niryuu/sni-each-converted huggingface dataset:
Context: The dark chocolate is one of the favourite food choices by many. The taste is simply irresistible , the smell is inviting and the feel of every bite is surely what you are longing for. Apart from the taste, you simply cannot resist it because it has a lot of benefits when it comes to your health. Our health is our priority when it comes to the choice of our foods. If you worry that the chocolate is bad for your health, then here is a list of the effects of dark chocolate to health especially when taken with the right amount every day. First of all , it contains a component called falconoid which acts as an antioxidant . The antioxidants fight the common signs of aging. The antioxidants are also good for the heart. Studies have shown that people who ate foods rich in antioxidants have low risk of heart diseases. In addition to the anti-aging and healthy heart benefits, the dark chocolate can also lower blood pressure and reduce bad cholesterol to as high as 10%. Lowering of blood pressure in patients of high blood level is good because it will lower the risks of stroke and certain health crisis. Low levels of blood cholesterol are also good for the heart and take away the risk of blood vessels which may harden for too much cholesterol in them. Lastly, do you know the feeling of being overjoyed after jogging? This feeling is like extreme happiness. Dark chocolates will give you the feeling of pleasure and happiness. If you are feeling that the world has turned against you, then a chocolate can be a mood lifter. It can help fight depression. Usually when we feel so bad, we would crave to eat more food. If you are looking for something to eat during your bad moments, try to take a bite from a dark chocolate and feel good somehow after it. These are commonly the effects of chocolates to health. It can benefit you especially if taken in moderate amounts. Approximately, 100 grams of chocolate or less a day is already enough according to studies. If you have taken too much, try to lessen on your other meals for the day. It is all about nutrition and taking the right amount of food in order to get the health benefits that it can provide for you. 
 Question: What do we consider most important when choosing our foods?
Output: our health.
Context: Coming off their bye week, the Jets stayed at home for a Week 10 duel with the Jacksonville Jaguars. New York would trail early in the first quarter with running back Maurice Jones-Drew's 33-yard touchdown run. The Jets would respond with kicker Jay Feely getting a 32-yard field goal, followed by rookie quarterback Mark Sanchez completing a 7-yard touchdown pass to wide receiver Jerricho Cotchery. In the second quarter, Jacksonville would take the lead as quarterback David Garrard got an 11-yard touchdown run and completed a 26-yard touchdown pass to wide receiver Mike Sims-Walker. New York would close out the half as Feely made a 37-yard field goal. After a scoreless third quarter, the Jets would regain the lead in the fourth quarter with a 40-yard field goal from Feely and a 1-yard touchdown run from running back Thomas Jones (with a failed 2-point conversion). However, the Jaguars got the last laugh as kicker Josh Scobee booted the game-winning 21-yard field goal. 
 Question: Which team scored less during the first quarter?
Output: jaguars
Context: James R. Redmond is Emeritus Professor of Zoology in the Iowa State University department of Ecology, Evolution and Organismal Biology. 
 Question: What is James R. Redmond's place of employment?
Output: iowa state university
Context: Thalaivaa (English: Leader) is a 2013 Indian Tamil action film written and directed by A. L. Vijay. 
 Question: Who was the main director of Thalaivaa?
Output: a. l. vijay
Context: Marquis Xuan of Cai () (? - 715 BC), born Ji Cuofu (), was the eleventh ruler of the State of Cai from 750 BC to 715 BC. He was the only known son of Marquis Dai of Cai (), his predecessor. 
 Question: Who fathered Marquis Xuan of Cai?
Output: marquis dai of cai
Context: Britomart Redeems Faire Amoret is an oil painting on canvas by English artist William Etty, first exhibited in 1833 and now in Tate Britain. 
 Question: What is the name of the place where Britomart Redeems Faire Amoret can be found?
Output: tate britain
Context: Parkinson's disease and dementia with Lewy bodies are very frequent neurological disorders of the elderly. Mutations in the alpha-synuclein (alphaSYN) gene cause Parkinson's disease, often associated with dementia. Neuropathologically these diseases are characterized by the presence of Lewy bodies and Lewy neurites, intraneuronal inclusions mostly composed of alphaSYN protein fibrils. Moreover, alphaSYN is phosphorylated at S129 (phospho-serine-129 [PSer129]) in neuropathological lesions. Using our (Thy1)-[A30P]alphaSYN transgenic mouse model that develops age-dependent impairment in fear conditioning behavior, we investigated PSer129 immunostaining in the brain. We found distinct staining patterns using new, sensitive monoclonal antibodies. Somal and nuclear PSer129 immunoreactivity increased with age in hippocampal and cortical areas as well as the lateral/basolateral amygdalar nuclei and was present also in young, pre-symptomatic mice, but not wild-type controls. The tendency of PSer129 immunostaining to accumulate in the nucleus was confirmed in cell culture. (Thy1)-[A30P]alphaSYN transgenic mice further developed age-dependent, specific neuritic/terminal alphaSYN pathology in the medial parts of the central amygdalar nucleus and one of its projection areas, the lateral hypothalamus. Interestingly, this type of PSer129 neuropathology was thioflavine S negative, unlike the Lewy-like neuropathology present in the brain stem of (Thy1)-[A30P]alphaSYN mice. Thus, alphaSYN becomes phosphorylated in distinct parts of the brain in this alpha-synucleinopathy mouse model, showing age-dependent increases of nuclear PSer129 in cortical brain areas and the formation of neuritic/terminal PSer129 neuropathology with variable amyloid quality within the fear conditioning circuitry and the brain stem. 
 Question: Against which protein is the antibody used for immonostaining of Lewy bodies raised?
Output: alpha-synuclein
Context: Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) is triggered by constitutively activated BCR-ABL and SRC family tyrosine kinases.They account for the activations of multiple growth-signaling pathways, including Raf/MEK/ERK, Akt/mTOR and STAT5 pathways. The BCR-ABL tyrosine kinase inhibitor imatinib is the standard treatment for Ph+ leukemia and plays efficacious role in CML. However, imatinib has few inhibitory effects on SRC tyrosine kinase with response rate of Ph+ ALL lower and relapse more frequent and quicker compared with CML. Previous studies showed that oridonin inhibits proliferation and induces apoptosis in many tumor cells. However, the anticancer activity and mechanism of oridonin in Ph+ ALL is unknown. To investigate the anticancer activity of oridonin, we examined its role in constitutively activated Akt/mTOR, Raf/MEK/ERK, STAT5 and SRC pathway, mRNA level of bcr/abl gene, cell viability and apoptosis in Ph+ ALL SUP-B15 cells. Furthermore, we detected synergetic effect of oridonin plus imatinib. Our results showed that oridonin inhibiting activations of LYN (one of SRC family kinases) and ABL and their downstream Akt/mTOR, Raf/MEK/ERK and STAT5 pathways, downregulated Bcl-2 but upregulated Bax protein and then induced apoptosis in Ph+ ALL cells. Oridonin plus imatinib exerted synergetic effects by overcoming imatinib defect of upregulating Akt/mTOR and LYN signaling. Additionally, we examined the effect of oridonin on the signaling pathways in the primary specimens from Ph+ ALL patients. Our data showed that oridonin remarkably suppressed activations of Akt/mTOR, Raf/MEK and STAT5 pathway in these primary specimens and oridonin with imatinib exerted synergetic suppressive effects on mTOR, STAT5 and LYN signaling in one imatinib resistant patient specimen. Additional evaluation of oridonin as a potential therapeutic agent for Ph+ ALL seems warranted. 
 Question: What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?
Output: bcr-abl
Context: Chikondi Banda (28 December 1979 -- 8 August 2013) was a Malawian international footballer who played as a midfielder. 
 Question: In which position does Chikondi Banda play?
Output: midfielder
Context: Ruby Hunter died of a heart attack on 17 February 2010, aged 54. 
 Question: Due to which disease did Ruby Hunter die?
Output: heart attack
Context: The Pyrgi Tablets, found in a 1964 excavation of a sanctuary of ancient Pyrgi on the Tyrrhenian coast of Italy (today the town of Santa Severa), are three golden leaves that record a dedication made around 500 BCE by Thefarie Velianas, king of Caere, to the Phoenician goddess E"Ashtaret. 
 Question: When did the discovery or creation of Pyrgi Tablets occur?
Output: 1964
Context: The police must investigate a series of robberies along a strip of land in the city. The new mayor of the city (Kenneth Mars) assigns Captain Harris (G.W. Bailey) and Lt. Proctor (Lance Kinsey) to the case, but while on stakeout the Wilson gang manages to slip through their fingers.The Mayor wants Harris and Proctor to work with Police Academy head Commandant Lassard (George Gaynes) on apprehending the gang. Lassard assembles a seven-man team consisting of Hightower (Bubba Smith), Tackleberry (David Graf), Jones (Michael Winslow), Hooks (Marion Ramsey), Callahan (Leslie Easterbrook), Fackler (Bruce Mahler), and Lassard's nephew, Nick (Matt McCoy) who transfers from Miami (in the previous film Police Acdemy 5) to the city to remain close to his friends and dull-witted uncle.After distributing flyers as to the information of the Wilson gang and getting nowhere, Nick McCoy stumbles upon a paper heading of an antique diamond heading to a museum, and gets an idea to use it as bait: however the robbers nab the diamond anyway by cutting a hole in the truck and escaping through the sewer system. McCoy then decides to go undercover to get information regarding a possible hideout, but Harris decides to go undercover to get a confession.It turns out that Harris goes undercover as a window washer at a tall building, for which he has a fear of heights, and gets a confession of himself on tape after his loyal but numb-skull lacky, Proctor, accidentally knocks him over the balcony.It is revealed here that the robberies are committed by a group of three dim-witted criminals who do not seem to be able to do this on their own, and it is revealed they are being guided by a literally shadow figure known as the "Mastermind", who speaks to the three behind a wall of glass and uses a voice distortion device. He devises a plan to get the cops out of the way.Commandant Lassard and his men are later suspended after stolen jewellery from the last robbery is planted in Lassard's locker, pending an investigation. The misfit cops decide to clear Lassard's name by nabbing the gang and the ringleader. Accessing data files from a computer, McCoy deduces that the robberies are occurring along a bus route, thus intentionally lowering property values in that part of the city. They also learn that someone must be 'leaking' information to the bad guys, which is why they are always one step ahead of the Police Academy.The Police Academy force finds and does battle with the Wilson gang, while Nick chases the leader. A pursuit follows, which leads to Commissioner Hurst's (George Robertson) office. It is revealed that the Mayor is the "Mastermind" and that Captain Harris has been unwittingly leaking information during his daily meetings with the Mayor. Hurst apologizes and reinstates the force, and a plaque is given to honor the officers' bravery the next day.As the movie closes, Harris is sitting in a chair when a string tying the balloon float is cut, lifting his chair and floating him up into the air as he shouts Proctor's name. 
 Question: who is guiding the group of three dimwitted criminals ?
Output: mastermind
Context: The DeLorean DMC-12 (commonly referred to simply as the DeLorean as it was the only model ever produced by the company) is a sports car manufactured by John DeLorean's DeLorean Motor Company for the American market from 1981--83. 
 Question: What year did DeLorean DMC-12 start?
Output: 1981
Context: The film is a comedy of middle-class French life ' examining culture clashes, puncturing smugness, exposing fault lines, finding strength in romantic and familial relationships and discovering an underlying sadness that stops some way short of tragedy.'[3] The film is set in a small town in Provence during a rainy August. Following the death of her widowed mother Agathe Villanova comes from Paris to deal with the sale of the home where she and her younger sister Florence were brought up, and to announce her entry into politics. She is the author of a feminist best-seller and a divorced film-maker Michel wants to make a TV documentary about her. Michel is having an affair with Agathe's sister. His collaborator is a young Algerian hotel clerk Karim, whose elderly mother has worked for most of her life as a servant with the Villanova family. Agathe's prejudice is put under the microscope when she records a series of interviews with Karim. 'The characters weave around each other for a week or so, occasionally colliding...everyone comes to have a better knowledge of themselves..the dialogue rings true..the ensemble acting is perfect..The film compares favourably with the best of Eric Rohmer.' [4] 
 Question: Where is Agathe Villanova's family home?
Output: provence
Context: Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower glycemia by enhancing urinary glucose excretion. The physiologic response to pharmacologically induced acute or chronic glycosuria has not been investigated in human diabetes. We evaluated 66 patients with type 2 diabetes (62 7 years, BMI = 31.6 4.6 kg/m(2), HbA1c = 55 8 mmol/mol, mean SD) at baseline, after a single dose, and following 4-week treatment with empagliflozin (25 mg). At each time point, patients received a mixed meal coupled with dual-tracer glucose administration and indirect calorimetry. Both single-dose and chronic empagliflozin treatment caused glycosuria during fasting (median, 7.8 [interquartile range {IQR}, 4.4] g/3 hours and 9.2 [IQR, 5.2] g/3 hours) and after meal ingestion (median, 29.0 [IQR, 12.5] g/5 hours and 28.2 [IQR, 15.4] g/5 hours). After 3 hours of fasting, endogenous glucose production (EGP) was increased 25%, while glycemia was 0.9 0.7 mmol/l lower (P < 0.0001 vs. baseline). After meal ingestion, glucose and insulin AUC decreased, whereas the glucagon response increased (all P < 0.001). While oral glucose appearance was unchanged, EGP was increased (median, 40 [IQR, 14] g and 37 [IQR, 11] g vs. 34 [IQR, 11] g, both P < 0.01). Tissue glucose disposal was reduced (median, 75 [IQR, 16] g and 70 [IQR, 21] g vs. 93 [IQR, 18] g, P < 0.0001), due to a decrease in both glucose oxidation and nonoxidative glucose disposal, with a concomitant rise in lipid oxidation after chronic administration (all P < 0.01). Cell glucose sensitivity increased (median, 55 [IQR, 35] pmol min(-1) m(-2) mM(-1) and 55 [IQR, 39] pmol min(-1) m(-2) mM(-1) vs. 44 [IQR, 32] pmol min(-1) m(-2) mM(-1), P < 0.0001), and insulin sensitivity was improved. Resting energy expenditure rates and those after meal ingestion were unchanged. In patients with type 2 diabetes, empagliflozin-induced glycosuria improved cell function and insulin sensitivity, despite the fall in insulin secretion and tissue glucose disposal and the rise in EGP after one dose, thereby lowering fasting and postprandial glycemia. Chronic dosing shifted substrate utilization from carbohydrate to lipid. Trial registration. ClinicalTrials.Gov NCT01248364 (EudraCT no. 2010-018708-99). Funding. This study was funded by Boehringer Ingelheim. 
 Question: Which protein does empagliflozin inhibit?
Output: sglt2
Context: Carpal tunnel syndrome is a complex of symptoms as a result of compression of the median nerve in the carpal tunnel. As nerve entrapment induces impairment of somatic fibres followed by clinical symptoms and signs of the syndrome, one can assume that sympathetic fibres are involved too. Results of studies focused on this problem show presence of sympathetic symptoms in about half of patients, including Raynaud phenomenon, blanching of hands, painful swelling of fingers, dry or excessive sweating of palms. Activity of sympathetic system can be investigated by means of sympathetic skin response and vasomotor response. Eight papers presenting the results of sympathetic skin response from median nerve in carpal tunnel syndrome were analysed. Results of 4 studies showed decreased sympathetic activity, in 2 findings were equivocal and 2 studies failed to reveal any abnormalities. The following variables were considered in the interpretation of sympathetic skin response curve: amplitude, latency and area under the chart, each of them having limited diagnostic value due to inter-and intrasubject variation of these parameters. Vasomotor response was investigated in 2 studies by means of Doppler ultrasound flow examination in digital arteries. Results of both studies showed decreased vasomotor response in carpal tunnel syndrome. The review of current knowledge on sympathetic impairment in carpal tunnel syndrome fails to provide a definitive determination of its range and clinical consequences. It confirms, however, that routine examination of sympathetic disturbances is unnecessary due to their minor clinical significance. 
 Question: What nerve is involved in carpal tunnel syndrome?
Output: median
Context: In 1740, the Mon of Lower Burma revolted against the Toungoo Dynasty and founded the Restored Hanthawaddy Kingdom based in Pegu . Throughout the 1740s, the Hanthawaddy forces were winning against Upper Burma-based Toungoo armies. The Siamese were concerned by another rising power in Burma since a strong Burma historically meant future invasions to Siam. Concerned, the Siamese court readily gave protection to the Burmese governors of Martaban and Tavoy who had fled to Siam. In 1745, they sent a diplomatic mission to Ava to evaluate the political situation there, and were received by the Burmese king Mahadhammaraza Dipadi. They saw an Ava court that was on its last legs. By 1751, Restored Hanthawaddy forces were closing in on Ava. The Siamese concerns about the emergence of another strong dynasty based in Pegu appeared imminent. Perhaps as a precautionary measure, the Siamese decided to move their forward base into the upper coast in 1751. While it remains unclear as to whether the Siamese ever intended to go beyond the coast into mainland Lower Burma, the Siamese action nonetheless rang alarm bells in Pegu. Deeply concerned, the Hanthawaddy leadership withdrew two-thirds of their army back down to Lower Burma immediately after they had toppled the last Toungoo king in April 1752. This redeployment of Hanthawaddy troops proved a critical turning point in Burmese history as it gave nascent Upper Burmese resistance groups much needed breathing room. The Hanthawaddy command left less than 10,000 men to pacify all of Upper Burma. Taking advantage of light Hanthawaddy troops, one resistance group, the Konbaung Dynasty led by Alaungpaya, drove out Hanthawaddy troops from Upper Burma by May 1754. Konbaung armies invaded Lower Burma in 1755, and captured Pegu in 1757, ending the 17-year-old Mon kingdom. 
 Question: Who sent diplomatic missions to Ava in 1745?
Output: siamese court
Context: In 1740, the Mon of Lower Burma revolted against the Toungoo Dynasty and founded the Restored Hanthawaddy Kingdom based in Pegu . Throughout the 1740s, the Hanthawaddy forces were winning against Upper Burma-based Toungoo armies. The Siamese were concerned by another rising power in Burma since a strong Burma historically meant future invasions to Siam. Concerned, the Siamese court readily gave protection to the Burmese governors of Martaban and Tavoy who had fled to Siam. In 1745, they sent a diplomatic mission to Ava to evaluate the political situation there, and were received by the Burmese king Mahadhammaraza Dipadi. They saw an Ava court that was on its last legs. By 1751, Restored Hanthawaddy forces were closing in on Ava. The Siamese concerns about the emergence of another strong dynasty based in Pegu appeared imminent. Perhaps as a precautionary measure, the Siamese decided to move their forward base into the upper coast in 1751. While it remains unclear as to whether the Siamese ever intended to go beyond the coast into mainland Lower Burma, the Siamese action nonetheless rang alarm bells in Pegu. Deeply concerned, the Hanthawaddy leadership withdrew two-thirds of their army back down to Lower Burma immediately after they had toppled the last Toungoo king in April 1752. This redeployment of Hanthawaddy troops proved a critical turning point in Burmese history as it gave nascent Upper Burmese resistance groups much needed breathing room. The Hanthawaddy command left less than 10,000 men to pacify all of Upper Burma. Taking advantage of light Hanthawaddy troops, one resistance group, the Konbaung Dynasty led by Alaungpaya, drove out Hanthawaddy troops from Upper Burma by May 1754. Konbaung armies invaded Lower Burma in 1755, and captured Pegu in 1757, ending the 17-year-old Mon kingdom. 
 Question: Who sent diplomatic missions to Ava in 1745?
Output: the siamese
Context: In 1740, the Mon of Lower Burma revolted against the Toungoo Dynasty and founded the Restored Hanthawaddy Kingdom based in Pegu . Throughout the 1740s, the Hanthawaddy forces were winning against Upper Burma-based Toungoo armies. The Siamese were concerned by another rising power in Burma since a strong Burma historically meant future invasions to Siam. Concerned, the Siamese court readily gave protection to the Burmese governors of Martaban and Tavoy who had fled to Siam. In 1745, they sent a diplomatic mission to Ava to evaluate the political situation there, and were received by the Burmese king Mahadhammaraza Dipadi. They saw an Ava court that was on its last legs. By 1751, Restored Hanthawaddy forces were closing in on Ava. The Siamese concerns about the emergence of another strong dynasty based in Pegu appeared imminent. Perhaps as a precautionary measure, the Siamese decided to move their forward base into the upper coast in 1751. While it remains unclear as to whether the Siamese ever intended to go beyond the coast into mainland Lower Burma, the Siamese action nonetheless rang alarm bells in Pegu. Deeply concerned, the Hanthawaddy leadership withdrew two-thirds of their army back down to Lower Burma immediately after they had toppled the last Toungoo king in April 1752. This redeployment of Hanthawaddy troops proved a critical turning point in Burmese history as it gave nascent Upper Burmese resistance groups much needed breathing room. The Hanthawaddy command left less than 10,000 men to pacify all of Upper Burma. Taking advantage of light Hanthawaddy troops, one resistance group, the Konbaung Dynasty led by Alaungpaya, drove out Hanthawaddy troops from Upper Burma by May 1754. Konbaung armies invaded Lower Burma in 1755, and captured Pegu in 1757, ending the 17-year-old Mon kingdom. 
 Question: Who sent diplomatic missions to Ava in 1745?
Output: siam
Context: In 1740, the Mon of Lower Burma revolted against the Toungoo Dynasty and founded the Restored Hanthawaddy Kingdom based in Pegu . Throughout the 1740s, the Hanthawaddy forces were winning against Upper Burma-based Toungoo armies. The Siamese were concerned by another rising power in Burma since a strong Burma historically meant future invasions to Siam. Concerned, the Siamese court readily gave protection to the Burmese governors of Martaban and Tavoy who had fled to Siam. In 1745, they sent a diplomatic mission to Ava to evaluate the political situation there, and were received by the Burmese king Mahadhammaraza Dipadi. They saw an Ava court that was on its last legs. By 1751, Restored Hanthawaddy forces were closing in on Ava. The Siamese concerns about the emergence of another strong dynasty based in Pegu appeared imminent. Perhaps as a precautionary measure, the Siamese decided to move their forward base into the upper coast in 1751. While it remains unclear as to whether the Siamese ever intended to go beyond the coast into mainland Lower Burma, the Siamese action nonetheless rang alarm bells in Pegu. Deeply concerned, the Hanthawaddy leadership withdrew two-thirds of their army back down to Lower Burma immediately after they had toppled the last Toungoo king in April 1752. This redeployment of Hanthawaddy troops proved a critical turning point in Burmese history as it gave nascent Upper Burmese resistance groups much needed breathing room. The Hanthawaddy command left less than 10,000 men to pacify all of Upper Burma. Taking advantage of light Hanthawaddy troops, one resistance group, the Konbaung Dynasty led by Alaungpaya, drove out Hanthawaddy troops from Upper Burma by May 1754. Konbaung armies invaded Lower Burma in 1755, and captured Pegu in 1757, ending the 17-year-old Mon kingdom. 
 Question: Who sent diplomatic missions to Ava in 1745?
Output: siamese
Context: In 1740, the Mon of Lower Burma revolted against the Toungoo Dynasty and founded the Restored Hanthawaddy Kingdom based in Pegu . Throughout the 1740s, the Hanthawaddy forces were winning against Upper Burma-based Toungoo armies. The Siamese were concerned by another rising power in Burma since a strong Burma historically meant future invasions to Siam. Concerned, the Siamese court readily gave protection to the Burmese governors of Martaban and Tavoy who had fled to Siam. In 1745, they sent a diplomatic mission to Ava to evaluate the political situation there, and were received by the Burmese king Mahadhammaraza Dipadi. They saw an Ava court that was on its last legs. By 1751, Restored Hanthawaddy forces were closing in on Ava. The Siamese concerns about the emergence of another strong dynasty based in Pegu appeared imminent. Perhaps as a precautionary measure, the Siamese decided to move their forward base into the upper coast in 1751. While it remains unclear as to whether the Siamese ever intended to go beyond the coast into mainland Lower Burma, the Siamese action nonetheless rang alarm bells in Pegu. Deeply concerned, the Hanthawaddy leadership withdrew two-thirds of their army back down to Lower Burma immediately after they had toppled the last Toungoo king in April 1752. This redeployment of Hanthawaddy troops proved a critical turning point in Burmese history as it gave nascent Upper Burmese resistance groups much needed breathing room. The Hanthawaddy command left less than 10,000 men to pacify all of Upper Burma. Taking advantage of light Hanthawaddy troops, one resistance group, the Konbaung Dynasty led by Alaungpaya, drove out Hanthawaddy troops from Upper Burma by May 1754. Konbaung armies invaded Lower Burma in 1755, and captured Pegu in 1757, ending the 17-year-old Mon kingdom. 
 Question: Who sent diplomatic missions to Ava in 1745?
Output: the siamese court
Context: Eponine Thenardier (/eponin tenrdie/; French: (epnin tenadje)), also referred to as the ''Jondrette girl'', is a fictional character in the 1862 novel Les Miserables by Victor Hugo. 
 Question: In which fictional work is Eponine a character?
Output: les misérables
Context: Polar Boy is a fictional character from the 30th century of the DC Universe, initially suggested by reader Buddy Lavigne of Northbrook, Illinois in the letters page of Adventure Comics #304, January, 1963. 
 Question: What is the name of the fictional universe that Polar Boy is from?
Output: dc universe
Context: Joy Tivy was born in Carlow, Ireland in 1924 and she commenced studies at the University College Dublin in 1942 where she studied geography as her primary subject with botany and geology as her secondary areas. 
 Question: What is the name of university that educated Joy Tivy?
Output: university college dublin
Context: Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Contrary to that of its phagocyte counterpart NOX2, the molecular basis of NOX1 regulation is not clear. Because NOXO1 lacks the phosphorylated region found in its homolog p47(PHOX), the current view is that NOX1 activation occurs without NOXO1 phosphorylation. Here, however, we demonstrate that phorbol myristate acetate (PMA) stimulates NOXO1 phosphorylation in a transfected human embryonic kidney (HEK) 293 epithelial cell model via protein kinase C and identify Ser-154 as the major phosphorylated site. Endogenous NOXO1 from T84 colon epithelial cells was also phosphorylated, suggesting that NOXO1 phosphorylation is physiologically relevant. In transfected HEK-293 cells, PMA-induced phosphorylation on Ser-154 enhanced NOXO1 binding to NOXA1 (+97%) and to the p22(PHOX) C-terminal region (+384%), increased NOXO1 colocalization with p22(PHOX), and allowed optimal ROS production by NOX1 as demonstrated by the use of S154A and S154D mutants compared with that by wild-type NOXO1 (P<0.05). Pulldown experiments revealed that phos-phorylation on Ser-154 was sufficient to markedly enhance NOXO1 binding to NOXA1, which in turn acts as a molecular switch, allowing optimal interaction of NOXO1 with p22(PHOX). This study unexpectedly revealed that full assembly and activation of NOX1 is a tightly regulated process in which NOXO1 phosphorylation on Ser-154 is the initial trigger. 
 Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nadph oxidase 1
Context: Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Contrary to that of its phagocyte counterpart NOX2, the molecular basis of NOX1 regulation is not clear. Because NOXO1 lacks the phosphorylated region found in its homolog p47(PHOX), the current view is that NOX1 activation occurs without NOXO1 phosphorylation. Here, however, we demonstrate that phorbol myristate acetate (PMA) stimulates NOXO1 phosphorylation in a transfected human embryonic kidney (HEK) 293 epithelial cell model via protein kinase C and identify Ser-154 as the major phosphorylated site. Endogenous NOXO1 from T84 colon epithelial cells was also phosphorylated, suggesting that NOXO1 phosphorylation is physiologically relevant. In transfected HEK-293 cells, PMA-induced phosphorylation on Ser-154 enhanced NOXO1 binding to NOXA1 (+97%) and to the p22(PHOX) C-terminal region (+384%), increased NOXO1 colocalization with p22(PHOX), and allowed optimal ROS production by NOX1 as demonstrated by the use of S154A and S154D mutants compared with that by wild-type NOXO1 (P<0.05). Pulldown experiments revealed that phos-phorylation on Ser-154 was sufficient to markedly enhance NOXO1 binding to NOXA1, which in turn acts as a molecular switch, allowing optimal interaction of NOXO1 with p22(PHOX). This study unexpectedly revealed that full assembly and activation of NOX1 is a tightly regulated process in which NOXO1 phosphorylation on Ser-154 is the initial trigger. 
 Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nicotinamide adenine dinucleotide phosphate-oxidase 1
Context: Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Contrary to that of its phagocyte counterpart NOX2, the molecular basis of NOX1 regulation is not clear. Because NOXO1 lacks the phosphorylated region found in its homolog p47(PHOX), the current view is that NOX1 activation occurs without NOXO1 phosphorylation. Here, however, we demonstrate that phorbol myristate acetate (PMA) stimulates NOXO1 phosphorylation in a transfected human embryonic kidney (HEK) 293 epithelial cell model via protein kinase C and identify Ser-154 as the major phosphorylated site. Endogenous NOXO1 from T84 colon epithelial cells was also phosphorylated, suggesting that NOXO1 phosphorylation is physiologically relevant. In transfected HEK-293 cells, PMA-induced phosphorylation on Ser-154 enhanced NOXO1 binding to NOXA1 (+97%) and to the p22(PHOX) C-terminal region (+384%), increased NOXO1 colocalization with p22(PHOX), and allowed optimal ROS production by NOX1 as demonstrated by the use of S154A and S154D mutants compared with that by wild-type NOXO1 (P<0.05). Pulldown experiments revealed that phos-phorylation on Ser-154 was sufficient to markedly enhance NOXO1 binding to NOXA1, which in turn acts as a molecular switch, allowing optimal interaction of NOXO1 with p22(PHOX). This study unexpectedly revealed that full assembly and activation of NOX1 is a tightly regulated process in which NOXO1 phosphorylation on Ser-154 is the initial trigger. 
 Question: Which NADPH oxidase family member requires interaction with NOXO1 for function?
Output: nox1
Context: In week 11 following their bye-week, the Lions hosted the Jacksonville Jaguars. The Jaguars opened the scoring in the first quarter via a 27-yard field goal from Jason Myers. The Lions' first score came in the second quarter on a 55-yard punt return from Andre Roberts, but the extra point try by Matt Prater was partially blocked and failed. The Jaguars responded with a three-yard touchdown pass from Blake Bortles to Allen Robinson, but the conversion attempt by Myers also failed. The Lions then scored on a 27-yard field goal from Matt Prater, which tied the score at 9-9 at halftime. The Lions took the lead in the third quarter via a 39-yard interception return from Rafael Bush. The Jaguars responded with 10 points in the third quarter via a 52-yard field goal from Myers, and a three-yard touchdown pass from Bortles to Marqise Lee, giving them a 19-16 lead. The Lions, trailing for the ninth straight game when entering the fourth quarter, would score the final 10 points of the game. The Lions offense scored its first and only touchdown on a one-yard run from Eric Ebron, and Matt Prater added a 43-yard field goal with 22 seconds left in the game. On the final drive for the Jaguars, Tavon Wilson intercepted a pass from Bortles, sealing the Lions 26-19 victory. The Lions became the first team in NFL history to have its first ten games of a season all decided by seven or fewer points. 
 Question: Who threw the last interception of the game?
Output: blake bortles
Context: Shprintzen-Goldberg syndrome is one of a group of disorders characterized by craniosynostosis and marfanoid habitus. Eleven cases were reported previously. We present 4 new patients and review one of the patients of the original report of Shprintzen and Goldberg [1982: J Craniofac Genet Dev Biol 2:65-74], 15 years later. The clinical and radiologic findings on our patients are compared with those of the previously reported patients and also with those of Furlong et al. [1987: Am J Med Genet 26:599-604] and Lacombe and Battin [1993: Clin Dysmorphol 2: 220-224], who share many of the characteristics of Shprintzen-Goldberg syndrome. Some of the clinical data are helpful in determining if the patients of Furlong et al. [1987: Am J Med Genet 26:599-604] and Lacombe and Battin [1993: Clin Dysmorphol 2: 220-224] have a separate syndrome or represent a variant of Shprintzen-Goldberg syndrome. However, radiologic investigations appear to be more specific, since an abnormality of the first and second cervical vertebrae, hydrocephalus, dilatation of the lateral ventricles, and a Chiari-I malformation of the brain were found only in the patients with Shprintzen-Goldberg syndrome. The apparently diagnostic findings of the 15 patients with this syndrome may be helpful in differentiating between Shprintzen-Goldberg syndrome and other syndromes with craniosynostosis and marfanoid habitus. 
 Question: Which disease is included as an additional feature in the Goldberg-Shprintzen syndrome?
Output: craniosynostosis
Context: Can you name some fossils? How about dinosaur bones or dinosaur footprints? Animal skeletons, teeth, shells, coprolites (otherwise known as feces), or any other remains or traces from a living creature that becomes rock is a fossil. The same processes that formed these fossils also created some of our most important energy resources, fossil fuels. Coal, oil, and natural gas are fossil fuels. Fossil fuels come from living matter starting about 500 million years ago. Millions of years ago, plants used energy from the Sun to form sugars, carbohydrates, and other energy-rich carbon compounds. As plants and animals died, their remains settled on the ground on land and in swamps, lakes, and seas (Figure 1.1). Over time, layer upon layer of these remains accumulated. Eventually, the layers were buried so deeply that they were crushed by an enormous mass of earth. The weight of this earth pressing down on these plant and animal remains created intense heat and pressure. After millions of years of heat and pressure, the material in these layers turned into chemicals called hydrocarbons (Figure 1.2). Hydrocarbons are made of carbon and hydrogen atoms. This molecule with one carbon and four hydrogen atoms is methane. Hydrocarbons can be solid, liquid, or gaseous. The solid form is what we know as coal. The liquid form is petroleum, or crude oil. Natural gas is the gaseous form. The solar energy stored in fossil fuels is a rich source of energy. Although fossil fuels provide very high quality energy, they are non-renewable. Click image to the left or use the URL below. URL: 
 Question: fossil fuels are compounds of _________________.
Output: carbon and hydrogen
Context: Clozapine reduces L-3,4-dihydroxyphenylalanine (L-Dopa)-induced dyskinesias in parkinsonian patients. To test if the antidyskinetic effect of clozapine is related to antagonism at the dopamine D(4) receptor, we investigated the effect of 8-methyl-6-(4-methyl-1-piperazinyl)-11H-pyrido[2,3-b][1, 4]benzodiazepine (JL-18), a structural analog of clozapine which is more selective for this receptor. Four 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP)-treated cynomolgus monkeys with a stable parkinsonian syndrome and reproducible dyskinesias to L-Dopa were used in this study. They were injected subcutaneously (s.c.) with L-Dopa methyl ester (125 mg per animal) plus benserazide (50 mg per animal; L-Dopa/benserazide) alone or in combination with JL-18 (at the doses of 0.1, 0.3, or 0.9 mg/kg, s.c.). Subcutaneous injection of sterile saline was used as control. L-Dopa/benserazide increased locomotion and improved parkinsonism but also induced dyskinesias. Co-administration of JL-18, at low doses (0.1, 0.3 mg/kg) with L-Dopa/benserazide, produced a dose-dependent reduction in L-Dopa-induced dyskinesias without a parallel return to parkinsonism. The present results suggest that novel selective dopamine D(4) receptor antagonists may represent a useful tool to reduce L-Dopa-induced dyskinesias. 
 Question: Which drug is benserazide usually co-administered with?
Output: l-dopa
Context: Chediak-Higashi syndrome, a rare autosomal recessive disorder, was described over 50 years ago. Patients show hypopigmentation, recurrent infections, mild coagulation defects and varying neurologic problems. Treatment is bone marrow transplant, which is effective in treating the hematologic and immune defects, however the neurologic problems persist. The CHS1/LYST gene was identified over 10 years ago and homologous CHS1/LYST genes are present in all eukaryotes. This review will discuss the advances made in understanding the clinical aspects of the syndrome and the function of CHS1/LYST/Beige. Clinical reports of Chediak-Higashi syndrome have identified mutations throughout the CHS1/LYST gene. The nature of the mutation can be a predictor of the severity of the disease. Over the past decade the CHS1/LYST family of proteins has been analyzed using model organisms, two-hybrid analysis, overexpression phenotypes and dominant negatives. These studies suggest that the CHS1/LYST protein is involved in either vesicle fusion or fission. Although CHS is a rare disease, the Chediak-like family of proteins is providing insight into the regulation of vesicle trafficking. Understanding the basic mechanisms that govern vesicle trafficking will provide essential information regarding how loss of CHS1/LYST affects hematologic, immunologic and neurologic processes. 
 Question: Which syndrome is associated with mutations in the LYST gene?
Output: chediak-higashi syndrome
Context: Coming off their divisional home win over the Cardinals, the 49ers flew to the Edward Jones Dome for a Week 2 divisional duel against their NFC West rival, the St. Louis Rams. In the first quarter, the Niners trailed early as Rams QB Marc Bulger completed a 12-yard TD pass to WR Torry Holt for the only score of the period. In the second quarter, San Francisco would tie the game up with RB Frank Gore getting a 1-yard TD run. St. Louis would take the halftime lead with kicker Jeff Wilkins getting a 29-yard field goal In the third quarter, the 49ers took the lead with Gore breaking through a gang of tacklers for a 43-yard TD run, along with the only score of the period. In the fourth quarter, the Rams retook the lead with Wiklins getting a 53-yard field goal. Fortunately, thanks to a St. Louis goof-up on special teams, the Niners took the lead with kicker Joe Nedney getting a 40-yard field goal. Near the end the game, the Rams had one last chance to win the game. Fortunately for San Francisco, Wilkins' 56-yard field goal attempt fell about a yard short of the crossbar. With the win, the 49ers improved to 2-0 for the first time since 1998. Q1 - STL - 6:04 - 12-yard TD pass from Marc Bulger to Torry Holt (Wilkins kick) (STL 7-0) Q2 - SF - 14:57 - Frank Gore 1-yard TD run (Nedney kick) (7-7) Q2 - STL - 9:04 - Jeff Wilkins 27-yard FG (STL 10-7) Q2 - STL - 1:51 - Jeff Wilkins 29-yard FG (STL 13-7) Q3 - SF - 2:43 - Frank Gore 43-yard TD run (Nedney kick) (SF 14-13) Q4 - STL - 10:04 - Jeff Wilkins 53-yard FG (STL 16-14) Q4 - SF - 3:23 - Joe Nedney 40-yard FG (SF 17-16) 
 Question: Who scored the first touchdown of the game?
Output: torry holt
Context: Saltburn, Marske and New Marske is a civil parish in Redcar and Cleveland in north east England. 
 Question: What was replaced Saltburn, Marske and New Marske?
Output: cleveland
Context: Tippity Witchet was a son of the great sire Broomstick who was the son of Ben Brush. 
 Question: Who was Tippity Witchet's paternal figure?
Output: broomstick
Context: Baron Mayer Amschel de Rothschild (29 June 1818 -- 6 February 1874) was an English businessman and politician of the English branch of the Rothschild family. 
 Question: What family lineage was Mayer Amschel de Rothschild part of?
Output: rothschild family
Context: The Girl and the Oak (Serbo-Croatian: Djevojka i hrast) is a 1955 Yugoslav film directed by Kreso Golik. 
 Question: Under whose direction was The Girl and the Oak produced?
Output: krešo golik
Context: Almost nothing is left of the Bastille except some remains of its stone foundation that were relocated to the side of the Boulevard Henri IV. Historians were critical of the Bastille in the early 19th century, and believe the fortress to have been a relatively well-administered institution, but deeply implicated in the system of French policing and political control during the 18th century. 
 Question: What material was used for Bastille?
Output: stone
Context: Miguel Angel Garcia Tebar (born 26 September 1979), known as Miguel Garcia, is a Spanish retired footballer who played as a defensive midfielder. 
 Question: What role does Miguel Angel Garcia Tebar play in football?
Output: midfielder
Context: IDLE (Integrated DeveLopment Environment or Integrated Development and Learning Environment) is an integrated development environment for Python, which has been bundled with the default implementation of the language since 1.5.2b1. 
 Question: Which programming language is IDLE written in?
Output: python
Context: As of the census of 2000, there were 120,546 people, 41,668 households, and 32,292 families residing in the county. The population density was 262 people per square mile (101/km). There were 43,903 housing units at an average density of 95 per square mile (37/km). The racial makeup of the county was 68.51% Race (United States Census), 26.06% Race (United States Census) or Race (United States Census), 0.75% Race (United States Census), 1.82% Race (United States Census), 0.06% Race (United States Census), 0.72% from Race (United States Census), and 2.08% from two or more races. 2.26% of the population were Race (United States Census) or Race (United States Census) of any race. 11.6% were of german people, 10.8% irish people, 10.2% english people, 9.3% American and 5.3% italian people ancestry. 
 Question: Which ancestral group is larger: Irish or English?
Output: irish
Context: Mesothelin is a 40 kDa protein present on normal mesothelial cells and overexpressed in several human tumors, including mesothelioma and ovarian and pancreatic adenocarcinoma. 
 Question: In what living being can Mesothelin be found?
Output: human
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 player caught the longest touchdown of the game?
Output: jermaine kearse
Context: Don Carlos Smith (March 25, 1816 -- August 7, 1841) was the youngest brother of Joseph Smith and a leader, missionary, and periodical editor in the early days of the Latter Day Saint movement. 
 Question: Who was the brother of Don Carlos Smith?
Output: joseph smith
Context: David T. Friendly (born May 1, 1956) is an American film producer best known for co-producing the 2006 film Little Miss Sunshine, for which he was nominated for an Academy Award for Best Picture. 
 Question: What award was David T. Friendly nominated for?
Output: academy award for best picture