niryuu/sni-each-converted huggingface dataset:
Context: Brink (Sir Cedric Hardwicke) has recently taken Pud's (Bobs Watson) parents in an auto wreck. Brink later comes for Gramps (Lionel Barrymore). Believing Brink to be an ordinary stranger, the crotchety old Gramps orders Mr. Brink off the property. Pud comes out of the house and asks who the stranger was. Gramps is surprised and relieved that someone else could see the stranger; he was not merely a dream or apparition. Pud tells Gramps that when he does a good deed, he will be able to make a wish. Because his apples are constantly being stolen, Gramps wishes that anyone who climbs up his apple tree will have to stay there until he permits them to climb down. Pud inadvertently tests the wish when he has trouble coming down from the tree himself, becoming free only when Gramps says he can. Pud's busybody Aunt Demetria (Eily Malyon) has designs on Pud and the money left him by his parents. Gramps spends much time fending off her efforts to adopt the boy. Brink takes Granny Nellie (Beulah Bondi) in a peaceful death just after she finishes a bit of knitting. When Mr. Brink returns again for Gramps, the old man finally realizes who his visitor is. Determined not to leave Pud to Demetria, Gramps tricks Mr. Brink into climbing the apple tree. While stuck in the tree, he cannot take Gramps or anyone else. The only way anyone or anything can die is if they touch Mr. Brink or the apple tree. Demetria plots to have Gramps committed to a psychiatric hospital when he claims that Death is trapped in his apple tree. Gramps proves his story first by proving that his doctor, Dr. Evans (Henry Travers), can not even kill a fly they have captured. He offers further proof of his power by shooting Mr. Grimes (Nat Pendleton), the orderly who has come to take him to the asylum; Grimes lives when he should have died. Dr. Evans is now a believer, but he tries to convince Gramps to let Death down so people who are suffering can find release. Gramps refuses, so the doctor arranges for the local sheriff to commit Gramps while Pud is delivered to Demetria's custody. With the help of his housekeeper (Una Merkel), Gramps tricks both of them into believing they are scheduled to go with Mr. Brink when he comes down from the tree. They beg Gramps to convince Brink otherwise, and Demetria vows never to bother Gramps or Pud again. Gramps realizes that sooner or later he will have to let Brinks downDeath is an ultimately unavoidable part of life. He tries to say goodbye to Pud, who reacts angrily and tries to run away. Mr. Brink sees Pud in the yard and dares him to climb the tree. Pud gets over the fence Gramps has had built around the tree, but falls and is crippled for life. Distraught, Gramps lets Death down from the tree. He takes both Gramps and Pud, who find they can walk again. In the final scene, they walk together up a beautiful country lane and hear Granny Nellie calling to them from beyond a brilliant light. 
 Question: What was blocking Pud's way?
Output: fence
Context: Brink (Sir Cedric Hardwicke) has recently taken Pud's (Bobs Watson) parents in an auto wreck. Brink later comes for Gramps (Lionel Barrymore). Believing Brink to be an ordinary stranger, the crotchety old Gramps orders Mr. Brink off the property. Pud comes out of the house and asks who the stranger was. Gramps is surprised and relieved that someone else could see the stranger; he was not merely a dream or apparition. Pud tells Gramps that when he does a good deed, he will be able to make a wish. Because his apples are constantly being stolen, Gramps wishes that anyone who climbs up his apple tree will have to stay there until he permits them to climb down. Pud inadvertently tests the wish when he has trouble coming down from the tree himself, becoming free only when Gramps says he can. Pud's busybody Aunt Demetria (Eily Malyon) has designs on Pud and the money left him by his parents. Gramps spends much time fending off her efforts to adopt the boy. Brink takes Granny Nellie (Beulah Bondi) in a peaceful death just after she finishes a bit of knitting. When Mr. Brink returns again for Gramps, the old man finally realizes who his visitor is. Determined not to leave Pud to Demetria, Gramps tricks Mr. Brink into climbing the apple tree. While stuck in the tree, he cannot take Gramps or anyone else. The only way anyone or anything can die is if they touch Mr. Brink or the apple tree. Demetria plots to have Gramps committed to a psychiatric hospital when he claims that Death is trapped in his apple tree. Gramps proves his story first by proving that his doctor, Dr. Evans (Henry Travers), can not even kill a fly they have captured. He offers further proof of his power by shooting Mr. Grimes (Nat Pendleton), the orderly who has come to take him to the asylum; Grimes lives when he should have died. Dr. Evans is now a believer, but he tries to convince Gramps to let Death down so people who are suffering can find release. Gramps refuses, so the doctor arranges for the local sheriff to commit Gramps while Pud is delivered to Demetria's custody. With the help of his housekeeper (Una Merkel), Gramps tricks both of them into believing they are scheduled to go with Mr. Brink when he comes down from the tree. They beg Gramps to convince Brink otherwise, and Demetria vows never to bother Gramps or Pud again. Gramps realizes that sooner or later he will have to let Brinks downDeath is an ultimately unavoidable part of life. He tries to say goodbye to Pud, who reacts angrily and tries to run away. Mr. Brink sees Pud in the yard and dares him to climb the tree. Pud gets over the fence Gramps has had built around the tree, but falls and is crippled for life. Distraught, Gramps lets Death down from the tree. He takes both Gramps and Pud, who find they can walk again. In the final scene, they walk together up a beautiful country lane and hear Granny Nellie calling to them from beyond a brilliant light. 
 Question: What was blocking Pud's way?
Output: a fence
Context: -Synuclein is the major protein component of Lewy bodies--the pathological hallmark of Parkinson's disease (PD) and Dementia with Lewy bodies (DLB). Its accumulation into intracellular aggregates is implicated in the process of Lewy body formation. However, its roles in both normal function, and disease, remain controversial. Using a novel model of chronic oxidative stress in cultured dopaminergic and cortical neurons, we report that endogenous -synuclein is upregulated in response to low dose toxicity. This response is conserved between subpopulations of cortical and dopaminergic neurons, and confers relative resistance to apoptosis following secondary insult. Additional acute oxidative stress leads to intracellular accumulation of -synuclein. These punctate deposits colocalize with ubiquitin, which is central to proteosome-mediated protein degeneration, and is the second major component of Lewy bodies. The current results imply that differential levels of -synuclein expression may influence neuronal vulnerability in chronic neurodegenerative diseases. They further support a 'two hit' hypothesis for Lewy body formation, whereby mild stress causes a protective upregulation of -synuclein. However, such increased levels of -synuclein may drive its accumulation, following additional toxic insult. Finally, these results support a common mechanism for degeneration of dopaminergic and cortical neurons, affected in PD, and DLB, respectively. 
 Question: Which is the primary protein component of Lewy bodies?
Output: αsyn
Context: -Synuclein is the major protein component of Lewy bodies--the pathological hallmark of Parkinson's disease (PD) and Dementia with Lewy bodies (DLB). Its accumulation into intracellular aggregates is implicated in the process of Lewy body formation. However, its roles in both normal function, and disease, remain controversial. Using a novel model of chronic oxidative stress in cultured dopaminergic and cortical neurons, we report that endogenous -synuclein is upregulated in response to low dose toxicity. This response is conserved between subpopulations of cortical and dopaminergic neurons, and confers relative resistance to apoptosis following secondary insult. Additional acute oxidative stress leads to intracellular accumulation of -synuclein. These punctate deposits colocalize with ubiquitin, which is central to proteosome-mediated protein degeneration, and is the second major component of Lewy bodies. The current results imply that differential levels of -synuclein expression may influence neuronal vulnerability in chronic neurodegenerative diseases. They further support a 'two hit' hypothesis for Lewy body formation, whereby mild stress causes a protective upregulation of -synuclein. However, such increased levels of -synuclein may drive its accumulation, following additional toxic insult. Finally, these results support a common mechanism for degeneration of dopaminergic and cortical neurons, affected in PD, and DLB, respectively. 
 Question: Which is the primary protein component of Lewy bodies?
Output: α-synuclein
Context: -Synuclein is the major protein component of Lewy bodies--the pathological hallmark of Parkinson's disease (PD) and Dementia with Lewy bodies (DLB). Its accumulation into intracellular aggregates is implicated in the process of Lewy body formation. However, its roles in both normal function, and disease, remain controversial. Using a novel model of chronic oxidative stress in cultured dopaminergic and cortical neurons, we report that endogenous -synuclein is upregulated in response to low dose toxicity. This response is conserved between subpopulations of cortical and dopaminergic neurons, and confers relative resistance to apoptosis following secondary insult. Additional acute oxidative stress leads to intracellular accumulation of -synuclein. These punctate deposits colocalize with ubiquitin, which is central to proteosome-mediated protein degeneration, and is the second major component of Lewy bodies. The current results imply that differential levels of -synuclein expression may influence neuronal vulnerability in chronic neurodegenerative diseases. They further support a 'two hit' hypothesis for Lewy body formation, whereby mild stress causes a protective upregulation of -synuclein. However, such increased levels of -synuclein may drive its accumulation, following additional toxic insult. Finally, these results support a common mechanism for degeneration of dopaminergic and cortical neurons, affected in PD, and DLB, respectively. 
 Question: Which is the primary protein component of Lewy bodies?
Output: alpha-synuclein
Context: The authors describe a family with six patients with muscular dystrophy with a variable course. One is a compound heterozygote for CAPN3 mutations (calpainopathy) and the others have a single CAPN3 mutation. Linkage analysis and sequencing revealed a XK gene mutation (McLeod syndrome). This illustrates the variable phenotype of XK mutations and suggests the possibility that CAPN3 heterozygotes may have their condition caused by nonallelic mutations in other unrelated genes. 
 Question: Mutation of which gene is associated with McLeod syndrome?
Output: xk
Context: Chettinad Palace in Karaikudi seen in the film. Natesan (Cheran) works as an engineer in electricity board in Karaikudi and leads a joint family with more 30 of his relatives living in the same house. On the other hand, Visalakshi aka Sala (Sneha) is the only daughter to her parents and she is about to complete her college education in Karaikudi. Sala feels bored while being alone and she always prefers to have her friends surrounding her. Sala's parents start searching for a groom and they get a reference for Natesan. Sala and her family meet Natesan's family in a function. Sala is surprised to see so many people living as a joint family together and she is very much impressed and agrees for the wedding. Natesan and Sala get married. Sala loves being accompanied by all the relatives in Natesan's home. When Sala and Natesan go on a honeymoon, Sala purchases gifts for everyone in the family. All the family members are also impressed seeing Sala. But Natesan feels sad that he does not get private time to spend with his wife as they are always surrounded by relatives. Now Natesan gets transferred to a hill station named Attakatti, near Pollachi. Natesan feels happy as he believes this will provide him time to spend with Sala. Although Sala feels sad leaving all her relatives, she also goes with Natesan to the hill station. Over there in the hill station, Sala feels lonely and gets bored and she longs for the life she had in Karaikudi. Their house is located in a remote place with no neighbours and friends. Natesan also gets busy with work and has very little time to spend with his wife. Slowly Sala gets psychologically disturbed due to loneliness and she behaves as if the house is filled with so many people. Also, she repairs the fan, lights etc. purposefully in their home so that the nearby electrician (Kanja Karuppu) comes to fix them and at least she gets a chance to speak to someone. She also starts recording all the sounds around her such as birds chirping, etc. and listens to the recordings when alone. One day, she records a neighbour's child's laughter sound following which the child faints. Sala is scared but the child is saved. Doctor Ramalingam (Jayaram) sees Sala and understands that she is suffering from a disorder and warns Natesan. But Natesan does not take it seriously. One day Sala consumes too much of sleeping pills to come out of her depression. But Natesan spots her lying in bed and rushes her to the hospital. Sala is saved. Ramalingam explains the disorder to Natesan and mentions that the best cure for her would be to lead a happy life surrounded by relatives. Natesan agrees and moves back to Karaikudi. The movie ends showing Natesan and Sala leading a happy life again. 
 Question: After moving out with her husband, Sala slowly becomes what?
Output: psychologically disturbed due to loneliness
Context: Juvenile neuronal ceroid-lipofuscinosis (JNCL) or Batten/Spielmeyer-Vogt-Sjogren disease (OMIM #204200) is one of a group of nine clinically related inherited neurodegenerative disorders (CLN1-9). JNCL results from mutations in CLN3 on chromosome 16p12.1. The neuronal loss in Batten disease has been shown to be due to a combination of apoptosis and autophagy suggesting that CLN3P, the defective protein, may have an anti-neuronal death function. PANDER (PANcreatic-DERived factor) is a novel cytokine that was recently cloned from pancreatic islet cells. PANDER is specifically expressed in the pancreatic islets, small intestine, testis, prostate, and neurons of the central nervous system, and has been demonstrated to induce apoptosis. In this study, we over-expressed CLN3P in SH-SY5Y neuroblastoma cells and monitored the effects on PANDER-induced apoptosis. CLN3P significantly increased the survival rate of the SH-SY5Y cells in this system. This study provides additional evidence that the function of CLN3P is related to preventing neuronal apoptosis. 
 Question: What is the effect of a defective CLN3 gene?
Output: jncl
Context: Juvenile neuronal ceroid-lipofuscinosis (JNCL) or Batten/Spielmeyer-Vogt-Sjogren disease (OMIM #204200) is one of a group of nine clinically related inherited neurodegenerative disorders (CLN1-9). JNCL results from mutations in CLN3 on chromosome 16p12.1. The neuronal loss in Batten disease has been shown to be due to a combination of apoptosis and autophagy suggesting that CLN3P, the defective protein, may have an anti-neuronal death function. PANDER (PANcreatic-DERived factor) is a novel cytokine that was recently cloned from pancreatic islet cells. PANDER is specifically expressed in the pancreatic islets, small intestine, testis, prostate, and neurons of the central nervous system, and has been demonstrated to induce apoptosis. In this study, we over-expressed CLN3P in SH-SY5Y neuroblastoma cells and monitored the effects on PANDER-induced apoptosis. CLN3P significantly increased the survival rate of the SH-SY5Y cells in this system. This study provides additional evidence that the function of CLN3P is related to preventing neuronal apoptosis. 
 Question: What is the effect of a defective CLN3 gene?
Output: batten disease
Context: Juvenile neuronal ceroid-lipofuscinosis (JNCL) or Batten/Spielmeyer-Vogt-Sjogren disease (OMIM #204200) is one of a group of nine clinically related inherited neurodegenerative disorders (CLN1-9). JNCL results from mutations in CLN3 on chromosome 16p12.1. The neuronal loss in Batten disease has been shown to be due to a combination of apoptosis and autophagy suggesting that CLN3P, the defective protein, may have an anti-neuronal death function. PANDER (PANcreatic-DERived factor) is a novel cytokine that was recently cloned from pancreatic islet cells. PANDER is specifically expressed in the pancreatic islets, small intestine, testis, prostate, and neurons of the central nervous system, and has been demonstrated to induce apoptosis. In this study, we over-expressed CLN3P in SH-SY5Y neuroblastoma cells and monitored the effects on PANDER-induced apoptosis. CLN3P significantly increased the survival rate of the SH-SY5Y cells in this system. This study provides additional evidence that the function of CLN3P is related to preventing neuronal apoptosis. 
 Question: What is the effect of a defective CLN3 gene?
Output: juvenile-onset neuronal ceroid lipofuscinosis
Context: The China Davis Cup team represents the People's Republic of China in Davis Cup tennis competition and are governed by the Chinese Tennis Association. 
 Question: Which sport has connection with China Davis Cup team?
Output: tennis
Context: In the fictional Forgotten Realms campaign setting of the Dungeons & Dragons fantasy role-playing game, Shou Lung is a country in the continent of Kara-Tur, which is located to the east of Faerun. 
 Question: With which fictional universe is the character Shou Lung associated?
Output: forgotten realms
Context: The 1933 Imperial Airways Ruysselede crash occurred on 30 December 1933 when an Imperial Airways Avro Ten collided with a radio mast at Ruysselede, West Flanders, Belgium and crashed killing all ten people on board. 
 Question: When did 1933 Imperial Airways Ruysselede crash occur?
Output: 30 december 1933
Context: Pamela Drury is single and works as a serious journalist. She spends her birthday alone and becomes lonely and reflects upon her life and the choices she made and secretly wishes she had gotten married and had children. In a box of photos of old boyfriends, she reflects upon why she broke up with one in particular, Robert Dickson, 13 years earlier. She also meets an interesting man, Ben and follows him home, only to see through his window that he is with his family and looks very happy. Shortly afterwards, she is hit by a car while crossing the street. The woman who was driving the car is also Pamela, but is Pamela Dickson; she is from an alternate universe in which she married Robert 13 years earlier. Pamela Dickson takes Pamela Drury to the Dickson family home and the two of them talk in the kitchen. Suddenly, Pamela Dickson's kids come home and she disappears, leaving the unmarried Pamela Drury in a house she has never seen before with three children she does not know. The children assume she is their mother, although they do not quite recognize her sometimes. She soon finds out that her alternate version Pamela Dickson lives in a dull marriage and writes lightweight fluff articles for a mainstream ladies magazine, rather than being the serious reporter that Drury is. She meets Ben again, but in this time-line he was never married and still mourns the loss of the great love of his life, who was killed just before their graduation from college. At first, Pamela Drury was pleased to be with Robert again after all these years apart, but she is soon unhappy and annoyed with married life, and quarrels with Robert. She embarks on an affair with Ben, not mentioning to him that she has a husband and kids (because she still doesn't think of herself as married or a mother). Ben visits her and learns the truth, and walks away angry and disappointed. Soon, Pamela Drury embraces having a family and falls for Robert again, and even stimulates him and enlivens her marriage. Then when Pamela Drury is in a restaurant bathroom, Pamela Dickson shows up again, and the two women switch back to their former lives. Pamela Dickson had been living the life of single Pamela Drury and enjoyed it but ultimately missed her husband and kids so she came back. Pamela Drury is single once more and embraces her life with a new appreciation of all that being single and having a career has to offer. She learns that while she was gone, Pamela Dickson began dating Ben, who actually is divorced from the woman she saw through the window, the same woman who alternate-Ben had thought was his soul mate. Ultimately she sees that both lives are appealing and offer a lot to appreciate. 
 Question: Who is Pamela married to in another life?
Output: robert
Context: Jacques Nicolas Bellavene (20 October 1770, in Verdun -- 8 February 1826, in Milly) was a French general. 
 Question: Which was the nationality of Jacques Nicolas Bellavene?
Output: french
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: Which group from the census is larger: white or African American?
Output: white
Context: Progress M-3 was launched at 23:10:57 GMT on 28 February 1990, atop a Soyuz-U2 carrier rocket flying from Site 1/5 at the Baikonur Cosmodrome. 
 Question: What day was Progress M-3 launched?
Output: 28 february 1990
Context: Sailing Through History A group of 1,309 passengers boarded the MSBalmoralon Sunday, in Southampton, England, on a voyage to retrace the path of theTitanic. TheTitanicwas the biggest ship in the world when it sailed on its ill-fated maiden voyage in 1912. Of the 2,227 passengers and crew aboard, more than 1,500 died. The ship, which was headed to New York City, carried the rich and famous on its first voyage. It also carried immigrants, who were seeking a better life in America. Relatives of people who sailed on theTitanic, historians, authors and people fascinated by the story of the unsinkable ship, are on theBalmoral. They want to remember the doomed ship and those who died on her first and last voyage. The historic liner had set sail on April 10, 1912, from Southampton. Late at night on April 14, she hit an iceberg. In the early morning hours of April 15, theTitanicsank. TheBalmoralis followingTitanic's original route from Southampton. First, the modern-day cruise liner docked in the port of Cherbourg, France, where theTitanichad picked up more passengers. On Monday afternoon, theBalmoralstops in Cobh, Ireland, theTitanic's last port of call before sailing to New York. Balmoralwill then cruise the North Atlantic Ocean to the location whereTitanichit an iceberg that ripped the ship's hull . On Sunday, April 15, at 2:20 a.m.--the time theTitanicwent down--passengers and crew will hold a memorial service. The next two days will be spent in Halifax, Canada, where many victims of the sinking are buried. Then, theBalmoralwill reach its final destination in New York City, whereTitanicwas supposed to dock--but never did. Until today, several teams of divers have explored the site. They have recovered some items such as dishes and silverware and put them on public display. And more trips are planned to the wreckage in the future. TheTitanicand its passengers and crew have been remembered in books, movies and TV programs. But there's a much more important contribution thatTitanicgave us. After she sank, lawmakers and shipbuilders made ships safer. It took a terrible tragedy to make ship travel safer for all. 
 Question: How many countries does the Balmoral reach before sailing to New York?
Output: two.
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: stuck together by minerals that fill in spaces between sediments
Output: cemented
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: Which type of feature may form in open spaces inside rocks?
Output: geode
Context: Trying to snap a four-game losing skid, the Panthers went home for a Week 12 NFC South rematch with the New Orleans Saints. In the first quarter, Carolina got the early lead as kicker John Kasay managed to get a 45-yard field goal for the only score of the period. In the second quarter, the Saints took the lead as QB Drew Brees completed a 1-yard TD pass to WR Lance Moore, along with kicker Olindo Mare getting a 46-yard field goal. The Panthers would end the half as Kasay nailed a 29-yard field goal. In the third quarter, New Orleans pulled away with Brees completing a 1-yard TD pass to TE Billy Miller, getting an 8-yard TD run, and completing a 4-yard TD pass to WR Marques Colston. With their fifth straight loss, not only did Carolina fall to 4-7, but they had also lost seven straight home games (they have yet to win a home game this year). Also, the Panthers offense only managed to get 4 touchdowns in the last five games. 
 Question: Which player scored the second longest field goal?
Output: john kasay
Context: Coming off their road win over the Steelers, the Colts went home for a Week 11 AFC South rematch with the Houston Texans. In the first quarter, Indianapolis trailed early as Texans kicker Kris Brown got a 28-yard field goal. The Colts responded with kicker Adam Vinatieri getting a 40-yard field goal. Houston would answer with Brown making a 34-yard field goal. In the second quarter, Indy tied the game as Vinatieri got a 39-yard field goal. The Texans retook the lead as RB Ahman Green got a 1-yard TD run. Indianapolis closed out the half as Vinatieri made a 32-yard field goal. In the third quarter, the Colts took the lead as QB Peyton Manning completed a 23-yard TD pass to RB Joseph Addai. Houston would reply as RB Steve Slaton got a 71-yard TD run, yet Indy regained the lead as Addai got a 7-yard TD run. In the fourth quarter, the Texans tried to come back as Green got a 2-yard field goal, yet Indianapolis pulled away with Vinatieri nailing a 31-yard field goal. On the Texans' final drive, QB Sage Rosenfels was intercepted by safety Melvin Bullitt (who was filling in again for the injured Bob Sanders). Ironically, it was Bullitt who picked off Rosenfels on the Texans' final drive when they played the Colts in Week 5. Manning then took a knee, preserving the Colts' third consecutive victory. 
 Question: Which player kicked the longest field goal?
Output: adam vinatieri
Context: Marino finished the game with 29 out of 50 pass completions for 318 yards, 1 touchdown, and 2 interceptions. Clayton was the top receiver of the game, with 6 receptions for 92 yards. Walker returned 4 kickoffs for 93 yards and gained 15 yards on 2 punt returns. Nathan was the Dolphins leading rusher with 18 yards, while also catching 10 passes for 83 yards. Craig had 58 rushing yards, 77 receiving yards, and 3 touchdowns. He was the first player ever to score 3 touchdowns in a Super Bowl, and his 2 touchdown catches also tied a Super Bowl record. Tyler led San Francisco in rushing with 65 yards, and also caught 4 passes for 70 yards. Clark caught 6 passes for 77 yards. Board recorded 2 sacks. McLemore recorded 51 punt return yards, the second most in Super Bowl history. Sports Illustrated called 49ers defensive tackle Gary Johnson (American football) the Super Bowls "unofficial defensive MVP" after he recorded one sack, flushed Marino out of the passing pocket numerous times, and had four unassisted tackles. 
 Question: Who had more sacks Board or Johnson?
Output: board
Context: In 1908 the U.S. Supreme Court decided Loewe v. Lawlor . In 1902 the Hatters' Union instituted a nationwide boycott of the hats made by a nonunion company in Connecticut. Owner Dietrich Loewe brought suit against the union for unlawful combinations to restrain trade in violation of the Sherman Antitrust Act. The Court ruled that the union was subject to an injunction and liable for the payment of triple damages. In 1915 Justice Oliver Wendell Holmes, speaking for the Court, again decided in favor of Loewe, upholding a lower federal court ruling ordering the union to pay damages of $252,130. . This was not a typical case in which a few union leaders were punished with short terms in jail; specifically, the life savings of several hundreds of the members were attached. The lower court ruling established a major precedent, and became a serious issue for the unions. The Clayton Act of 1914 presumably exempted unions from the antitrust prohibition and established for the first time the Congressional principle that "the labor of a human being is not a commodity or article of commerce". However, judicial interpretation so weakened it that prosecutions of labor under the antitrust acts continued until the enactment of the Norris-La Guardia Act in 1932. 
 Question: Who won the 1908 Supreme Court case Loewe v. Lawlor?
Output: loewe
Context: V849 Ophiuchi or Nova Ophiuchi 1919 was a nova that lit up in 1919 in the constellation Ophiuchus and reached a brightness of 7.4 mag. 
 Question: What constellation is V849 Ophiuchi a part of?
Output: ophiuchus
Context: This Burning Effigy were an Irish gothic rock/ethereal wave band, originally formed in Dublin in 1993, and consisting of members Stephen Carey (guitar and keyboards), Ger Egan (vocals), Micheal Cowley (bass), Brian Fallon (drums). 
 Question: What was the name of the city or state where This Burning Effigy was formed?
Output: dublin
Context: Hatra defeated the Iranians at the battle of Shahrazoor in 238, but fell to the Iranian Sassanid Empire of Shapur I in 241 and was destroyed. 
 Question: When was Hatra abolished?
Output: 241
Context: Bruce Gradkowski came into the game as Oakland's starter at Quarterback, trying to cap on his gamewinning performance last week vs. St. Louis Arizona started the game with a 102-yard kickoff return from LaRod Stephens-Howling. The Raiders answered quickly though when Gradkowski completed a 22-yard pass to tight-end Zach Miller. This was followed by three field goals, two for Oakland, one for Arizona, and Oakland led 13-10 at the end of the first quarter. Both Gradkowski and Derek Anderson then traded touchdowns and the Raiders led 20-17 at the half. Anderson helped Arizona take the lead late in the third quarter with an 8-yard touchdown pass to Larry Fitzgerald. Arizona led 24-20 at the end of the third quarter. Sebastian Janikowski made the lead 24-23 with another field goal in the fourth quarter. Arizona held on for the win after Janikowski missed a 32-yard field goal as time expired. Both the Raiders and Cardinals committed numerous mistakes, including two muffed punts by Arizona. Oakland committed 11 penalties for 123yards, Arizona seven for 104. 
 Question: Who team did Oakland beat the week prior to this game?
Output: st. louis
Context: Facioscapulohumeral dystrophy (FSHD) is characterized by chromatin relaxation of the D4Z4 macrosatellite array on chromosome 4 and expression of the D4Z4-encoded DUX4 gene in skeletal muscle. The more common form, autosomal dominant FSHD1, is caused by contraction of the D4Z4 array, whereas the genetic determinants and inheritance of D4Z4 array contraction-independent FSHD2 are unclear. Here, we show that mutations in SMCHD1 (encoding structural maintenance of chromosomes flexible hinge domain containing 1) on chromosome 18 reduce SMCHD1 protein levels and segregate with genome-wide D4Z4 CpG hypomethylation in human kindreds. FSHD2 occurs in individuals who inherited both the SMCHD1 mutation and a normal-sized D4Z4 array on a chromosome 4 haplotype permissive for DUX4 expression. Reducing SMCHD1 levels in skeletal muscle results in D4Z4 contraction-independent DUX4 expression. Our study identifies SMCHD1 as an epigenetic modifier of the D4Z4 metastable epiallele and as a causal genetic determinant of FSHD2 and possibly other human diseases subject to epigenetic regulation. 
 Question: Which disease is associated with the ectopic expression of the protein encoded by the gene DUX4?
Output: fshd
Context: Facioscapulohumeral dystrophy (FSHD) is characterized by chromatin relaxation of the D4Z4 macrosatellite array on chromosome 4 and expression of the D4Z4-encoded DUX4 gene in skeletal muscle. The more common form, autosomal dominant FSHD1, is caused by contraction of the D4Z4 array, whereas the genetic determinants and inheritance of D4Z4 array contraction-independent FSHD2 are unclear. Here, we show that mutations in SMCHD1 (encoding structural maintenance of chromosomes flexible hinge domain containing 1) on chromosome 18 reduce SMCHD1 protein levels and segregate with genome-wide D4Z4 CpG hypomethylation in human kindreds. FSHD2 occurs in individuals who inherited both the SMCHD1 mutation and a normal-sized D4Z4 array on a chromosome 4 haplotype permissive for DUX4 expression. Reducing SMCHD1 levels in skeletal muscle results in D4Z4 contraction-independent DUX4 expression. Our study identifies SMCHD1 as an epigenetic modifier of the D4Z4 metastable epiallele and as a causal genetic determinant of FSHD2 and possibly other human diseases subject to epigenetic regulation. 
 Question: Which disease is associated with the ectopic expression of the protein encoded by the gene DUX4?
Output: facioscapulohumeral dystrophy
Context: In 1908 the U.S. Supreme Court decided Loewe v. Lawlor . In 1902 the Hatters' Union instituted a nationwide boycott of the hats made by a nonunion company in Connecticut. Owner Dietrich Loewe brought suit against the union for unlawful combinations to restrain trade in violation of the Sherman Antitrust Act. The Court ruled that the union was subject to an injunction and liable for the payment of triple damages. In 1915 Justice Oliver Wendell Holmes, speaking for the Court, again decided in favor of Loewe, upholding a lower federal court ruling ordering the union to pay damages of $252,130. . This was not a typical case in which a few union leaders were punished with short terms in jail; specifically, the life savings of several hundreds of the members were attached. The lower court ruling established a major precedent, and became a serious issue for the unions. The Clayton Act of 1914 presumably exempted unions from the antitrust prohibition and established for the first time the Congressional principle that "the labor of a human being is not a commodity or article of commerce". However, judicial interpretation so weakened it that prosecutions of labor under the antitrust acts continued until the enactment of the Norris-La Guardia Act in 1932. 
 Question: What did Lawlor do?
Output: nationwide boycott
Context: 1. In order to investigate the biological function of the human CLN3 gene that is defective in Batten disease, we created a yeast strain by PCR-targeted disruption of the yeast gene (YHC3), which is a homologue of the human CLN3 gene. 2. The phenotypic characterization revealed that the yhc3 delta mutants are more sensitive to combined heat and alkaline stress than the wild-type strains as determined by inhibition of cell proliferation. 3. This suggests that the yhc3 delta mutant is a good model to investigate the biological function of human CLN3 gene in mammalian cells and to understand the pathophysiology of juvenile Batten disease. 
 Question: What is the effect of a defective CLN3 gene?
Output: jncl
Context: 1. In order to investigate the biological function of the human CLN3 gene that is defective in Batten disease, we created a yeast strain by PCR-targeted disruption of the yeast gene (YHC3), which is a homologue of the human CLN3 gene. 2. The phenotypic characterization revealed that the yhc3 delta mutants are more sensitive to combined heat and alkaline stress than the wild-type strains as determined by inhibition of cell proliferation. 3. This suggests that the yhc3 delta mutant is a good model to investigate the biological function of human CLN3 gene in mammalian cells and to understand the pathophysiology of juvenile Batten disease. 
 Question: What is the effect of a defective CLN3 gene?
Output: batten disease
Context: 1. In order to investigate the biological function of the human CLN3 gene that is defective in Batten disease, we created a yeast strain by PCR-targeted disruption of the yeast gene (YHC3), which is a homologue of the human CLN3 gene. 2. The phenotypic characterization revealed that the yhc3 delta mutants are more sensitive to combined heat and alkaline stress than the wild-type strains as determined by inhibition of cell proliferation. 3. This suggests that the yhc3 delta mutant is a good model to investigate the biological function of human CLN3 gene in mammalian cells and to understand the pathophysiology of juvenile Batten disease. 
 Question: What is the effect of a defective CLN3 gene?
Output: juvenile-onset neuronal ceroid lipofuscinosis
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: Which team scored more touchdowns?
Output: seattle seahawks
Context: In cancer research, background models for mutation rates have been extensively calibrated in coding regions, leading to the identification of many driver genes, recurrently mutated more than expected. Noncoding regions are also associated with disease; however, background models for them have not been investigated in as much detail. This is partially due to limited noncoding functional annotation. Also, great mutation heterogeneity and potential correlations between neighboring sites give rise to substantial overdispersion in mutation count, resulting in problematic background rate estimation. Here, we address these issues with a new computational framework called LARVA. It integrates variants with a comprehensive set of noncoding functional elements, modeling the mutation counts of the elements with a -binomial distribution to handle overdispersion. LARVA, moreover, uses regional genomic features such as replication timing to better estimate local mutation rates and mutational hotspots. We demonstrate LARVA's effectiveness on 760 whole-genome tumor sequences, showing that it identifies well-known noncoding drivers, such as mutations in the TERT promoter. Furthermore, LARVA highlights several novel highly mutated regulatory sites that could potentially be noncoding drivers. We make LARVA available as a software tool and release our highly mutated annotations as an online resource (larva.gersteinlab.org). 
 Question: Which tool is used for the identification of recurrent variants in noncoding regions?
Output: larva
Context: Miami trailed 10-0 with just over four minutes remaining, but touchdown passes from quarterback Ryan Tannehill to Jarvis Landry and DeVante Parker put the Dolphins up by four points with 36 seconds left on the clock. The Rams' rookie quarterback Jared Goff attempted a hail mary pass to try and give the Rams the win, but the pass was incomplete, resulting in a 14-10 win for the Dolphins. With the win, the Dolphins improved to 6-4. They also improved to 11-2 all-time against the Rams. 
 Question: How many points was the total at the end of the game?
Output: resulting in a 14-10 win
Context: The Miraculous Mandarin is scored for 3 flutes (2nd and 3rd doubling piccolo), 3 oboes (3rd doubling English horn), 3 clarinets, (2nd doubling E-flat clarinet and 3rd doubling bass clarinet ), 3 bassoons (2nd and 3rd doubling contrabassoon), 4 horns (2nd and 4th doubling Wagner tuba), 3 trumpets in C, 3 trombones, bass tuba, timpani, snare drum, tenor drum, bass drum, cymbals, triangle, tam-tam, xylophone, celesta, harp, piano, organ, choir, and strings. 
 Question: On which instrument(s) was The Miraculous Mandarin created to be played on?
Output: organ