dkoterwa/mlqa_filtered huggingface dataset:
The Nagorno-Karabakh War was an ethnic and territorial conflict that took place in the late 1980s to May 1994, in the enclave of Nagorno-Karabakh in southwestern Azerbaijan, between the majority ethnic Armenians of Nagorno-Karabakh backed by the Republic of Armenia, and the Republic of Azerbaijan. As the war progressed, Armenia and Azerbaijan, both former Soviet Republics, entangled themselves in  protracted, undeclared mountain warfare in the mountainous heights of Karabakh as Azerbaijan attempted to curb the secessionist movement in Nagorno-Karabakh. The enclave's parliament had voted in favor of uniting itself with Armenia and a referendum, boycotted by the Azerbaijani population of Nagorno-Karabakh, was held, whereby most of the voters voted in favor of independence. The demand to unify with Armenia began in a relatively peaceful manner in 1988; in the following months, as the Soviet Union disintegrated, it gradually grew into an increasingly violent conflict between Armenians and Azerbaijanis, resulting in claims of ethnic cleansing by both sides.Inter-ethnic clashes between the two broke out shortly after the parliament of the Nagorno-Karabakh Autonomous Oblast (NKAO) in Azerbaijan voted to unify the region with Armenia on 20 February 1988.  The declaration of secession from Azerbaijan was the final result of a territorial conflict regarding the land. As Azerbaijan declared its independence from the Soviet Union and removed the powers held by the enclave's government, the Armenian majority voted to secede from Azerbaijan and in the process proclaimed the unrecognized Republic of Nagorno-Karabakh.Full-scale fighting erupted in early 1992. International mediation by several groups including the Organization for Security and Co-operation in Europe (OSCE) failed to bring an end resolution that both sides could work with. In early 1993, Armenian forces captured regions outside the enclave itself, threatening the involvement of other countries in the region. By the end of the war in 1994, the Armenians were in full control of the enclave (with the exception of the Shahumyan Region) in addition to surrounding areas of Azerbaijan proper, most notably the Lachin Corridor, a mountain pass that links Nagorno-Karabakh with mainland Armenia. A Russian-brokered ceasefire was signed in May 1994, but regular peace talks between Armenia and Azerbaijan mediated by the OSCE Minsk Group have failed to result in a peace treaty. This has left the Nagorno-Karabakh area in a state of legal limbo, with the Republic of Artsakh remaining de facto independent but internationally unrecognized while Armenian forces currently control approximately 9% of Azerbaijan's territory outside the enclave. As many as 230,000 Armenians from Azerbaijan and 800,000 Azerbaijanis from Armenia and Karabakh have been displaced as a result of the conflict.

Question: When did the Nagorno-Karabakh War end?
Answer: May 1994
The loss of Shusha led the Azerbaijani parliament to lay the blame on Yaqub Mammadov, then acting President of Azerbaijan, which removed him from power and cleared Mutalibov of any responsibility after the loss of Khojaly, reinstating him as President on 15 May 1992. Many Azerbaijanis saw this act as a coup, in addition to forestalling parliamentary elections due in June of that year. The Azerbaijani parliament at that time was made up of former leaders from the country's communist regime, and the losses of Khojaly and Shusha led to further agitation for free elections.To contribute to the turmoil, an offensive was launched by Armenian forces on 18 May to take the city of Lachin in the narrow corridor separating Armenia and Nagorno-Karabakh. The city itself was poorly guarded and, within the next day, Armenian forces took control of the town and cleared any remaining Azerbaijanis to open the road that linked the region to Armenia. The taking of the city then allowed an overland route to be connected with Armenia itself with supply convoys beginning to trek up the mountainous region of Lachin to Karabakh.The loss of Lachin was the final blow to Mutalibov's regime. Demonstrations were held despite Mutalibov's ban and an armed coup was staged by Popular Front activists. Fighting between government forces and Popular Front supporters escalated as the political opposition seized the parliament building in Baku as well as the airport and presidential office. On 16 June 1992 Abulfaz Elchibey was elected leader of Azerbaijan with many political leaders from the Azerbaijan Popular Front Party were elected into the parliament. The instigators lambasted Mutalibov as an undedicated and weak leader in the war in Karabakh. Elchibey was staunchly against receiving any help from the Russians, instead favoring closer ties to Turkey.The fighting also spilled into nearby Nakhchivan, which was shelled by Armenian troops in May 1992.

Question: Who formed a closer relationship with Turkey?
Answer: Azerbaijan
Carter meets Lee at Los Angeles International Airport and proceeds to take him on a sightseeing tour of LA, simultaneously keeping Lee away from the embassy and contacting several of his underworld informants about the kidnapping. Lee finally escapes and makes his way to the Chinese Consulate, where a nervous Han and a group of FBI agents are awaiting news about his daughter. While arguing with Agent-in-charge Warren Russ, Carter accidentally involves himself in a phone conversation with Sang, where he arranges a ransom drop of $50 million in a couple of hours.

Question: Where did Carter meet Lee?
Answer: Los Angeles International Airport
New Britain (Tok Pisin: Niu Briten) is the largest island in the Bismarck Archipelago of Papua New Guinea. It is separated from the island of New Guinea by the Dampier and Vitiaz Straits and from New Ireland by St. George's Channel. The main towns of New Britain are Rabaul/Kokopo and Kimbe. The island is roughly the size of Taiwan. While the island was part of German New Guinea, it was named Neupommern ("New Pomerania").

Question: which are the two main towns?
Answer: Rabaul/Kokopo and Kimbe
Its distribution has been greatly reduced and is now discontinuous. Decades of poaching for its velvety pelt, peaking in the 1950s and 1960s, considerably diminished population numbers. The species was listed as endangered in 1999 and wild population estimates are typically below 5,000. The Guianas are one of the last real strongholds for the species, which also enjoys modest numbers — and significant protection — in the Peruvian Amazonian basin. It is one of the most endangered mammal species in the neotropics. Habitat degradation and loss is the greatest current threat. The giant otter is also rare in captivity; in 2003, only 60 animals were being held.The giant otter shows a variety of adaptations suitable to an amphibious lifestyle, including exceptionally dense fur, a wing-like tail, and webbed feet. The species prefers freshwater rivers and streams, which are usually seasonally flooded, and may also take to freshwater lakes and springs. It constructs extensive campsites close to feeding areas, clearing large amounts of vegetation. The giant otter subsists almost exclusively on a diet of fish, particularly characins and catfish, but may also eat crabs, turtles, snakes and small caiman. It has no serious natural predators other than humans, although it must compete with other species, including the neotropical otter and caiman species, for food resources.

Question: Who are the giant otters' competitors?
Answer: neotropical otter and caiman species
A B cell identifies pathogens when antibodies on its surface bind to a specific foreign antigen. This antigen/antibody complex is taken up by the B cell and processed by proteolysis into peptides. The B cell then displays these antigenic peptides on its surface MHC class II molecules. This combination of MHC and antigen attracts a matching helper T cell, which releases lymphokines and activates the B cell. As the activated B cell then begins to divide, its offspring (plasma cells) secrete millions of copies of the antibody that recognizes this antigen. These antibodies circulate in blood plasma and lymph, bind to pathogens expressing the antigen and mark them for destruction by complement activation or for uptake and destruction by phagocytes. Antibodies can also neutralize challenges directly, by binding to bacterial toxins or by interfering with the receptors that viruses and bacteria use to infect cells.

Question: What do T cells produce in order to activate B cells?
Answer: lymphokines

Question: Antibodies bind to what to neutralize challenges?
Answer: bacterial toxins
Another important role of the immune system is to identify and eliminate tumors. This is called immune surveillance. The transformed cells of tumors express antigens that are not found on normal cells. To the immune system, these antigens appear foreign, and their presence causes immune cells to attack the transformed tumor cells. The antigens expressed by tumors have several sources; some are derived from oncogenic viruses like human papillomavirus, which causes cervical cancer, while others are the organism's own proteins that occur at low levels in normal cells but reach high levels in tumor cells. One example is an enzyme called tyrosinase that, when expressed at high levels, transforms certain skin cells (e.g. melanocytes) into tumors called melanomas. A third possible source of tumor antigens are proteins normally important for regulating cell growth and survival, that commonly mutate into cancer inducing molecules called oncogenes.The main response of the immune system to tumors is to destroy the abnormal cells using killer T cells, sometimes with the assistance of helper T cells. Tumor antigens are presented on MHC class I molecules in a similar way to viral antigens. This allows killer T cells to recognize the tumor cell as abnormal. NK cells also kill tumorous cells in a similar way, especially if the tumor cells have fewer MHC class I molecules on their surface than normal; this is a common phenomenon with tumors. Sometimes antibodies are generated against tumor cells allowing for their destruction by the complement system.Clearly, some tumors evade the immune system and go on to become cancers. Tumor cells often have a reduced number of MHC class I molecules on their surface, thus avoiding detection by killer T cells. Some tumor cells also release products that inhibit the immune response; for example by secreting the cytokine TGF-β, which suppresses the activity of macrophages and lymphocytes. In addition, immunological tolerance may develop against tumor antigens, so the immune system no longer attacks the tumor cells.Paradoxically, macrophages can promote tumor growth  when tumor cells send out cytokines that attract macrophages, which then generate cytokines and growth factors such as tumor-necrosis factor alpha that nurture tumor development or promote stem-cell-like plasticity.  In addition, a combination of hypoxia in the tumor and a cytokine produced by macrophages induces tumor cells to decrease production of a protein that blocks metastasis and thereby assists spread of cancer cells.

Question: What to tumors express?
Answer: antigens
Both innate and adaptive immunity depend on the ability of the immune system to distinguish between self and non-self molecules. In immunology, self molecules are those components of an organism's body that can be distinguished from foreign substances by the immune system. Conversely, non-self molecules are those recognized as foreign molecules. One class of non-self molecules are called antigens (short for antibody generators) and are defined as substances that bind to specific immune receptors and elicit an immune response.Newborn infants have no prior exposure to microbes and are particularly vulnerable to infection. Several layers of passive protection are provided by the mother.   During pregnancy, a particular type of antibody, called IgG, is transported from mother to baby directly through the placenta, so human babies have high levels of antibodies even at birth, with the same range of antigen specificities as their mother. Breast milk or  colostrum also contains antibodies that are transferred to the gut of the infant and protect against bacterial infections until the newborn can synthesize its own antibodies. This is passive immunity because the fetus does not actually make any memory cells or antibodies—it only borrows them. This passive immunity is usually short-term, lasting from a few days up to several months. In medicine, protective passive immunity can also be transferred artificially from one individual to another via antibody-rich serum.

Question: How does a fetus acquire memory cells?
Answer: borrows them
Helper T cells express T cell receptors (TCR) that recognize antigen bound to Class II MHC molecules. The MHC:antigen complex is also recognized by the helper cell's CD4 co-receptor, which recruits molecules inside the T cell (e.g., Lck) that are responsible for the T cell's activation. Helper T cells have a weaker association with the MHC:antigen complex than observed for killer T cells, meaning many receptors (around 200–300) on the helper T cell must be bound by an MHC:antigen in order to activate the helper cell, while killer T cells can be activated by engagement of a single MHC:antigen molecule. Helper T cell activation also requires longer duration of engagement with an antigen-presenting cell. The activation of a resting helper T cell causes it to release cytokines that influence the activity of many cell types. Cytokine signals produced by helper T cells enhance the microbicidal function of macrophages and the activity of killer T cells. In addition, helper T cell activation causes an upregulation of molecules expressed on the T cell's surface, such as CD40 ligand (also called CD154), which provide extra stimulatory signals typically required to activate antibody-producing B cells.

Question: TCR recognize antigen that is connected to what kind of molecules?
Answer: Class II MHC molecules
Immunology is a science that examines the structure and function of the immune system. It originates from medicine and early studies on the causes of immunity to disease. The earliest known reference to immunity was during the plague of Athens in 430 BC. Thucydides noted that people who had recovered from a previous bout of the disease could nurse the sick without contracting the illness a second time. In the 18th century, Pierre-Louis Moreau de Maupertuis made experiments with scorpion venom and observed that certain dogs and mice were immune to this venom. In the 10th century, Persian physician al-Razi (also known as Rhazes) wrote the first recorded theory of acquired immunity, noting that a smallpox bout protected its survivors from future infections. Although he explained the immunity in terms of "excess moisture" getting expelled from the blood—therefore preventing the disease to occur for a second time—this theory explained many observations about smallpox known during this time.These and other observations of acquired immunity were later exploited by Louis Pasteur in his development of vaccination and his proposed germ theory of disease. Pasteur's theory was in direct opposition to contemporary theories of disease, such as the miasma theory. It was not until Robert Koch's 1891 proofs, for which he was awarded a Nobel Prize in 1905, that microorganisms were confirmed as the cause of infectious disease. Viruses were confirmed as human pathogens in 1901, with the discovery of the yellow fever virus by Walter Reed.Immunology made a great advance towards the end of the 19th century, through rapid developments, in the study of humoral immunity and cellular immunity. Particularly important was the work of Paul Ehrlich, who proposed the side-chain theory to explain the specificity of the antigen-antibody reaction; his contributions to the understanding of humoral immunity were recognized by the award of a Nobel Prize in 1908, which was jointly awarded to the founder of cellular immunology, Elie Metchnikoff.

Question: When was there any record of a reference to immunity?
Answer: 430 BC
Microorganisms or toxins that successfully enter an organism encounter the cells and mechanisms of the innate immune system.  The innate response is usually triggered when microbes are identified by pattern recognition receptors, which recognize components that are conserved among broad groups of microorganisms, or when damaged, injured or stressed cells send out alarm signals, many of which (but not all) are recognized by the same receptors as those that recognize pathogens. Innate immune defenses are non-specific, meaning these systems respond to pathogens in a generic way. This system does not confer long-lasting immunity against a pathogen. The innate immune system is the dominant system of host defense in most organisms.

Question: What is the system that is dominant as a host of defense in most life forms?
Answer: innate immune system
Overactive immune responses comprise the other end of immune dysfunction, particularly the autoimmune disorders. Here, the immune system fails to properly distinguish between self and non-self, and attacks part of the body. Under normal circumstances, many T cells and antibodies react with "self" peptides. One of the functions of specialized cells (located in the thymus and bone marrow) is to present young lymphocytes with self antigens produced throughout the body and to eliminate those cells that recognize self-antigens, preventing autoimmunity.

Question: What does the immune system attack?
Answer: part of the body
The success of any pathogen depends on its ability to elude host immune responses. Therefore, pathogens evolved several methods that allow them to successfully infect a host, while evading detection or destruction by the immune system. Bacteria often overcome physical barriers by secreting enzymes that digest the barrier, for example, by using a type II secretion system. Alternatively, using a type III secretion system, they may insert a hollow tube into the host cell, providing a direct route for proteins to move from the pathogen to the host. These proteins are often used to shut down host defenses.An evasion strategy used by several pathogens to avoid the innate immune system is to hide within the cells of their host (also called intracellular pathogenesis). Here, a pathogen spends most of its life-cycle inside host cells, where it is shielded from direct contact with immune cells, antibodies and complement. Some examples of intracellular pathogens include viruses, the food poisoning bacterium Salmonella and the eukaryotic parasites that cause malaria (Plasmodium falciparum) and leishmaniasis (Leishmania spp.). Other bacteria, such as Mycobacterium tuberculosis, live inside a protective capsule that prevents lysis by complement. Many pathogens secrete compounds that diminish or misdirect the host's immune response. Some bacteria form biofilms to protect themselves from the cells and proteins of the immune system. Such biofilms are present in many successful infections, e.g., the chronic Pseudomonas aeruginosa and Burkholderia cenocepacia infections characteristic of cystic fibrosis. Other bacteria generate surface proteins that bind to antibodies, rendering them ineffective; examples include Streptococcus (protein G), Staphylococcus aureus (protein A), and Peptostreptococcus magnus (protein L).The mechanisms used to evade the adaptive immune system are more complicated. The simplest approach is to rapidly change non-essential epitopes (amino acids and/or sugars) on the surface of the pathogen, while keeping essential epitopes concealed. This is called antigenic variation. An example is HIV, which mutates rapidly, so the proteins on its viral envelope that are essential for entry into its host target cell are constantly changing. These frequent changes in antigens may explain the failures of vaccines directed at this virus. The parasite Trypanosoma brucei uses a similar strategy, constantly switching one type of surface protein for another, allowing it to stay one step ahead of the antibody response. Masking antigens with host molecules is another common strategy for avoiding detection by the immune system. In HIV, the envelope that covers the virion is formed from the outermost membrane of the host cell; such "self-cloaked" viruses make it difficult for the immune system to identify them as "non-self" structures.

Question: What is the pathogen shielded from during its life-cycle?
Answer: immune cells, antibodies and complement
In its original American broadcast on October 15, 2009, "Sister City" was seen by 4.69 million household viewers, according to Nielsen Media Research. It was a drop from the previous week's episode, "Practice Date". "Sister City" received a 2.0 rating/6 share among viewers aged between 18 and 49. The episode received generally positive reviews. Entertainment Weekly writer Henning Fog said "Sister City" continued a trend of excellence in the second season that has established Parks and Recreation as NBC's best comedy. Fog said the episode also further expanded its characters, by showing Leslie is not a complete pushover and Tom is a kind person.Salon.com writer Heather Havrilesky called the episode an "instant classic", and particularly praised the guest performance of Fred Armisen. She said the episode "benefits from the show's writers' increasing habit of giving everything from political scandals to lame local events the Onion treatment". Alan Sepinwall of The Star-Ledger said it was "another strong one", and said the Leslie character is growing less clueless and more three-dimensional. Robert Philpot of the Fort Worth Star-Telegram said he believed the show still too closely resembled The Office, but that "Sister City" "showed that Parks and Recreation can equal The Office for comic discomfort". Fowler of IGN said the anti-American sentiment demonstrated by the Venezuelan delegation "was a funny twist that didn't completely wear itself out, although it came close". Fowler particularly praised Armisen, who he said risked overshadowing the regular cast, and the sardonic comedy of Plaza. Not all reviews were positive. The A.V. Club writer Leonard Pierce, who said he felt the second season had been excellent so far, described "Sister City" as "easily the weakest episode of the season, maybe the series". Pierce called the political overtones "ham-handed", the humor was too over-the-top, and the episode suffered from the absence of most of the supporting cast.

Question: When did Sister City premier?
Answer: October 15, 2009
Leslie calls a meeting and apologizes to Raul, who in turn apologizes as well and offers Leslie a check for $35,000 to fill in the pit. Leslie fears it may be "dirty money", but accepts. During a photo opportunity later, Raul sets up a video camera and asks Leslie say "Viva Venezuela" and "Viva Chavez" to it. Against her wishes, Leslie reluctantly does so. When Raul starts speaking Spanish to the camera, Leslie asks April to translate, and learns Raul is discussing his "Committee to Humiliate and Shame America". A furious Leslie tears up the $35,000 check and shouts "Viva America", prompting Raul to declare Pawnee is no longer their sister city and storm out. Leslie insists she will raise the money to build the park without them and Tom, inspired by her example, secretly puts all the tip money he made from the Venezuelans into the park donation jar. The episode ends with Leslie and Tom later receiving an online video from April, who tells them she and Donna are vacationing with Jhonny (JC Gonzalez) in his Venezuelan palace, which is watched over by armed guards.

Question: What type of people are protecting Toms Venezuelan palace?
Answer: armed guards