tested for their association with PTSD. Among 1558 participants, 87% had a history of trauma, and 38% had current PTSD. The population was comprised predominantly of white middle-class women, half of whom were married. More than 90% were first-time users of the site. Factors associated with PTSD included death of, or harm to, a loved one; personal history of incest, rape, or physical abuse; lower age; lower income; unemployment; missed work; increased medical care; dissatisfaction with psychotropic medication; depressive symptoms; and lower resilience. In this selective convenience sample, there were high rates of traumatization and PTSD. The demographics of this group are similar to those seen in previously studied populations that had contacted the ADAA. Furthermore, the factors associated with PTSD were like those in many community surveys. The ADAA Web site has the opportunity to benefit large numbers of highly distressed individuals. 
 Question: Symptoms of which disorder are evaluated with the Davidson Trauma Scale?
Output: post-traumatic stress disorder
Context: Last year, over 206,000 students from the United States studied abroad. Does that number surprise you? These students already know the benefits of studying abroad. You may be wondering why you should study abroad. Here are some answers for you. * Timing The absolutely best time in your life to study abroad is when you are in college. If you miss this opportunity, it's almost impossible for you to do it later in life. * To gain cross-cultural experience Life overseas makes you see your everyday world in a whole new light. You don't even realize it, but our culture shapes the way we view the world and affects us every minute of the day. Differences in culture are more than just differences in language, food, clothing and art. * To improve your communication skills and your self-confidence People who study abroad tend to be willing to take risks, willing to put themselves in unusual situations, and able to solve problems. * To become more fluent in a language or to learn a new language The world market is becoming smaller, and many companies require a second language. Foreign languages are not only valuable in the job market but also valuable in the real world. * For the adventure Travel to other cities within your host country and around neighboring countries. As you get to know your new classmates, roommates, and host family, you will gain a unique view on the host culture. Discover the differences and, more importantly, the many similarities between your worlds. The friendships you make will last long after the program. * To learn more about yourself Find out who you really are. What are your limits? How do you overcome the difficulties you've never _ before? How independent are you? These questions are hard to answer until you are removed from your usual surroundings. After solving difficult problems on your own overseas, you'll find that almost nothing will confuse you at home. Students who study abroad commonly report that their study abroad experience actually changed their lives. 
 Question: What is the best time in your life to study abroad according to the passage?
Output: when you are in college.
Context: Henry Keogh (born 1954) is an Australian convicted of murder. 
 Question: Which crime led to the conviction of Henry Keogh?
Output: murder
Context: Chediak-Higashi syndrome (CHS) is a rare multiorgan disease entity with autosomal recessive inheritance characterized by oculocutaneous albinism, bleeding tendency, recurrent bacterial infections and various neurological symptoms. Intracellular vesicle formation is deficient, resulting in giant granules in many cells, e.g. giant melanosomes in the melanocytes. Diagnosis has been based on morphological examination of peripheral blood and bone marrow, with giant granules seen in cells of the myeloid lineage and in lymphocytes. The ultimate diagnostic test is to look for a mutated LYST gene. Most patients develop an accelerated phase of the disease with deposition of lymphohistiocytes in the liver, spleen, lymph nodes and bone marrow, resulting in hepatosplenomegaly, bone marrow infiltration and haemophagocytosis. Peripheral blood neutropenia becomes more profound as anaemia and thrombocytopenia develop. Most patients succumb before the age of 10 years. Four patients with CHS are described, one of whom is a long-term survivor after successful allogeneic bone marrow transplantation, two succumbed during the accelerated phase and one is living with a chronic form of the disease. Allogeneic bone marrow transplantation from an HLA-matched sibling is the therapy of choice and should be performed early. If there is no matched family donor, an unrelated donor or a placental blood graft is a good alternative. The clinical picture of CHS is heterogeneous and therapeutic decisions need to be made on an individual basis. 
 Question: Which mutated gene causes the ChediakHigashi Syndrome?
Output: lysosomal trafficking regulator gene
Context: Chediak-Higashi syndrome (CHS) is a rare multiorgan disease entity with autosomal recessive inheritance characterized by oculocutaneous albinism, bleeding tendency, recurrent bacterial infections and various neurological symptoms. Intracellular vesicle formation is deficient, resulting in giant granules in many cells, e.g. giant melanosomes in the melanocytes. Diagnosis has been based on morphological examination of peripheral blood and bone marrow, with giant granules seen in cells of the myeloid lineage and in lymphocytes. The ultimate diagnostic test is to look for a mutated LYST gene. Most patients develop an accelerated phase of the disease with deposition of lymphohistiocytes in the liver, spleen, lymph nodes and bone marrow, resulting in hepatosplenomegaly, bone marrow infiltration and haemophagocytosis. Peripheral blood neutropenia becomes more profound as anaemia and thrombocytopenia develop. Most patients succumb before the age of 10 years. Four patients with CHS are described, one of whom is a long-term survivor after successful allogeneic bone marrow transplantation, two succumbed during the accelerated phase and one is living with a chronic form of the disease. Allogeneic bone marrow transplantation from an HLA-matched sibling is the therapy of choice and should be performed early. If there is no matched family donor, an unrelated donor or a placental blood graft is a good alternative. The clinical picture of CHS is heterogeneous and therapeutic decisions need to be made on an individual basis. 
 Question: Which mutated gene causes the ChediakHigashi Syndrome?
Output: lyst gene
Context: However, the Seven Years' War ended on February 10, 1763 with the signing of the Treaty of Paris in Paris, France. Also, Silang was assassinated on May 28, 1763 by an Indio under the employ of the friars. The Spanish were then able to focus on the uprising and mustered forces to surround Palaris. The Spanish friars, who were allowed to stay in the province, also started a campaign to persuade Pangasinan residents of the futility of the Palaris Revolt. By September 1763, news of the peace treaty reached Pangasinan and army of Palaris' men surrendered and returned to normal life amid the Spanish offensive. Palaris tried to fend off the offensive at the village of Mabalitec near the Agno River between Binalatongan and Bayambang in December 1763. To prevent the Spanish from seeking lodging in his hometown, he ordered his men to raze Binalatongan. But the Spanish won the Battle of Mabalitec, demoralizing Palaris' forces. The town of Binalatongan was rebuilt in another site between December 1763 to June 1764 and renamed San Carlos , in honor of the reigning King Carlos III of Spain. Palaris' forces made a last stand at the town of San Jacinto, Pangasinan, but they were defeated. Palaris' advisers, Andres Lopez and Juan de Vera Oncantin, were captured. They would later be hanged. 
 Question: Who assassin employed by? Silang
Output: friars
Context: Daniel Caligiuri (pronounced (kaliduri); born 15 January 1988 in Villingen-Schwenningen) is a German-born Italian professional footballer who plays as a midfielder for VfL Wolfsburg in the Bundesliga and the Italy national team. 
 Question: What position was played by Daniel Caligiuri?
Output: midfielder
Context: Women, Race & Class Angela Y Davis PS7.99 Analysing the differences and similarities between the experiences of black and white women, Davis casts new light on the struggle for human rights. The Words to Say it (an autobiographical novel) Marie Cardinal translated by Pat Goodheart PS7.99 Marie Cardinal's groundbreaking book was the first and remains the complete book about the personal experience of psychoanalysis . It reveals her traumatic childhood and institutionalisation , followed by her escape to the cul-de-sac where her analyst lived. There, for many years, she made the journey towards recovery through Freudian psychoanalysis. A worldwide bestseller, translated into eighteen languages, it remains one of the most highly-praised books of our age. Jade Millie Murray PS4.99 Jade Wilson is smart, young, black and ambitious. And she's just been given the chance of a lifetime - a try-out for the Commonwealth Games swimming team. Jade lives with her mum, Jojo, a successful business woman. Jojo is overprotective of Jade, but she has her reasons. As a young model with a wonderful career ahead of her, she fell pregnant with Jade, and, much as she loves her daughter, she's determined not to let anything get in the way of Jade's success. So when Jade starts dating Dicey, there is hell to pay. Will Jade survive her Mum's constant nagging ? And what if she were to get pregnant - would she, could she, do the same as Jojo and give up her career? As things start hotting up with Dicey, Jade is faced with some very tough choices... . The book is very popular with people all over the world. 
 Question: Which book do you buy if you want to read about women's rights?
Output: women, race & class
Context: As of the census of 2000, there were 325,957 people, 149,937 households, and 94,460 families residing in the county. The population density was 570 people per square mile (220/km2). There were 182,467 housing units at an average density of 319 per square mile (123/km2). The racial makeup of the county was 92.65% Race (United States Census), 4.18% Race (United States Census) or Race (United States Census), 0.22% Race (United States Census), 0.77% Race (United States Census), 0.03% Race (United States Census), 1.14% from Race (United States Census), and 1.02% from two or more races. 4.34% of the population were Race (United States Census) or Race (United States Census) of any race. 89.7% spoke only English language at home; 4.4% spoke Spanish language, 1.3% German language, and 1.0% French language at home. 
 Question: What was the second most common language spoken at home?
Output: spanish
Context: The Jets started slow by accruing no passing yards during the first quarter, but the Patriots went down the field in two long drives taking up most of the time in the first half. In the second quarter, the Patriots took the early lead as quarterback Tom Brady completed a 6-yard touchdown pass to wide receiver Wes Welker, but the Jets replied with quarterback Mark Sanchez completing a 10-yard touchdown pass to wide receiver Braylon Edwards. The Patriots scored again with Brady finding wide receiver Randy Moss on a 34-yard touchdown pass. The Jets narrowed the Patriots' lead when kicker Nick Folk nailed a 49-yard field goal, followed by him making a 36-yard field goad in the third quarter. The Jets got the lead when Sanchez completed a 2-yard touchdown pass to wide receiver Jerricho Cotchery (with a successful 2-point conversion). The Jets extended their lead in the fourth quarter when Sanchez making a 1-yard touchdown pass to tight end Dustin Keller. 
 Question: Who caught the last touchdown of the game?
Output: dustin keller
Context: In February 2009, James L. Jones, then-chairman of the Atlantic Council, stepped down in order to serve as President Obama's new National Security Advisor and was succeeded by Senator Chuck Hagel. 
 Question: Who led Atlantic Council?
Output: chuck hagel
Context: Mowat-Wilson syndrome (MWS) is a multiple congenital anomaly-mental retardation complex caused by mutations in the Zinc Finger Homeobox 1 B gene (ZFHX1B). MWS has been reported in association with Hirschsprung disease (HSCR). MWS is sometimes difficult to diagnose clinically, especially when HSCR is absent. Thus, it is necessary to detect gene abnormalities at the molecular level. Here we report two Japanese girls with MWS, who showed a distinct facial phenotype, severe intellectual disability and epileptic seizures. Major congenital anomalies of the patients were very different. Patient 1 suffered from severe congenital heart disease, but did not show apparent HSCR. Patient 2 suffered from typical HSCR and underwent surgical treatment, but did not have congenital heart disease. According to the gene analysis using white blood cells, they had nonsense mutations in ZFHX1B, R695X and Q433X, respectively. In conclusion, molecular genetic analysis of ZFHX1B is important for a definite diagnosis of MWS which has a wide phenotypic spectrum of congenital anomalies. 
 Question: Which gene is responsible for the development of the Mowat-Wilson syndrome?
Output: zeb2
Context: Mowat-Wilson syndrome (MWS) is a multiple congenital anomaly-mental retardation complex caused by mutations in the Zinc Finger Homeobox 1 B gene (ZFHX1B). MWS has been reported in association with Hirschsprung disease (HSCR). MWS is sometimes difficult to diagnose clinically, especially when HSCR is absent. Thus, it is necessary to detect gene abnormalities at the molecular level. Here we report two Japanese girls with MWS, who showed a distinct facial phenotype, severe intellectual disability and epileptic seizures. Major congenital anomalies of the patients were very different. Patient 1 suffered from severe congenital heart disease, but did not show apparent HSCR. Patient 2 suffered from typical HSCR and underwent surgical treatment, but did not have congenital heart disease. According to the gene analysis using white blood cells, they had nonsense mutations in ZFHX1B, R695X and Q433X, respectively. In conclusion, molecular genetic analysis of ZFHX1B is important for a definite diagnosis of MWS which has a wide phenotypic spectrum of congenital anomalies. 
 Question: Which gene is responsible for the development of the Mowat-Wilson syndrome?
Output: zfhx1b
Context: Mowat-Wilson syndrome (MWS) is a multiple congenital anomaly-mental retardation complex caused by mutations in the Zinc Finger Homeobox 1 B gene (ZFHX1B). MWS has been reported in association with Hirschsprung disease (HSCR). MWS is sometimes difficult to diagnose clinically, especially when HSCR is absent. Thus, it is necessary to detect gene abnormalities at the molecular level. Here we report two Japanese girls with MWS, who showed a distinct facial phenotype, severe intellectual disability and epileptic seizures. Major congenital anomalies of the patients were very different. Patient 1 suffered from severe congenital heart disease, but did not show apparent HSCR. Patient 2 suffered from typical HSCR and underwent surgical treatment, but did not have congenital heart disease. According to the gene analysis using white blood cells, they had nonsense mutations in ZFHX1B, R695X and Q433X, respectively. In conclusion, molecular genetic analysis of ZFHX1B is important for a definite diagnosis of MWS which has a wide phenotypic spectrum of congenital anomalies. 
 Question: Which gene is responsible for the development of the Mowat-Wilson syndrome?
Output: sip-1
Context: All electromagnetic waves travel at the same speed through empty space. That speed, called the speed of light, is 300 million meters per second (3.0 108 m/s). Nothing else in the universe is known to travel this fast. If you could move that fast, you would be able to travel around Earth 7.5 times in just 1 second! The sun is about 150 million kilometers (93 million miles) from Earth, but it takes electromagnetic radiation only 8 minutes to reach Earth from the sun. Electromagnetic waves travel more slowly through a medium, and their speed may vary from one medium to another. For example, light travels more slowly through water than it does through air (see Figure 21.4). You can learn more about the speed of light at this URL: [Link] Although all electromagnetic waves travel at the same speed, they may differ in their wavelength and frequency. Wavelength and frequency are defined in the same way for electromagnetic waves as they are for mechanical waves. Both properties are illustrated in Figure 21.5. Wavelength is the distance between corresponding points of adjacent waves. Wavelengths of electromagnetic waves range from many kilometers to a tiny fraction of a millimeter. Frequency is the number of waves that pass a fixed point in a given amount of time. Frequencies of electro- magnetic waves range from thousands to trillions of waves per second. Higher frequency waves have greater energy. The speed of a wave is a product of its wavelength and frequency. Because all electromagnetic waves travel at the same speed through space, a wave with a shorter wavelength must have a higher frequency, and vice versa. This relationship is represented by the equation: Speed = Wavelength Frequency The equation for wave speed can be rewritten as: Frequency = Speed Speed or Wavelength = Wavelength Frequency Therefore, if either wavelength or frequency is known, the missing value can be calculated. Consider an electromag- netic wave that has a wavelength of 3 meters. Its speed, like the speed of all electromagnetic waves, is 3.0 108 meters per second. Its frequency can be found by substituting these values into the frequency equation: Frequency = 3.0 108 m/s = 1.0 108 waves/s, or 1.0 108 hertz (Hz) 3.0 m You Try It! Problem: What is the wavelength of an electromagnetic wave that has a frequency of 3.0 108 hertz? For more practice calculating the frequency and wavelength of electromagnetic waves, go to these URLs: 
 Question: distance between corresponding points of adjacent waves
Output: wavelength
Context: The acromelic dysplasia group is characterized by short stature, short hands and feet, stiff joint, and "muscular" build. Four disorders can now be ascribed to this group, namely Weill-Marchesani syndrome (WMS), geleophysic dysplasia (GD), acromicric dysplasia (AD), and Myhre syndrome (MS). Although closely similar, they can be distinguished by subtle clinical features and their pattern inheritance. WMS is characterized by the presence of dislocation of microspherophakia and has autosomal dominant or recessive mode of inheritance. GD is the more severe one, with a progressive cardiac valvular thickening, tracheal stenosis, bronchopulmonary insufficiency, often leading to an early death. AD has an autosomal dominant mode of inheritance, distinct facial and skeleton features (a hoarse voice and internal notch of the femoral head). Finally, MS is sporadic, characterized by prognathism, deafness, developmental delay, thickened calvarium, and large vertebrae with short and large pedicles. We first identified mutations in Fibrillin-1 (FBN1) in the dominant form of WMS and then mutations in A Disintegrin-like And Metalloproteinase domain with ThromboSpondin type 1 repeats 10 (ADAMTS10) in the recessive form of WMS. The function of ADAMTS10 is unknown but these findings support a direct interaction between ADAMTS10 and FBN1. We then identified mutations in ADAMTSL2 in the recessive form of GD and a hotspot of mutations in FBN1 in the dominant form of GD and in AD (exon 41-42, encoding TGF binding protein-like domain 5 (TB5) of FBN1). The function of ADAMTSL2 is unknown. Using a yeast double hybrid screen, we identified latent transforming growth factor- (TGF) binding protein 1 as a partner of ADAMTSL2. We found an increased level of active TGF in the fibroblast medium from patients with FBN1 or ADAMTSL2 mutations and an enhanced phosphorylated SMAD2 level, allowing us to conclude at an enhanced TGF signaling in GD and AD. Finally, a direct interaction between ADAMTSL2 and FBN1 was demonstrated suggesting a dysregulation of FBN1/ADAMTSL2 interrelationship as the underlying mechanism of the short stature phenotypes. Using exome sequencing in MS probands, we identified de novo SMAD4 missense mutations, all involving isoleucine residue at position 500, in the MH2 domain. In MS fibroblasts, we found decreased ubiquitination level of SMAD4 and increased level of SMAD4 supporting a stabilization of SMAD4 protein. Functional SMAD4 is required for canonical signal transduction through the oligomerization with phosphorylated SMAD2/3 and SMAD1/5/8. We therefore studied the nuclear localization of mutant SMAD complexes and found that the complexes translocate to the nucleus. We finally observed a decreased expression of downstream TGF target genes supporting impaired TGF driven transcriptional control in MS. Our findings support a direct link between the short stature phenotypes and the TGF signaling. However, the finding of enhanced TGF signaling in Marfan phenotypes supports the existence of yet unknown mechanisms regulating TGF action. 
 Question: What is the mode of inheritance of Acromicric dysplasia?
Output: autosomal dominant
Context: Coming off their win over the Dolphins, the Falcons stayed at home, donned their throwback uniforms, and prepared for a Week 2 NFC South showdown against the Carolina Panthers. Atlanta would trail early in the first quarter as Panthers kicker John Kasay got a 38-yard field goal. Afterwards, the Falcons would answer with quarterback Matt Ryan completing a 24-yard touchdown pass to tight end Tony Gonzalez. In the second quarter, Carolina would reply with running back DeAngelo Williams getting a 3-yard touchdown run. Atlanta would strike back as Ryan completed a 10-yard touchdown pass to fullback Jason Snelling. The Panthers would creep close as Kasay nailed a 50-yard field goal, yet the Falcons would increase their lead prior to halftime as Ryan completed a 7-yard touchdown pass to wide receiver Roddy White. After a scoreless third quarter, Atlanta would get some necessary distance from Carolina as running back Michael Turner got a 1-yard touchdown run. Afterwards, Carolina mustered an 11-yard touchdown pass from quarterback Jake Delhomme to tight end Dante Rosario. On another Panthers possession, Delhomme threw an interception to cornerback Chris Houston. After yet another possession, with time running out, the Panthers tried to rally as Delhomme threw a deep desperation pass, but it resulted incomplete as cornerback Brent Grimes batted it down. 
 Question: who scored first?
Output: panthers
Context: Min and Bill is a 1930 American Pre-Code comedy-drama film starring Marie Dressler and Wallace Beery and based on Lorna Moon's novel Dark Star, adapted by Frances Marion and Marion Jackson. 
 Question: The Min and Bill is based upon what?
Output: lorna moon
Context: KazSat-3 (Kazakh: -3) is a telecommunications satellite which was launched 28 April 2014 at 10:25 GMT Astana Time from Cosmodrome Baikonur in Kazakhstan. 
 Question: On what date was KazSat-3 launched?
Output: 28 april 2014
Context: The acromelic dysplasia group includes three rare disorders: Weill-Marchesani syndrome (WMS), Geleophysic dysplasia (GD) and Acromicric dysplasia (AD) all characterized by short stature, short hands and stiff joints. The clinical overlap between the three disorders is striking. Indeed, in addition to the diagnostic criteria, they all share common features including delayed bone age, cone shaped epiphyses, thick skin and heart disease. In contrast, a microspherophakic lens seems to be a characteristic feature of WMS whereas hepatomegaly and a severe outcome are encountered only in the most severe forms of GD. Finally, WMS is transmitted either by an autosomal dominant or an autosomal recessive (AR) mode of inheritance, GD by an autosomal recessive mode of inheritance and AD by an autosomal dominant mode of inheritance. Using genetic approaches, we have identified the molecular basis of WMS and GD which both involved the same superfamily of proteins, the ADAMTS [A Disintegrin-like And Metalloproteinase domain (reprolysin type) with ThromboSpondin type 1 repeats (TSR)]. We have found ADAMTS10 mutations in the recessive form of WMS and Fibrillin 1 mutations in the dominant form of WMS. More recently, we have identified ADAMTSL2 mutations in GD. The function of ADAMTS1 0 and AD AMTSL 2 are unknown. But the findings of FBN1 and ADAMTS10 mutations in WMS suggest a direct link between the two proteins. Using a yeast double hybrid screen, we have identified LTBP1 (Latent TGFbeta Binding protein 1) as a partner of ADAMTSL2. The combination of these findings suggests that ADAMTS10 and ADAMTSL2 are both involved in the microfibrillar network. 
 Question: What is the mode of inheritance of Acromicric dysplasia?
Output: autosomal dominant
Context: Guo Jingming is a best-selling author in China. He was born in Zigong, Sichuan Province on June 6, 1983. He is well-known for his essays and fictions, such as On the Edge of Love and Hurt, City of Fantasy, and Tiny Times. His essays and fictions are especially popular with teenagers. He is also a director and once directed his movie Tiny Times successfully. In June 2013, Guo was awarded the Best New Director at the Shanghai International Film Festival for his first movie Tiny Times. The movie has sold 6.7 million copies. In 2001, Guo Jingming started to gain _ after winning the New Concept Writing Competition's top award. Lots of young people got to know Guo Jingming little by little. A year later, Guo entered the writing competition again and won the top prize for the second time. At the same time, a collection of his prose On the Edge of Love and Hurt was published. In 2003, his first novel City of Fantasy came out. It was the novel that made Guo Jingming famous all over the country. In 2008, Guo was elected to the Chinese Writers' Association. He became the youngest member of the association. Guo's Tiny Times series was published between 2008 and 2012. 
 Question: What's Guo Jingming's first novel?
Output: city of fantasy.
Context: As a result of continued decline in the traditional Gaelic heartlands, today no Civil parishes in Scotland in Scotland has a proportion of Gaelic speakers greater than 65% (the highest value is in Barvas, Isle of Lewis, with 64.1%). In addition, no civil parish on mainland Scotland has a proportion of Gaelic speakers greater than 20% (the highest value is in Ardnamurchan, Highland (council area), with 19.3%). Out of a total of 871 civil parishes in Scotland, the proportion of Gaelic speakers exceeds 50% in 7 parishes, exceeds 25% in 14 parishes, and exceeds 10% in 35 parishes. Decline in traditional areas has recently been balanced by growth in the Scottish Lowlands. Between the 2001 and 2011 censuses, the number of Gaelic speakers rose in nineteen of the countrys 32 council areas. The largest absolute gains were in Aberdeenshire (council area) (+526), North Lanarkshire (+305), City of Aberdeen (+216), and East Ayrshire (+208). The largest relative gains were in Aberdeenshire (+0.19%), East Ayrshire (+0.18%), Moray (+0.16%), and Orkney Islands (+0.13%). 
 Question: Which area has a greater percentage of people that speak Gaelic, Barvas or Ardnamurchan?
Output: barvas
Context: Teenage Catgirls in Heat (originally titled Catgirls) is a 1993 comedy film co-written and directed by Scott Perry and distributed by Troma Entertainment. 
 Question: What studio produced Teenage Catgirls in Heat?
Output: troma entertainment
Context: This article needs an improved plot summary. (November 2015) Sidhu (Akshay Kumar) is a lowly vegetable cutter at a roadside food stall in the Chandni Chowk section of Delhi, who consults astrologers, tarot card readers, and fake fakirs despite his foster father Dada's (Mithun Chakraborty) exhortations. When two strangers from China claim him as a reincarnation of war hero 'Liu Shen' and take him to China, Sidhu, encouraged by trickster Chopstick (Ranvir Shorey), believes he will be feted as a hero, unaware of his own recruitment to assassinate the smuggler Hojo (Gordon Liu). Sidhu travels to China with Chopstick. Along the way he meets Sakhi (Deepika Padukone), the Indian-Chinese spokesmodel known as Ms. Tele Shoppers Media, or Ms. TSM, who also appears in China. Her twin sister Suzy, known as the femme fatale Meow Meow, works for Hojo, not knowing Hojo tried to kill her father, Inspector Chiang (Roger Yuan). Sidhu, through a series of accidents, initially eludes Hojo, but Hojo eventually exposes him as a fraud. Thereupon Hojo kills Dada, and Sidhu is beaten and urinated on by Hojo. Injured and disgraced Sidhu vows revenge. He thereafter encounters an amnesiac vagrant, whom he later identifies to Sakhi as Inspector Chiang. Chiang later recovers his memory and trains Sidhu in kung fu. When Hojo again meets with Sidhu, Suzy injures Chiang; but upon seeing Sakhi, betrays Hojo. Sidhu fights Hojo in single combat, eventually using a modified vegetable-cutting technique to overwhelm him. In the aftermath, Sidhu opens a vegetable stall in China, but is recruited to fight for some African pygmies. The film thereupon concludes with the announcement "To be Continued Chandni Chowk to Africa". 
 Question: What is the vicious smugglers name?
Output: hojo
Context: The Seattle Seahawks kicked off their 2013 campaign with a hard-fought, ugly win over the Carolina Panthers, 12-7. This game marked Russell Wilson's first 300-yard passing game, and Cam Newton's worst career performance, posting 125 yards through the air, a career low. The first quarter ended equal for both teams, as both sides exchanged a couple of punts. Seattle took their third drive of the game in the second quarter, and drove into the red zone, capping it with a Steven Hauschka 27-yard field goal. Carolina responded immediately, and taking advantage of a couple of Seattle penalties, and some big runs by DeAngelo Williams, with Cam Newton hitting Steve Smith for a 3-yard TD. Seattle responded with a drive to around the Carolina 27 yard line, but Charles Godfrey sacked Russell Wilson and stripped the football, which Carolina recovered. So the first half ended 7-3, Carolina. The second half began with a defensive battle between both sides. Seattle then broke the deadlock with a Steven Hauschka 40-yard field goal, on a drive that lasted over 4 minutes, cutting the lead to 7-6. After forcing Carolina to punt midway through the fourth quarter, Seattle's offense produced its finest drive of the day. A couple of Russell Wilson passes, followed by a Robert Turbin 15-yard scamper, set up Seattle at the Panthers' 43 yard line. Russell Wilson overthrew receiver Stephen Williams on first down, but on second down and 10, by using exactly the same play, Wilson connected with second-year man Jermaine Kearse for a 43-yard score, with 10 minutes left to play. They failed the two-point conversion however, so Seattle had a 12-7 lead. Carolina responded by using DeAngelo Williams on some big runs. Inside the Seattle 35 yard line, Williams took off for a 24-yard scamper, and looked like he was going to score, however at the last possible moment, Earl Thomas forced Williams to fumble inside the 10 yard line. 
 Question: Who threw for more yards, Wilson or Newton?
Output: wilson