document_title: Acid rain

question_text: where does acid rain fall in the us

question_tokens: where does acid rain fall in the us

text: Acid rain

text: Definition

text: "Acid rain" is a popular term referring to the deposition of a mixture from wet (rain, snow, sleet, fog, cloudwater, and dew) and dry (acidifying particles and gases) acidic components. Distilled water, once carbon dioxide is removed, has a neutral pH of 7. Liquids with a pH less than 7 are acidic, and those with a pH greater than 7 are alkaline. "Clean" or unpolluted rain has an acidic pH, but usually no lower than 5.7, because carbon dioxide and water in the air react together to form carbonic acid, a weak acid according to the following reaction:

text: Carbonic acid then can ionize in water forming low concentrations of hydronium and carbonate ions:

text: However, unpolluted rain can also contain other chemicals which affect its pH (acidity level). A common example is nitric acid produced by electric discharge in the atmosphere such as lightning.[1] Acid deposition as an environmental issue (discussed later in the article) would include additional acids other than H2CO3.

text: History

text: The corrosive effect of polluted, acidic city air on limestone and marble was noted in the 17th century by John Evelyn, who remarked upon the poor condition of the Arundel marbles.[2] Since the Industrial Revolution, emissions of sulfur dioxide and nitrogen oxides into the atmosphere have increased.[3][4] In 1852, Robert Angus Smith was the first to show the relationship between acid rain and atmospheric pollution in Manchester, England.[5]

text: Though acidic rain was discovered in 1853, it was not until the late 1960s that scientists began widely observing and studying the phenomenon.[6] The term "acid rain" was coined in 1872 by Robert Angus Smith.[7] Canadian Harold Harvey was among the first to research a "dead" lake. Public awareness of acid rain in the U.S increased in the 1970s after The New York Times published reports from the Hubbard Brook Experimental Forest in New Hampshire of the myriad deleterious environmental effects shown to result from it.[8][9]

text: Occasional pH readings in rain and fog water of well below 2.4 have been reported in industrialized areas.[3] Industrial acid rain is a substantial problem in China and Russia[10][11] and areas downwind from them. These areas all burn sulfur-containing coal to generate heat and electricity.[12]

text: The problem of acid rain has not only increased with population and industrial growth, but has become more widespread. The use of tall smokestacks to reduce local pollution has contributed to the spread of acid rain by releasing gases into regional atmospheric circulation.[13][14] Often deposition occurs a considerable distance downwind of the emissions, with mountainous regions tending to receive the greatest deposition (simply because of their higher rainfall). An example of this effect is the low pH of rain which falls in Scandinavia.

text: In the United States

text: The earliest report about acid rain in the United States was from the chemical evidence from Hubbard Brook Valley. In 1972, a group of scientists including Gene Likens discovered the rain that was deposited at White Mountains of New Hampshire was acidic. The pH of the sample was measured to be 4.03 at Hubbard Brook.[16] The Hubbard Brook Ecosystem Study followed up with a series of research that analyzed the environmental effects of acid rain. Acid rain that mixed with stream water at Hubbard Brook was neutralized by the alumina from soils.[17] The result of this research indicates the chemical reaction between acid rain and aluminum leads to increasing rate of soil weathering. Experimental research was done to examine the effects of increased acidity in stream on ecological species. In 1980, a group of scientists modified the acidity of Norris Brook, New Hampshire, and observed the change in species’ behaviors. There was a decrease in species diversity, an increase in community dominants, and a decrease in the food web complexity.[18]

text: In 1980, the U.S. Congress passed an Acid Deposition Act.[19] This Act established an 18-year assessment and research program under the direction of the National Acidic Precipitation Assessment Program (NAPAP). NAPAP looked at the entire problem from a scientific perspective. It enlarged a network of monitoring sites to determine how acidic the precipitation actually was, and to determine long-term trends, and established a network for dry deposition. It looked at the effects of acid rain and funded research on the effects of acid precipitation on freshwater and terrestrial ecosystems, historical buildings, monuments, and building materials. It also funded extensive studies on atmospheric processes and potential control programs.

text: From the start, policy advocates from all sides attempted to influence NAPAP activities to support their particular policy advocacy efforts, or to disparage those of their opponents.[19] For the U.S. Government's scientific enterprise, a significant impact of NAPAP were lessons learned in the assessment process and in environmental research management to a relatively large group of scientists, program managers and the public.[20]

text: In 1981, the National Academy of Sciences was looking into research about the controversial issues regarding acid rain.[21] President Ronald Reagan did not place a huge attention on the issues of acid rain[22] until his personal visit to Canada and confirmed that Canadian border suffered from the drifting pollution from smokestacks in Midwest of US. Reagan honored the agreement to Canadian Prime Minister Pierre Trudeau’s enforcement of anti-pollution regulation.[23] In 1982, US President Ronald Reagan commissioned William Nierenberg to sit on National Science Board.[24] Nierenberg selected scientists including Gene Likens to sit on a panel to draft a report on acid rain. In 1983, the panel of scientists came up with a draft report, which concluded that acid rain is a real problem and solutions should be sought.[25] White House Office of Science and Technology Policy reviewed the draft report and sent Fred Singer’s suggestions of the report, which cast doubt on the cause of acid rain.[26] The panelists revealed rejections against Singer’s positions and submitted the report to Nirenberg in April. In May 1983, the House of Representatives voted against legislations that aimed to control sulfur emissions. There was a debate about whether Nierenberg delayed to release the report. Nierenberg himself denied the saying about his suppression of the report and explained that the withheld of the report after the House's vote was due to the fact that the report was not ready to be published.[27]

text: In 1991, DENR provided its first assessment of acid rain in the United States. It reported that 5% of New England Lakes were acidic, with sulfates being the most common problem. They noted that 2% of the lakes could no longer support Brook Trout, and 6% of the lakes were unsuitable for the survival of many species of minnow. Subsequent Reports to Congress have documented chemical changes in soil and freshwater ecosystems, nitrogen saturation, decreases in amounts of nutrients in soil, episodic acidification, regional haze, and damage to historical monuments.

text: Meanwhile, in 1989, the U.S. Congress passed a series of amendments to the Clean Air Act. Title IV of these amendments established the Acid Rain Program, a cap and trade system designed to control emissions of sulfur dioxide and nitrogen oxides. Title IV called for a total reduction of about 10 million tons of SO2 emissions from power plants. It was implemented in two phases. Phase I began in 1995, and limited sulfur dioxide emissions from 110 of the largest power plants to a combined total of 8.7 million tons of sulfur dioxide. One power plant in New England (Merrimack) was in Phase I. Four other plants (Newington, Mount Tom, Brayton Point, and Salem Harbor) were added under other provisions of the program. Phase II began in 2000, and affects most of the power plants in the country.

text: During the 1990s, research continued. On March 10, 2005, the EPA issued the Clean Air Interstate Rule (CAIR). This rule provides states with a solution to the problem of power plant pollution that drifts from one state to another. CAIR will permanently cap emissions of SO2 and NOx in the eastern United States. When fully implemented, CAIR will reduce SO2 emissions in 28 eastern states and the District of Columbia by over 70% and NOx emissions by over 60% from 2003 levels.[28]

text: Overall, the program's cap and trade program has been successful in achieving its goals. Since the 1990s, SO2 emissions have dropped 40%, and according to the Pacific Research Institute, acid rain levels have dropped 65% since 1976.[29][30] Conventional regulation was used in the European Union, which saw a decrease of over 70% in SO2 emissions during the same time period.[31]

text: In 2007, total SO2 emissions were 8.9 million tons, achieving the program's long-term goal ahead of the 2010 statutory deadline.[32]

text: In 2007 the EPA estimated that by 2010, the overall costs of complying with the program for businesses and consumers would be $1 billion to $2 billion a year, only one fourth of what was originally predicted.[29] Forbes says: In 2010, by which time the cap and trade system had been augmented by the George W. Bush administration’s Clean Air Interstate Rule, SO2 emissions had fallen to 5.1 million tons. [33]

text: The term Citizen science can be traced back as far as January 1989 and a campaign by the Audubon Society to measure Acid rain. Scientist Muki Haklay cites in a policy report for the Wilson Center entitled 'Citizen Science and Policy: A European Perspective' a first use of the term 'citizen science' by R. Kerson in the magazine MIT Technology Review from January 1989.[34][35] Quoting from the Wilson Center report: "The new form of engagement in science received the name "citizen science". The first recorded example of the use of the term is from 1989, describing how 225 volunteers across the US collected rain samples to assist the Audubon Society in an acid-rain awareness raising campaign. The volunteers collected samples, checked for acidity, and reported back to the organization. The information was then used to demonstrate the full extent of the phenomenon."[34][35]

text: Emissions of chemicals leading to acidification

text: The most important gas which leads to acidification is sulfur dioxide. Emissions of nitrogen oxides which are oxidized to form nitric acid are of increasing importance due to stricter controls on emissions of sulfur containing compounds. 70 Tg(S) per year in the form of SO2 comes from fossil fuel combustion and industry, 2.8 Tg(S) from wildfires and 7–8 Tg(S) per year from volcanoes.[36]

text: Natural phenomena

text: The principal natural phenomena that contribute acid-producing gases to the atmosphere are emissions from volcanoes. Thus, for example, fumaroles from the Laguna Caliente crater of Poás Volcano create extremely high amounts of acid rain and fog, with acidity as high as a pH of 2, clearing an area of any vegetation and frequently causing irritation to the eyes and lungs of inhabitants in nearby settlements. Acid-producing gasses are also created by biological processes that occur on the land, in wetlands, and in the oceans. The major biological source of sulfur containing compounds is dimethyl sulfide.

text: Nitric acid in rainwater is an important source of fixed nitrogen for plant life, and is also produced by electrical activity in the atmosphere such as lightning.

text: Acidic deposits have been detected in glacial ice thousands of years old in remote parts of the globe.[13]

text: Soils of coniferous forests are naturally very acidic due to the shedding of needles, and the results of this phenomenon should not be confused with acid rain.

text: Human activity

text: The principal cause of acid rain is sulfur and nitrogen compounds from human sources, such as electricity generation, factories, and motor vehicles. Electrical power generation using coal is among the greatest contributors to gaseous pollutions that are responsible for acidic rain. The gases can be carried hundreds of kilometers in the atmosphere before they are converted to acids and deposited. In the past, factories had short funnels to let out smoke but this caused many problems locally; thus, factories now have taller smoke funnels. However, dispersal from these taller stacks causes pollutants to be carried farther, causing widespread ecological damage.

text: Chemical processes

text: Combustion of fuels produces sulfur dioxide and nitric oxides. They are converted into sulfuric acid and nitric acid.[37]

text: Gas phase chemistry

text: In the gas phase sulfur dioxide is oxidized by reaction with the hydroxyl radical via an intermolecular reaction:[5]

text: which is followed by:

text: In the presence of water, sulfur trioxide (SO3) is converted rapidly to sulfuric acid:

text: Nitrogen dioxide reacts with OH to form nitric acid:

text: Chemistry in cloud droplets

text: When clouds are present, the loss rate of SO2 is faster than can be explained by gas phase chemistry alone. This is due to reactions in the liquid water droplets.

text: Sulfur dioxide dissolves in water and then, like carbon dioxide, hydrolyses in a series of equilibrium reactions:

text: There are a large number of aqueous reactions that oxidize sulfur from S(IV) to S(VI), leading to the formation of sulfuric acid. The most important oxidation reactions are with ozone, hydrogen peroxide and oxygen (reactions with oxygen are catalyzed by iron and manganese in the cloud droplets).[5]

text: Acid deposition

text: Wet deposition

text: Wet deposition of acids occurs when any form of precipitation (rain, snow, and so on.) removes acids from the atmosphere and delivers it to the Earth's surface. This can result from the deposition of acids produced in the raindrops (see aqueous phase chemistry above) or by the precipitation removing the acids either in clouds or below clouds. Wet removal of both gases and aerosols are both of importance for wet deposition.

text: Dry deposition

text: Acid deposition also occurs via dry deposition in the absence of precipitation. This can be responsible for as much as 20 to 60% of total acid deposition.[38] This occurs when particles and gases stick to the ground, plants or other surfaces.

text: Adverse effects

text: Acid rain has been shown to have adverse impacts on forests, freshwaters and soils, killing insect and aquatic life-forms as well as causing damage to buildings and having impacts on human health.

text: Surface waters and aquatic animals

text: Both the lower pH and higher aluminium concentrations in surface water that occur as a result of acid rain can cause damage to fish and other aquatic animals. At pHs lower than 5 most fish eggs will not hatch and lower pHs can kill adult fish. As lakes and rivers become more acidic biodiversity is reduced. Acid rain has eliminated insect life and some fish species, including the brook trout in some lakes, streams, and creeks in geographically sensitive areas, such as the Adirondack Mountains of the United States.[39] However, the extent to which acid rain contributes directly or indirectly via runoff from the catchment to lake and river acidity (i.e., depending on characteristics of the surrounding watershed) is variable. The United States Environmental Protection Agency's (EPA) website states: "Of the lakes and streams surveyed, acid rain caused acidity in 75% of the acidic lakes and about 50% of the acidic streams".[39]

text: Soils

text: Soil biology and chemistry can be seriously damaged by acid rain. Some microbes are unable to tolerate changes to low pH and are killed.[40] The enzymes of these microbes are denatured (changed in shape so they no longer function) by the acid. The hydronium ions of acid rain also mobilize toxins such as aluminium, and leach away essential nutrients and minerals such as magnesium.[41]

text: Soil chemistry can be dramatically changed when base cations, such as calcium and magnesium, are leached by acid rain thereby affecting sensitive species, such as sugar maple (Acer saccharum).[42][43]

text: Forests and other vegetation

text: Adverse effects may be indirectly related to acid rain, like the acid's effects on soil (see above) or high concentration of gaseous precursors to acid rain. High altitude forests are especially vulnerable as they are often surrounded by clouds and fog which are more acidic than rain.

text: Other plants can also be damaged by acid rain, but the effect on food crops is minimized by the application of lime and fertilizers to replace lost nutrients. In cultivated areas, limestone may also be added to increase the ability of the soil to keep the pH stable, but this tactic is largely unusable in the case of wilderness lands. When calcium is leached from the needles of red spruce, these trees become less cold tolerant and exhibit winter injury and even death.[44][45]

text: Ocean acidification

text: This section needs expansion. You can help by adding to it. (July 2013)

text: Acid rain has a much less harmful effect on the oceans. However, acid rain can cause the oceans acidity to rise, making it more difficult for different coastal species to create their exoskeletons that they need to survive. These coastal species link together as part of the ocean's food chain and without them being a source for other marine life to feed off of more marine life will die.[46]

text: Coral's limestone skeletal is sensitive to pH drop, because the calcium carbonate, core component of the limestone dissolves in acidic (low pH) solutions.

text: Human health effects

text: Acid rain does not directly affect human health. The acid in the rainwater is too dilute to have direct adverse effects. However, the particulates responsible for acid rain (sulfur dioxide and nitrogen oxides) do have an adverse effect. Increased amounts of fine particulate matter in the air do contribute to heart and lung problems including asthma and bronchitis.[47]

text: Other adverse effects

text: Acid rain can damage buildings, historic monuments, and statues, especially those made of rocks, such as limestone and marble, that contain large amounts of calcium carbonate. Acids in the rain react with the calcium compounds in the stones to create gypsum, which then flakes off.

text: The effects of this are commonly seen on old gravestones, where acid rain can cause the inscriptions to become completely illegible. Acid rain also increases the corrosion rate of metals, in particular iron, steel, copper and bronze.[48][49]

text: Affected areas

text: Places significantly impacted by acid rain around the globe include most of eastern Europe from Poland northward into Scandinavia,[50] the eastern third of the United States,[51] and southeastern Canada. Other affected areas include the southeastern coast of China and Taiwan.[citation needed]

text: Prevention methods

text: Technical solutions

text: Many coal-firing power stations use flue-gas desulfurization (FGD) to remove sulfur-containing gases from their stack gases. For a typical coal-fired power station, FGD will remove 95% or more of the SO2 in the flue gases. An example of FGD is the wet scrubber which is commonly used. A wet scrubber is basically a reaction tower equipped with a fan that extracts hot smoke stack gases from a power plant into the tower. Lime or limestone in slurry form is also injected into the tower to mix with the stack gases and combine with the sulfur dioxide present. The calcium carbonate of the limestone produces pH-neutral calcium sulfate that is physically removed from the scrubber. That is, the scrubber turns sulfur pollution into industrial sulfates.

text: In some areas the sulfates are sold to chemical companies as gypsum when the purity of calcium sulfate is high. In others, they are placed in landfill. However, the effects of acid rain can last for generations, as the effects of pH level change can stimulate the continued leaching of undesirable chemicals into otherwise pristine water sources, killing off vulnerable insect and fish species and blocking efforts to restore native life.

text: Fluidized bed combustion also reduces the amount of sulfur emitted by power production.

text: Vehicle emissions control reduces emissions of nitrogen oxides from motor vehicles.

text: International treaties

text: A number of international treaties on the long-range transport of atmospheric pollutants have been agreed for example, the 1985 Helsinki Protocol on the Reduction of Sulphur Emissions under the Convention on Long-Range Transboundary Air Pollution. Canada and the US signed the Air Quality Agreement in 1991. Most European countries and Canada have signed the treaties.

text: Emissions trading

text: In this regulatory scheme, every current polluting facility is given or may purchase on an open market an emissions allowance for each unit of a designated pollutant it emits. Operators can then install pollution control equipment, and sell portions of their emissions allowances they no longer need for their own operations, thereby recovering some of the capital cost of their investment in such equipment. The intention is to give operators economic incentives to install pollution controls.

text: The first emissions trading market was established in the United States by enactment of the Clean Air Act Amendments of 1990. The overall goal of the Acid Rain Program established by the Act[52] is to achieve significant environmental and public health benefits through reductions in emissions of sulfur dioxide (SO2) and nitrogen oxides (NOx), the primary causes of acid rain. To achieve this goal at the lowest cost to society, the program employs both regulatory and market based approaches for controlling air pollution.


document_title: Bovine spongiform encephalopathy

question_text: when was bse first observed in great britain

root

text: Bovine spongiform encephalopathy

text: Classification[edit]

text: BSE is a transmissible disease that primarily affects the central nervous system; it is a form of transmissible spongiform encephalopathy, like Creutzfeldt–Jakob disease and kuru in humans and scrapie in sheep, and chronic wasting disease in cervids.[16][17][18]

tag: p

text: Signs and symptoms[edit]

text: Symptoms are not seen immediately in cattle due to the diseases’ extremely long incubation period.[19] Some cattle have been observed to have an abnormal gait, changes in behavior, tremors and hyper-responsiveness to certain stimuli.[20] Hindlimb ataxia affects the animal’s gait and occurs when muscle control is lost. This results in poor balance and coordination.[21] Behavioural changes may include aggression, anxiety relating to certain situations, nervousness, frenzy or an overall change in temperament. Some rare but previously observed symptoms also include persistent pacing, rubbing or licking. Additionally, nonspecific symptoms have also been observed which include weight loss, decreased milk production, lameness, ear infections and teeth grinding due to pain. Some animals may show a combination of these symptoms, while others may only be observed demonstrating one of the many reported. Once clinical symptoms arise, they typically get worse over the upcoming weeks and months, eventually leading to recumbency, coma and death.[20]

text: Cause[edit]

text: The infectious agent in BSE is a specific type of misfolded protein called a prion.[17]

text: Prions can be transmitted to humans by eating food contaminated with them.[17]

text: Prions are not destroyed even if the beef or material containing them is cooked or heat-treated. Prion proteins carry the disease between individuals and cause deterioration of the brain.[22] Transmissible spongiform encephalopathy (TSE)s like BSE can arise in animals that carry an allele which causes previously normal protein molecules to contort by themselves from an alpha helical arrangement to a beta pleated sheet, which is the disease-causing shape for the particular protein[citation needed]. Transmission can occur when healthy animals come in contact with tainted tissues from others with the disease. In the brain, these proteins cause native cellular prion protein to deform into the infectious state, which then goes on to deform further prion protein in an exponential cascade. This results in protein aggregates, which then form dense plaque fibers leading to the microscopic appearance of "holes" in the brain, degeneration of physical and mental abilities, and ultimately death[citation needed].

text: Different hypotheses exist for the origin of prion proteins in cattle. Two leading hypotheses suggest it may have jumped species from the disease scrapie in sheep, or that it evolved from a spontaneous form of "mad cow disease" that has been seen occasionally in cattle for many centuries.[23] In the 5th century BC, Hippocrates described a similar illness in cattle and sheep, which he believed also occurred in man.[24] Publius Flavius Vegetius Renatus recorded cases of a disease with similar characteristics in the fourth and fifth centuries AD.[25] The British Government enquiry took the view the cause was not scrapie, as had originally been postulated, but was some event in the 1970s that was not possible to identify.[26]

text: Other theories state that the agent is a virus,[27] virino,[28] Spiroplasma species, or Acinetobacter species.[29]

text: Pathogenesis[edit]

text: The pathogenesis of BSE is not well understood or documented like other diseases of this nature. Even though BSE is a disease that results in neurological defects, its pathogenesis occurs in areas that reside outside of the nervous system.[30] There was a strong deposition of PrPSc initially located in the Ileal Peyer’s patches of the small intestine.[31] The lymphatic system has been identified in the pathogenesis of scrapies, it has not, however, been determined to be an essential part of the pathogenesis of BSE. The Ileal Peyer’s patches have been the only organ from this system that has been found to play a major role in the pathogenesis.[30] Infectivity of the Ileal Peyer's patches has been observed as early as 4 months after inoculation.[31] PrPSc accumulation was found to occur mostly in tangible body macrophages of the Ileal Peyer’s patches. Tangible body macrophages involved in PrPSc clearance are thought to play a role in PrPSc accumulation in the Peyer’s patches. Accumulation of PrPSc was also found in follicular dendritic cells; however, it was of a lesser degree.[32] Six months after inoculation, there was no infectivity in any tissues, only that of the ileum. This led researchers to believe that the disease agent replicates here. In naturally confirmed cases, there have been no reports of infectivity in the Ileal Peyer’s patches. Generally, in clinical experiments, high doses of the disease are administered. In natural cases, it was hypothesized that low doses of the agent were present, and therefore, infectivity could not be observed.[33]

text: Diagnosis[edit]

text: Diagnosis of BSE continues to be a practical problem. It has an incubation period of months to years, during which no symptoms are noticed, though the pathway of converting the normal brain prion protein (PrP) into the toxic, disease-related PrPSc form has started. At present, virtually no way is known to detect PrPSc reliably except by examining post mortem brain tissue using neuropathological and immunohistochemical methods. Accumulation of the abnormally folded PrPSc form of PrP is a characteristic of the disease, but it is present at very low levels in easily accessible body fluids such as blood or urine. Researchers have tried to develop methods to measure PrPSc, but no methods for use in materials such as blood have been accepted fully.[by whom?]

text: The traditional method of diagnosis relies on histopathological examination of the medulla oblongata of the brain, and other tissues, post mortem. Immunohistochemistry can be used to demonstrate prion protein accumulation.[34]

text: In 2010, a team from New York described detection of PrPSc even when initially present at only one part in a hundred billion (10−11) in brain tissue. The method combines amplification with a novel technology called surround optical fiber immunoassay and some specific antibodies against PrPSc. After amplifying and then concentrating any PrPSc, the samples are labelled with a fluorescent dye using an antibody for specificity and then finally loaded into a microcapillary tube. This tube is placed in a specially constructed apparatus so it is totally surrounded by optical fibres to capture all light emitted once the dye is excited using a laser. The technique allowed detection of PrPSc after many fewer cycles of conversion than others have achieved, substantially reducing the possibility of artifacts, as well as speeding up the assay. The researchers also tested their method on blood samples from apparently healthy sheep that went on to develop scrapie. The animals’ brains were analysed once any symptoms became apparent. The researchers could, therefore, compare results from brain tissue and blood taken once the animals exhibited symptoms of the diseases, with blood obtained earlier in the animals’ lives, and from uninfected animals. The results showed very clearly that PrPSc could be detected in the blood of animals long before the symptoms appeared. After further development and testing, this method could be of great value in surveillance as a blood- or urine-based screening test for BSE.[35][36]

text: Prevention[edit]

text: A ban on feeding meat and bone meal to cattle has resulted in a strong reduction in cases in countries where the disease was present. In disease-free countries, control relies on import control, feeding regulations, and surveillance measures.[34]

text: In UK and US slaughterhouses, the brain, spinal cord, trigeminal ganglia, intestines, eyes, and tonsils from cattle are classified as specified risk materials, and must be disposed of appropriately.[34]

text: An enhanced BSE-related feed ban is in effect in both the United States and Canada to help improve prevention and elimination of BSE.[37]

text: Treatment[edit]

text: As of 2015 there was no cure for BSE; some of the symptoms like twitching can be managed but otherwise treatment is palliative care.[38]

text: Epidemiology[edit]

text: The table to the right summarizes reported cases of BSE and of vCJD by country. (The vCJD column is by country of residence of patient at time of diagnosis and not suspected origin of beef.) BSE is the disease in cattle, while vCJD is the disease in people.

text: The tests used for detecting BSE vary considerably, as do the regulations in various jurisdictions for when, and which cattle, must be tested. For instance in the EU, the cattle tested are older (30 months or older), while many cattle are slaughtered younger than that. At the opposite end of the scale, Japan tests all cattle at the time of slaughter. Tests are also difficult, as the altered prion protein has very low levels in blood or urine, and no other signal has been found. Newer tests[specify] are faster, more sensitive, and cheaper, so future figures possibly may be more comprehensive. Even so, currently the only reliable test is examination of tissues during a necropsy.

text: As for vCJD in humans, autopsy tests are not always done, so those figures, too, are likely to be too low, but probably by a lesser fraction. In the United Kingdom, anyone with possible vCJD symptoms must be reported to the Creutzfeldt–Jakob Disease Surveillance Unit. In the United States, the CDC has refused to impose a national requirement that physicians and hospitals report cases of the disease. Instead, the agency relies on other methods, including death certificates and urging physicians to send suspicious cases to the National Prion Disease Pathology Surveillance Center (NPDPSC) at Case Western Reserve University in Cleveland, which is funded by the CDC.

text: To control potential transmission of vCJD within the United States, the American Red Cross has established strict restrictions on individuals' eligibility to donate blood. Individuals who have spent a cumulative time of 3 months or more in the United Kingdom between 1980 and 1996, or a cumulative time of 5 years or more from 1980 to present in any combination of countries in Europe, are prohibited from donating blood.[39]

text: North America[edit]

text: The first reported case in North America was in December 1993 from Alberta, Canada.[40][41] Another Canadian case was reported in May 2003. The first known U.S. occurrence came in December of the same year, though it was later confirmed to be a cow of Canadian origin imported to the U.S.[42] Canada announced two additional cases of BSE from Alberta in early 2005.[43] In June 2005, John R. Clifford, chief veterinary officer for the United States Department of Agriculture animal health inspection service, confirmed a fully domestic case of BSE in Texas.[44]

text: Practices in the United States relating to BSE[edit]

text: Soybean meal is cheap and plentiful in the United States. Cottonseed meal, 1.5 million tons of which are produced in the U.S. every year, none of which is suitable for humans or any other simple-stomach animals, is even cheaper than soybean meal. Historically, meat and bone meal, blood meal, and meat scraps have almost always commanded a higher price as a feed additive than oilseed meals in the U.S., so not much incentive existed to use animal products to feed ruminants. As a result, the use of animal byproduct feeds was never common, as it was in Europe. However, U.S. regulations only partially prohibited the use of animal byproducts in feed. In 1997, regulations prohibited the feeding of mammalian byproducts to ruminants such as cattle and goats. However, the byproducts of ruminants can still be legally fed to pets or other livestock, including pigs and poultry. In addition, it is legal for ruminants to be fed byproducts from some of these animals.[45] Because of this, some authors have suggested that under certain conditions, it is still possible for BSE incidence to increase in U.S. cattle.[46] A proposal to end the use of cattle blood, restaurant scraps, and poultry litter (fecal matter, feathers, bedding material)[47] in January 2004 has yet to be implemented.[48][needs update]

text: In February 2001, the US Government Accountability Office reported the FDA, which is responsible for regulating feed, had not adequately enforced the various bans.[49] Compliance with the regulations was shown to be extremely poor before the discovery of a cow in Washington infected with BSE in 2003, but industry representatives report that compliance is now total. Even so, critics call the partial prohibitions insufficient. Indeed, US meat producer Creekstone Farms was forcibly prevented from conducting BSE testing by the USDA, which under an obscure 1913 law had the authority to restrict sales of BSE testing kits, allegedly to protect other producers from being forced to conduct the same tests to stay competitive.[50]

text: The USDA has issued recalls of beef supplies that involved introduction of downer cows into the food supply. Hallmark/Westland Meat Packing Company was found to have used electric shocks to prod downer cows into the slaughtering system in 2007.[51] Possibly due to pressure from large agribusiness, the United States has drastically cut back on the number of cows inspected for BSE.[52]

text: Effect on the US beef industry[edit]

text: This section needs to be updated. Please update this article to reflect recent events or newly available information. (November 2016)

tag: table

text: Japan was the top importer of US beef, buying 240,000 tons valued at $1.4 billion in 2003.[citation needed] After the discovery of the first case of BSE in the US on 23 December 2003, Japan halted US beef imports. In December 2005, Japan once again allowed imports of US beef, but reinstated its ban in January 2006 after a violation of the US-Japan beef import agreement: a vertebral column, which should have been removed prior to shipment, was included in a shipment of veal.

text: Tokyo yielded to US pressure to resume imports, ignoring consumer worries about the safety of US beef, said Japanese consumer groups. Michiko Kamiyama from Food Safety Citizen Watch and Yoko Tomiyama from Consumers Union of Japan[53] said about this: "The government has put priority on the political schedule between the two countries, not on food safety or human health."

text: Sixty-five nations implemented full or partial restrictions on importing US beef products because of concerns that US testing lacked sufficient rigor. As a result, exports of US beef declined from 1,300,000 metric tons in 2003, (before the first mad cow was detected in the US) to 322,000 metric tons in 2004. This has increased since then to 771,000 metric tons in 2007.[54]

text: On 31 December 2006, Hematech, Inc, a biotechnology company based in Sioux Falls, South Dakota, announced it had used genetic engineering and cloning technology to produce cattle that lacked a necessary gene for prion production – thus theoretically making them immune to BSE.[55]

text: In April 2012, some South Korean retailers ceased importing beef from the United States after a case of BSE was reported.[56] Indonesia also suspended imports of beef from the US after a dairy cow with mad cow disease was discovered in California.[57]

text: Japan[edit]

text: With 36 confirmed cases, Japan experienced one of the largest number of cases of BSE outside Europe.[58] It was the only country outside Europe and the Americas to report non-imported cases.[59] Reformation of food safety in light of the BSE cases resulted in the establishment of a governmental Food Safety Commission in 2003.[60]

text: Europe[edit]

text: Cattle are naturally herbivores, eating grasses. In modern industrial cattle-farming, though, various commercial feeds are used, which may contain ingredients including antibiotics, hormones, pesticides, fertilizers, and protein supplements. The use of meat and bone meal, produced from the ground and cooked leftovers of the slaughtering process, as well as from the carcasses of sick and injured animals such as cattle or sheep, as a protein supplement in cattle feed was widespread in Europe prior to about 1987.[4] Worldwide, soybean meal is the primary plant-based protein supplement fed to cattle. However, soybeans do not grow well in Europe, so cattle raisers throughout Europe turned to the cheaper animal byproduct feeds as an alternative. The British Inquiry dismissed suggestions that changes to processing might have increased the infectious agents in cattle feed, saying, "changes in process could not have been solely responsible for the emergence of BSE, and changes in regulation were not a factor at all."[61] (The prion causing BSE is not destroyed by heat treatment.)

text: The first confirmed instance in which an animal fell ill with the disease occurred in 1986 in the United Kingdom, and lab tests the following year indicated the presence of BSE; by November 1987, the British Ministry of Agriculture accepted it had a new disease on its hands.[62] Subsequently, 177 people (as of June 2014) contracted and died of a disease with similar neurological symptoms subsequently called (new) variant Creutzfeldt–Jakob disease (vCJD).[6][63] This is a separate disease from 'classical' Creutzfeldt–Jakob disease, which is not related to BSE and has been known about since the early 1900s. Three cases of vCJD occurred in people who had lived in or visited the UK – one each in the Republic of Ireland, Canada, and the United States of America. Also, some concern existed about those who work with (and therefore inhale) cattle meat and bone meal, such as horticulturists, who use it as fertilizer. Up-to-date statistics on all types of CJD are published by the National Creutzfeldt–Jakob Disease Surveillance Unit in Edinburgh, Scotland.

text: For many of the vCJD patients, direct evidence exists that they had consumed tainted beef, and this is assumed to be the mechanism by which all affected individuals contracted it.[citation needed] Disease incidence also appears to correlate with slaughtering practices that led to the mixture of nervous system tissue with ground meat (mince) and other beef. An estimated 400,000 cattle infected with BSE entered the human food chain in the 1980s.[citation needed] Although the BSE epizootic was eventually brought under control by culling all suspect cattle populations, people are still being diagnosed with vCJD each year (though the number of new cases currently has dropped to fewer than five per year). This is attributed to the long incubation period for prion diseases, which is typically measured in years or decades. As a result, the full extent of the human vCJD outbreak is still not known.

text: The scientific consensus is that infectious BSE prion material is not destroyed through cooking procedures, meaning that even contaminated beef foodstuffs prepared "well done" may remain infectious.[64][65] In fact the infectious agent remains viable over 600 °C (1,112 °F).

text: Alan Colchester, a professor of neurology at the University of Kent, and Nancy Colchester, writing in the 3 September 2005 issue of the medical journal The Lancet, proposed a theory that the most likely initial origin of BSE in the United Kingdom was the importation from the Indian Subcontinent of bone meal which contained CJD-infected human remains.[66] The government of India vehemently responded to the research, calling it "misleading, highly mischievous; a figment of imagination; absurd," further adding that India maintained constant surveillance and had not had a single case of either BSE or vCJD.[67][68] The authors responded in the 22 January 2006 issue of The Lancet that their theory is unprovable only in the same sense as all other BSE origin theories are and that the theory warrants further investigation.[69]

text: During the course of the investigation into the BSE epizootic, an enquiry was also made into the activities of the Department of Health Medicines Control Agency (MCA). On 7 May 1999, David Osborne Hagger, a retired civil servant who worked in the Medicines Division of the Department of Health between 1984 and 1994, produced a written statement to the BSE Inquiry in which he gave an account of his professional experience of BSE.[70]

text: In February 1989, the MCA had been asked to "identify relevant manufacturers and obtain information about the bovine material contained in children’s vaccines, the stocks of these vaccines and how long it would take to switch to other products." In July, "[the] use of bovine insulin in a small group of mainly elderly patients was noted and it was recognised that alternative products for this group were not considered satisfactory." In September, the BSE Working Party of the Committee on the Safety of Medicines (CSM) recommended that "no licensing action is required at present in regard to products produced from bovine material or using prepared bovine brain in nutrient media and sourced from outside the United Kingdom, the Channel Isles and the Republic of Ireland provided that the country of origin is known to be free of BSE, has competent veterinary advisers and is known to practise good animal husbandry."

text: In 1990, the British Diabetic Association became concerned regarding the safety of bovine insulin. The CSM assured them "[that] there was no insulin sourced from cattle in the UK or Ireland and that the situation in other countries was being monitored."

text: In 1991, the European Commission "[expressed] concerns about the possible transmission of the BSE/scrapie agent to man through use of certain cosmetic treatments."

text: Although most of the publicity accrued to the British epidemic, the highest number of confirmed cases was actually in France. In 1992, sources in France reported to the MCA "that BSE had now been reported in France and there were some licensed surgical sutures derived from French bovine material." Concerns were also raised at a CSM meeting "regarding a possible risk of transmission of the BSE agent in gelatin products."[70] For many years the French government and agricultural industry downplayed the extent of the epidemic, claiming just 923 confirmed cases. In 2004 this figure was challenged in an article in The Review of Veterinary Research which put the figure at 300,000.[71][72] The scientists behind this study later heavily criticised the surveillance system, indicating they believed there had been an official cover-up.[3] Epidemiologist Jean-Louis Thillier eventually concluded that between 1996 and 2006, over 300,000 cases of BSE had infected the national herd and that nine French people had died unnecessarily from the epidemic through the failure to report cases,[73] a finding accepted by the judge who ordered the report.[74]

text: For this failure, France was heavily criticised internationally. Thillier himself queried why there had never been a ban on French beef or basic safety precautions to stop the food chain becoming contaminated, suggesting "Perhaps because the French government forgot its role in guaranteeing the safety of food products, and this neglect cost the lives of nine people."[74] The Sydney Morning Herald added, "while blustering French politicians blamed Britain for the emergence of the disease - and tried to quarantine the country by banning imports of British beef - they failed to adopt measures to prevent a hidden epidemic at home."[75]

text: In 2016 France confirmed a further case of BSE.[76]

text: A number of other countries had isolated outbreaks of BSE confirmed, including Spain, Portugal, Belgium and Germany.[77] However, in all cases, including Britain and France, it is thought the full number of cases is far less than the number reported, so true incidences could be much higher.[3]

text: The ban on British beef[edit]

text: The BSE crisis led to the European Union banning exports of British beef with effect from March 1996; the ban lasted for 10 years before it was finally lifted on 1 May 2006[78] despite attempts in May 1996 by British prime minister John Major to get the ban lifted. The ban resulted in trade controversies between the UK and other EU states, dubbed "beef war" by media.[79] Restrictions remained for beef containing "vertebral material" and for beef sold on the bone.[80] France continued to impose a ban on British beef illegally long after the European Court of Justice had ordered it to lift its blockade, although it has never paid any fine for doing so.[74]

text: Russia was proceeding to lift the ban sometime after November 2012 after 16 years; the announcement was made during a visit by the UK's chief veterinary officer Nigel Gibbens.[81]

text: It was successfully negotiated that beef from Wales was allowed to be exported to the Dutch market, which had formerly been an important market for Northern Irish beef. Of two approved export establishments in the United Kingdom in 1999, one was in Scotland – an establishment to which live beef was supplied from Northern Ireland. As the incidence of BSE was very low in Northern Ireland – only six cases of BSE by 1999 – partly due to the early adoption of an advanced herd tagging and computerization system in the region, calls were made to remove the EU ban on exports with regard to Northern Irish beef.[82]

text: Similar wildcat bans from countries known to have BSE were imposed in various European countries, although these were mostly subsequently ruled illegal. The Economist magazine noted, "Unfortunately, much of the crisis in Europe can be blamed on politicians and bureaucrats. Even while some European countries were clamouring for bans on British beef, they were ignoring warnings from the European Commission about how to avoid the spread of BSE in their own herds."[77]


document_title: List of highest paid film actors

question_text: who is the highest paid actor per movie

question_tokens: who is the highest paid actor per movie

text: List of highest paid film actors

text: Salaries for the world's highest paid film actors currently range from $20–30 million, but an actor can earn substantially more by deferring all or part of their salary against a percentage of the film's gross, known within the industry as a "profit participation" deal. Since not all salaries are made public, this is a non-definitive list of actors who have received $30 million or more as compensation for their services. The figures are given at their nominal value, since earnings from profit based deals are accumulated over many years, making it unfeasible to adjust for inflation.

text:
Highest-earning actors in films

Actor

Film

Year

Salary

Total income

Ref

Keanu Reeves

The Matrix ReloadedThe Matrix Revolutions

2003

$30,000,000

$156,000,000

[1]

Bruce Willis

The Sixth Sense

1999

$14,000,000

$100,000,000

[1]

Tom Cruise

Mission: Impossible 2

2000

$100,000,000

[1]

Tom Cruise

War of the Worlds

2005

$100,000,000

[1]

Will Smith

Men in Black 3

2012

$100,000,000

[2]

Robert Downey, Jr.

Iron Man 3

2013

$75,000,000

[3]

Sandra Bullock

Gravity

2013

$20,000,000

$70,000,000+

[4]

Tom Hanks

Forrest Gump

1994

$70,000,000

[1]

Tom Cruise

Mission: Impossible

1996

$70,000,000

[1]

Harrison Ford

Indiana Jones and the Kingdom of the Crystal Skull

2008

$65,000,000

[5]

Jack Nicholson

Batman

1989

$6,000,000

$60,000,000

[1][6]

Leonardo DiCaprio

Inception

2010

$59,000,000

[7]

Robert Downey, Jr.

Captain America: Civil War

2014

$40,000,000

$40,000,000+

[3]

Robert Downey, Jr.

Avengers: Age of Ultron

2014

$40,000,000

[8]

Johnny Depp

Pirates of the Caribbean: On Stranger Tides

2011

$35,000,000

$55,000,000

[7][9]

Robert Downey, Jr.

The Avengers

2012

$50,000,000

[10]

Cameron Diaz

Bad Teacher

2011

$42,000,000

[11]

Leonardo DiCaprio

Titanic

1997

$40,000,000

[1]

Tom Hanks

Saving Private Ryan

1998

$40,000,000

[1]

Johnny Depp

Alice in Wonderland

2010

$40,000,000

[7]

Aamir Khan

Dangal

2016

$37,000,000+

[nb 1][12][13]

Jim Carrey

Yes Man

2008

$35,000,000

[14]

Arnold Schwarzenegger

Terminator 3: Rise of the Machines

2003

$29,250,000

$30,000,000+

[nb 2][1]

Mel Gibson

Lethal Weapon 4

1998

$30,000,000

$30,000,000

[1]

Brad Pitt

Ocean's Eleven

2001

$10,000,000

$30,000,000

[1]

text:
Jump up ^ ₹257 crore ($37–41 million at 2017 exchange rates).

Jump up ^ Arnold Schwarzenegger received a $29,250,000 salary for Terminator 3 plus a 20% royalty on the worldwide box office gross over $380 million. The film ultimately had a global gross of $433 million.

tag: ol


document_title: Robots (2005 film)

question_text: who does the voice of aunt fanny in robots

text: Robots (2005 film)

text: Plot[edit]

text: This section may require copy editing for grammar, style, cohesion, tone, or spelling. You can assist by editing it. (September 2017) (Learn how and when to remove this template message)

text: In Rivet Town, Rodney Copperbottom is a young inventor who dreams of making the world a better place, like his idol, Bigweld. During Rodney's adolescence, he invents the Wonderbot to help his father, Herb, clean dishes at a restaurant. When Herb's supervisor confronts them, Wonderbot breaks the dishes, causing Herb to be put in debt and Rodney to be dismissed. Rodney takes his invention to Robot City to work as an inventor at Bigweld Industries and help pay his father’s debt. After a spectacular but harrowing ride on the Crosstown Express, Rodney arrives at the gate of Bigweld Industries.

text: He learns that Phineas T. Ratchet has taken over Bigweld Industries and has put an end to manufacturing spare parts. Ratchet believes the company can improve if it focuses on selling upgrades; if the robots refuse, they are sent to the Chop Shop, where they are melted down by the owner of the Chop Shop, Madame Gasket, Ratchet's mother. Rodney is forced out and meets Fender Pinwheeler, and a group of other robots called "The Rusties" with whom Rodney stays at a low-rent boarding house owned by Aunt Fanny. Eventually, Rodney begins fixing old robots in the neighborhood. Upon discovering this, Gasket orders Ratchet to stop Rodney and destroy Bigweld.

text: Rodney later receives news that Herb needs replacement parts. Rodney decides to contact Bigweld directly to beg him to restart the manufacture of spare parts. Wonderbot reminds him that Bigweld will show up at the Bigweld Ball, which takes place that night. Rodney and Fender go to the ball in disguise only to hear Ratchet announce that Bigweld is unable to attend. Rodney confronts Ratchet, but security stops him. Cappy, a robot-executive of the company who dislikes Ratchet's plan, saves him, and together with Fender, they escape from the ball.

text: Afterwards, Fender is captured by a sweeper and taken to the Chop Shop, but manages to escape, losing his legs in the process and finding a replacement pair with a built-in skirt. Meanwhile, Rodney and Cappy fly to Bigweld's home and meet him. Rodney asks Bigweld to return to his company and make spare parts available again, but Bigweld refuses, explaining that Ratchet forced him out of the company. Rodney calls his parents, intending to give up his dream and return to Rivet Town, but Herb encourages Rodney to continue pursuing it. Rodney rallies the Rusties into fighting back against Ratchet and Gasket. Fender reveals that Ratchet has built a fleet of super-sweepers with the intention of rounding up and destroying all of the older robots. Bigweld eventually comes with the group, having realized what Rodney meant to him.

text: The group then heads back to Bigweld Industries where Bigweld attempts to fire Ratchet, but after a huge chase involving Ratchet chasing after Rodney, Bigweld, Cappy and the Rusties around the city, Bigweld ends up getting captured and sent to the Chop Shop. A battle ensues between the Rusties, Ratchet, and Gasket's henchmen. During the chaos, Rodney rescues Bigweld, the choppers and sweepers are destroyed, Wonderbot engages Gasket in combat, where she is destroyed when she gets tossed into a furnace, while Ratchet loses his upgrades. Retaking control of Bigweld Industries, Bigweld goes to Rivet Town to tell Rodney's parents that their son is now his right-hand inventor and eventual successor.

text: Cast[edit]

text:
Ewan McGregor as Rodney Copperbottom, a young blue robot and aspiring inventor.
Halle Berry as Cappy, a human-themed worker at Bigweld Industries and Rodney's love interest.
Robin Williams as Fender Pinwheeler, a red robot who befriends Rodney and is constantly falling apart.
Mel Brooks as Bigweld, the jolly inventor and owner of Bigweld Industries; until Rodney met him, Bigweld had slipped into depression at Madame Gasket's actions.
Greg Kinnear as Phineas T. Ratchet, a materialistic, arrogant, treacherous, greedy, and self-centered robot, Rodney's arch-rival, and Madame Gasket's son, partner and henchman.
Jim Broadbent as Madame Gasket, a twisted, malevolent, manipulative, and tyrannical robot, Rodney's arch-enemy, Bigweld's arch-rival, and Ratchet's mother, partner, leader, and boss.
Amanda Bynes as Piper Pinwheeler, a yellow robot who is Fender's younger sister.
Drew Carey as Crank Casey, an orange robot who befriends Rodney.
Jennifer Coolidge as Aunt Fanny, a kind, motherly robot who takes in "broken" robots; she has the unintentional effect of bumping people with her large aft.
Harland Williams as Lugnut, a large green robot who befriends Rodney along with his mute companion Diesel.
Stanley Tucci as Herb Copperbottom, Rodney's father and a dishwasher at Gunk's.
Dianne Wiest as Lydia Copperbottom, Rodney's mother.
Chris Wedge as Wonderbot / Phone Booth
Natasha Lyonne as Loretta Geargrinder, a receptionist at Bigweld Industries and Fender's love interest.
Paul Giamatti as Tim the Gate Guard
Dan Hedaya as Mr. Gunk, Herb's rude, inconsiderate boss.
Brian Scott McFadden as Trashcan Bot
Jay Leno as Fire Hydrant
Lucille Bliss as Pigeon Lady
Paula Abdul as Wristwatch #1
Randy Jackson as Wristwatch #2
Al Roker as Mailbox
Stephen Tobolowsky as Bigmouth Executive / Forge
Tim Nordquist as Tin Man
Lowell Ganz as Mr. Gasket, Madame Gasket's husband and Ratchet's father.
James Earl Jones as a Darth Vader voice box at a hardware store[6]

tag: ul

text: Locations[edit]

text: Rivet Town was rumored to be based on Watertown, New York, but director Chris Wedge dismissed this in an interview.[8]

text: Release[edit]

text: Robots was originally scheduled for a 2004 release,[9] but the release date was changed to 2005. The film premiered on March 6, 2005 in Westwood, Los Angeles,[1][7] and it was released theatrically on March 11, 2005. The film was the first to feature the new trailer for Star Wars: Episode III – Revenge of the Sith. The film also featured the exclusive trailer for Ice Age: The Meltdown, then called Ice Age 2.[10] Robots was digitally re-mastered into IMAX format (IMAX DMR) and released in select IMAX theatres around the world. It was the first Twentieth Century Fox's film that was released on the same day on IMAX and conventional 35mm screens. It was also the first IMAX DMR film released in the Spring season, and the second IMAX DMR film distributed by Fox.[11]

text: Home media[edit]

text: The film, released on DVD and VHS on September 27, 2005,[12] was accompanied by an original short animated film based on Robots, titled Aunt Fanny's Tour of Booty.[13][14] The film was released in high-definition on Blu-ray Disc on March 22, 2011.[15]

text: Reception[edit]

text: Critical reaction[edit]

text: On the review aggregator Rotten Tomatoes, the film has a rating of 64% based on 177 reviews. The site's consensus reads: "Robots delights on a visual level, but the story feels like it came off an assembly line."[16] Another review aggregator, Metacritic, gave a score of 64 based on 33 reviews.[17] Roger Ebert gave the film three-and-a-half stars out of four, stating that "this is a movie that is a joy to behold entirely apart from what it is about. It looks happy, and, more to the point, it looks harmonious."[18]

text: Box office[edit]

text: The film was released March 11, 2005, in the United States and Canada and grossed $36 million in 3,776 theaters its opening weekend, ranking #1 at the box office.[19] It grossed a total of $260.7 million worldwide—$128.2 million in the United States and Canada and $132.5 million in other territories.[20]

text: Accolades[edit]

text: The film was nominated for many awards in the category of best animated film, as well as awards for character design, best animated character, voice casting, and sound editing. However, it only won one, the MTV (Mexico) Movie Award for best song, "Un Héroe Real".[citation needed]

text: The film is recognized by American Film Institute in these lists:

text: 2008: AFI's 10 Top 10: Nominated Animation Film[21]

text: Music[edit]

text: Soundtrack[edit]

text:
Robots: Original Motion Picture Soundtrack

Soundtrack album by Various Artists

Released
March 1, 2005 (2005-03-01)

Genre
Pop, alternative rock, pop rock, R&B, hip hop, funk, soul

Length
41:09

Label
Virgin Records

text: Robots: Original Motion Picture Soundtrack was released on March 1, 2005 by Virgin Records.[22]

text:
No.
Title
Performer
Length

1.
"Shine"
Ricky Fanté
4:08

2.
"Right Thurr"
Chingy
4:12

3.
"Tell Me What You Already Did"
Fountains of Wayne
1:59

4.
"Wonderful Night"
Fatboy Slim featuring Lateef
2:46

5.
"Get Up Offa That Thing" (Ali Dee Remix)"
James Brown
3:40

6.
"(There's Gotta Be) More to Life"
Stacie Orrico
3:23

7.
"Love's Dance"
Earth, Wind & Fire
4:29

8.
"Low Rider"
War
3:15

9.
"I Like That"
Houston, Featuring Chingy, Nate Dogg and I-20
3:58

10.
"Silence"
Gomez
2:55

11.
"Walkie Talkie Man"
Steriogram
2:15

12.
"Robot City"
John Powell, Featuring Blue Man Group
4:09

Total length:
41:09

text:
"Underground" – Tom Waits
"Can't Get Enough of Your Love, Babe" – Barry White
"...Baby One More Time" – Britney Spears
"See Me" – Melanie Blatt
"Eye of the Tiger" – Survivor
"From Zero to Hero" – Sarah Connor
"Gonna Make You Sweat (Everybody Dance Now)" – C+C Music Factory and Freedom Williams

text: Score[edit]

text:
Robots: Original Motion Picture Score

Film score by John Powell

Released
March 15, 2005 (2005-03-15)

Genre
Score

Length
43:41

Label
Varèse Sarabande

text: Robots: Original Motion Picture Score was composed by John Powell and was released on March 15, 2005 by Varèse Sarabande Records.[23]

text:
No.
Title
Length

1.
"Opening Titles/ Building A Baby"
4:02

2.
"Rivet Town Parade"
0:54

3.
"Bigweld TV / Creating Wonderbot"
2:45

4.
"Wonderbot Wash"
2:08

5.
"Train Station"
3:50

6.
"The Crosstown Express"
1:19

7.
"Wild Ride"
1:36

8.
"Madame Gasket"
1:00

9.
"Chop Shop"
1:50

10.
"Meet The Rusties"
2:06

11.
"Bigweld Workshop"
3:13

12.
"Phone Booth"
1:29

13.
"Gathering Forces"
3:28

14.
"Escape"
4:42

15.
"Deciding to Fight Back"
1:13

16.
"Attack of the Sweepers"
1:26

17.
"Butt Whoopin'"
3:42

18.
"Homecoming"
1:33

19.
"Dad's Dream"
1:25

Total length:
43:41

text: Video game[edit]

text: Aunt Fanny's Tour of Booty[edit]

text: Aunt Fanny's Tour of Booty is a five-minute computer-animated film that was included as a bonus feature on the DVD and VHS releases of Robots and a prequel to the film. In the short, Aunt Fanny gives a tour of the Robot City Train Station to a motley collection of robots, including Fender Pinwheeler, Zinc, Tammy, Hacky, and an Old Lady-Bot.[13][14]


document_title: List of Minnesota Vikings starting quarterbacks

question_text: who was the starting quarterback for the vikings

text: History[edit]

text: This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (August 2017) (Learn how and when to remove this template message)

text: The Vikings' starting quarterback for the first game of their inaugural season against the Chicago Bears was George Shaw.[3] However, he was replaced by Fran Tarkenton early on, who passed for four touchdowns in the game and rushed for one more. Tarkenton went on to start in 10 of the Vikings' 14 regular season matches that year.[4] He played for the Vikings until 1967, when he was traded to the New York Giants,[5] and Joe Kapp took his place as the Vikings' starting quarterback .[6] Kapp led the Vikings to their first playoff appearance in 1968,[7] but he was traded to the Boston Patriots in 1970 and Gary Cuozzo stepped up to replace him.[6][8] Cuozzo remained in the position for two seasons, moving to the St. Louis Cardinals in 1972.[8]

text: Tarkenton returned for another seven-year spell as the Vikings' starting quarterback in 1972, continuing until his retirement in 1978,[5] at which point Tommy Kramer was promoted from the second string in his second season with the franchise.[9] Kramer was injured for most of the 1983 season, so Steve Dils served as the starting quarterback for most of the season,[10] before Kramer reclaimed the position in 1984.[9] For the 1987 season, Kramer shared quarterback duties with Wade Wilson, before Wilson took over on a permanent basis from 1988.[11] Wilson was replaced by the emerging Rich Gannon in 1990,[12] but Gannon was released after the 1992 season and veteran Jim McMahon took over for the 1993 season until the arrival of Warren Moon in 1994.[13]

text: Moon retained the starting quarterback spot for two seasons,[14] but suffered a broken collarbone halfway through his third season with the Vikings and was replaced by Brad Johnson for the remainder of the season.[15] The Vikings had three starting quarterbacks in the following three seasons – Johnson (1997),[15] Randall Cunningham (1998)[16] and Jeff George (1999)[17] – before Daunte Culpepper began a six-year spell in his second year in the NFL in 2000.[18] He suffered a serious knee injury during the 2005 season, and Johnson took over in the position again, having re-signed the previous summer after seven years away from the franchise.[15] Culpepper then joined the Miami Dolphins in 2006,[18] giving Johnson another full year as starting quarterback, [15] only to be replaced by sophomore Tarvaris Jackson in 2007.[19] The 2008 season commenced with Jackson starting at quarterback,[19] but he was replaced after two games by Gus Frerotte, who was returning to the Vikings from the St. Louis Rams after having been traded to the Miami Dolphins in 2005.[20] Jackson regained the job for the final three games and led the Vikings to their first divisional title since 2000, and their first NFC North title.[19]

text: In 2009, the Vikings recruited veteran quarterback Brett Favre out of retirement to be their new starting quarterback.[21] In Week 13 of the 2010 season, Favre suffered a chest injury that ended his NFL-record streak of consecutive starts at 297 (321 including postseason games), and Tarvaris Jackson reclaimed the starting spot for Week 14. However, Jackson was injured himself in Week 15, giving rookie Joe Webb a chance to stake a claim for the position. He was unable to hold onto the position as Donovan McNabb was signed as a free agent to replace Favre, who retired at the end of the 2010 season. After going 1–5 through the first six games of 2011, though, McNabb was replaced by first-round draft pick Christian Ponder, who retained the starting position for the remainder of the season and for the whole of 2012. However, he was plagued by indifferent form and the Vikings signed Matt Cassel – recently released by the Kansas City Chiefs. When Ponder suffered an injury early in the 2013 season, Cassel was given his first start for the Vikings in week 4 in the NFL International Series game against the Pittsburgh Steelers at Wembley Stadium, London. He started the following game, but was replaced in week 7 by Josh Freeman, recently signed after his release by the Tampa Bay Buccaneers. However, he was injured during the game and did not make another start for the Vikings, allowing Ponder to reclaim the starting role. Cassel then returned as the starter in week 14, and retained the role for the rest of the season and into 2014. After three games, he was placed on injured reserve and first-round draft pick Teddy Bridgewater took over for the week 4 game against the Atlanta Falcons. Bridgewater himself was injured late in the game, allowing Ponder the chance to come back in for the following week, but the rookie soon returned and has held the starting berth until suffering a knee injury in practice during the 2016 preseason. Shaun Hill started the season opener and Sam Bradford took over in week 2.

text: Seven Vikings quarterbacks have made at least one start in their rookie season: Tarkenton in 1961, Vander Kelen in 1963, Kramer in 1977, Jackson in 2006, Webb in 2010, Ponder in 2011 and Bridgewater in 2014.

text: Starting quarterbacks by season[edit]

text:
Year
Column links to corresponding team season

(#)
Number of games started in the regular season or post-season win–loss record

†
Inducted to the Pro Football Hall of Fame[2]

text: Regular season[edit]

text:
Season
Quarterback(s)
Ref(s)

1961
Fran Tarkenton† (10) / George Shaw (4)
[3][4][5]

1962
Fran Tarkenton† (14)
[22]

1963
Fran Tarkenton† (13) / Ron Vander Kelen (1)
[23][24]

1964
Fran Tarkenton† (14)
[25]

1965
Fran Tarkenton† (14)
[26]

1966
Fran Tarkenton† (12) / Bob Berry (1) / Ron Vander Kelen (1)
[27][28]

1967
Joe Kapp (11) / Ron Vander Kelen (3)
[6][29]

1968
Joe Kapp (14)
[7]

1969
Joe Kapp (13) / Gary Cuozzo (1)
[8][30]

1970
Gary Cuozzo (12) / Bob Lee (2)
[31][32]

1971
Gary Cuozzo (8) / Bob Lee (4) / Norm Snead (2)
[33][34]

1972
Fran Tarkenton† (14)
[35]

1973
Fran Tarkenton† (14)
[36]

1974
Fran Tarkenton† (13) / Bob Berry (1)
[37]

1975
Fran Tarkenton† (14)
[38]

1976
Fran Tarkenton† (13) / Bob Lee (1)
[39]

1977
Fran Tarkenton† (9) / Bob Lee (4) / Tommy Kramer (1)
[9][40]

1978[b]
Fran Tarkenton† (16)
[41]

1979
Tommy Kramer (16)
[42]

1980
Tommy Kramer (15) / Steve Dils (1)
[10][43]

1981
Tommy Kramer (14) / Steve Dils (2)
[44]

1982[c]
Tommy Kramer (9)
[45]

1983
Steve Dils (12) / Tommy Kramer (3) / Wade Wilson (1)
[11][46]

1984
Tommy Kramer (9) / Wade Wilson (5) / Archie Manning (2)
[47][48]

1985
Tommy Kramer (15) / Wade Wilson (1)
[49]

1986
Tommy Kramer (13) / Wade Wilson (3)
[50]

1987[c]
Wade Wilson (7) / Tommy Kramer (5) / Tony Adams (3)
[51][52]

1988
Wade Wilson (10) / Tommy Kramer (6)
[53]

1989
Wade Wilson (12) / Tommy Kramer (4)
[54]

1990
Rich Gannon (12) / Wade Wilson (4)
[12][55]

1991
Rich Gannon (11) / Wade Wilson (5)
[56]

1992
Rich Gannon (12) / Sean Salisbury (4)
[57][58]

1993
Jim McMahon (12) / Sean Salisbury (4)
[13][59]

1994
Warren Moon† (15) / Sean Salisbury (1)
[14][60]

1995
Warren Moon† (16)
[61]

1996
Warren Moon† (8) / Brad Johnson (8)
[15][62]

1997
Brad Johnson (13) / Randall Cunningham (3)
[16][63]

1998
Randall Cunningham (14) / Brad Johnson (2)
[64]

1999
Jeff George (10) / Randall Cunningham (6)
[17][65]

2000
Daunte Culpepper (16)
[18][66]

2001
Daunte Culpepper (11) / Todd Bouman (3) / Spergon Wynn (2)
[67][68][69]

2002
Daunte Culpepper (16)
[70]

2003
Daunte Culpepper (14) / Gus Frerotte (2)
[20][71]

2004
Daunte Culpepper (16)
[72]

2005
Brad Johnson (9) / Daunte Culpepper (7)
[73]

2006
Brad Johnson (14) / Tarvaris Jackson (2)
[19][74]

2007
Tarvaris Jackson (12) / Kelly Holcomb (3) / Brooks Bollinger (1)
[75][76][77]

2008
Gus Frerotte (11) / Tarvaris Jackson (5)
[78]

2009
Brett Favre† (16)
[21][79]

2010
Brett Favre† (13) / Tarvaris Jackson (1) / Joe Webb (2)
[80][81]

2011
Christian Ponder (10) / Donovan McNabb (6)
[82][83][84]

2012
Christian Ponder (16)
[85]

2013
Christian Ponder (9) / Matt Cassel (6) / Josh Freeman (1)
[86][87][88]

2014
Teddy Bridgewater (12) / Matt Cassel (3) / Christian Ponder (1)
[84][87][89]

2015
Teddy Bridgewater (16)
[89]

2016
Sam Bradford (15) / Shaun Hill (1)
[90][91]

2017
Case Keenum (14) / Sam Bradford (2)
[90][92]

text: Postseason[edit]

text:
Season
Quarterback(s)
Ref(s)

1968
Joe Kapp (0–1)
[6]

1969
Joe Kapp (2–1)
[6]

1970
Gary Cuozzo (0–1)
[8]

1971
Bob Lee (0–1)
[32]

1973
Fran Tarkenton (2–1)
[5]

1974
Fran Tarkenton (2–1)
[5]

1975
Fran Tarkenton (0–1)
[5]

1976
Fran Tarkenton (2–1)
[5]

1977
Bob Lee (1–1)
[32]

1978
Fran Tarkenton (0–1)
[5]

1980
Tommy Kramer (0–1)
[9]

1982
Tommy Kramer (1–1)
[9]

1987
Tommy Kramer (1–0) / Wade Wilson (1–1)
[9][11]

1988
Wade Wilson (1–1)
[11]

1989
Wade Wilson (0–1)
[11]

1992
Sean Salisbury (0–1)
[58]

1993
Jim McMahon (0–1)
[13]

1994
Warren Moon (0–1)
[14]

1996
Brad Johnson (0–1)
[15]

1997
Randall Cunningham (1–1)
[16]

1998
Randall Cunningham (1–1)
[16]

1999
Jeff George (1–1)
[17]

2000
Daunte Culpepper (1–1)
[18]

2004
Daunte Culpepper (1–1)
[18]

2008
Tarvaris Jackson (0–1)
[19]

2009
Brett Favre (1–1)
[21]

2012
Joe Webb (0–1)
[81]

2015
Teddy Bridgewater (0–1)
[89]

2017
Case Keenum (1–1)
[92]

text: Statistics[edit]

text: Having been the franchise's starting quarterback for 13 seasons (longer than any other Vikings player), Fran Tarkenton holds the record for the most starts in a Vikings jersey, and those for the most wins and ties.[93] He is also the franchise's leading passer in terms of numbers of attempts, completions, total yards gained and passing touchdowns, although Brett Favre has the best pass completion percentage.[93] However, Tarkenton has also thrown the most interceptions.[93] The record for the longest completed pass by a Vikings starting quarterback is held by Gus Frerotte, who threw a 99-yard touchdown pass to wide receiver Bernard Berrian in a home game against the Chicago Bears in the 2008 season.[93][94]

text: Tarkenton is also the franchise leader for rushing attempts and rushing yards as a quarterback, but it is Daunte Culpepper – with 72 fewer rushing yards on 10 fewer attempts than Tarkenton – who has the most rushing touchdowns.[95] Joe Webb holds the record for the longest rush with a 65-yard run in Minnesota's 34–28 road loss to the Detroit Lions in 2011.[95][96]

text:
Years
Years that the quarterback was on the Vikings' roster
Yds
Yards gained by passing

GP
Games played (regular season)
TD
Passing touchdowns

GS
Games started (regular season)
Int
Interceptions thrown

W
Number of wins as starting quarterback
Lng
Longest completed pass thrown (yards)

L
Number of losses as starting quarterback
Rate
Quarterback rating

T
Number of ties as starting quarterback
Att
Rushes attempted

Cmp
Passes completed
Yds
Yards gained by rushing

Att
Passes attempted
TD
Rushing touchdowns

Cmp%
Percentage of passes completed
Lng
Longest rushing attempt

text:
Name
Years
Passing statistics
Rushing statistics
Ref

GP
GS
W
L
T
Cmp
Att
Cmp%
Yds
TD
Int
Lng
Rate
Att
Yds
TD
Lng

Shaw, GeorgeGeorge Shaw
1961
8
4
1
3
0
46
91
50.5
530
4
4
42
64.8
10
39
0
19
[3]

Tarkenton, FranFran Tarkenton
1961–1966
1972–1978
177
170
91
73
6
2,635
4,569
57.7
33,098
239
194
89
80.1
464
2,548
22
52
[5]

Vander Kelen, RonRon Vander Kelen
1963–1967
29
5
1
4
0
107
252
42.5
1,375
6
11
53
50.0
26
116
1
20
[24]

Berry, BobBob Berry
1965–1967
1973–1975
24
2
1
1
0
63
124
50.8
708
7
8
52
60.1
7
25
0
8
[28]

Kapp, JoeJoe Kapp
1967–1969
40
38
23
12
3
351
699
50.2
4,807
37
47
85
62.2
99
540
5
27
[6]

Cuozzo, GaryGary Cuozzo
1968–1971
33
21
16
5
0
276
556
49.6
3,552
18
23
72
63.6
36
85
0
15
[8]

Lee, BobBob Lee
1969–1972
1975–1978
52
11
9
2
0
159
306
52.0
2,153
15
17
63
67.9
39
37
2
10
[32]

Snead, NormNorm Snead
1971
7
2
2
0
0
37
75
49.3
470
1
6
55
40.4
6
6
1
5
[34]

Kramer, TommyTommy Kramer
1977–1989
128
110
54
56
0
2,011
3,648
55.1
24,775
159
157
76
72.9
214
531
8
20
[9]

Dils, SteveSteve Dils
1979–1984
47
15
6
9
0
336
623
53.9
3,867
15
18
68
68.9
24
73
0
19
[10]

Wilson, WadeWade Wilson
1981–1991
76
48
27
21
0
929
1,665
55.8
12,135
66
75
75
73.4
159
679
9
38
[11]

Manning, ArchieArchie Manning
1983–1984
8
2
0
2
0
52
94
55.3
545
2
3
56
66.1
12
41
0
16
[48]

Adams, TonyTony Adams
1987
3
3
0
3
0
49
89
55.1
607
3
5
63
64.2
11
31
0
12
[52]

Gannon, RichRich Gannon
1987–1992
48
35
19
16
0
561
1,003
55.9
6,457
40
36
78
73.9
144
720
3
42
[12]

Salisbury, SeanSean Salisbury
1992–1994
22
9
5
4
0
228
404
56.4
2,772
14
9
55
80.0
24
1
0
6
[58]

Macmahon, JimJim McMahon
1993
12
12
8
4
0
200
331
60.4
1,968
9
8
58
76.2
33
96
0
16
[13]

Moon, WarrenWarren Moon
1994–1996
39
39
21
18
0
882
1,454
60.7
10,102
58
42
85
82.8
69
143
0
16
[14]

Johnson, BradBrad Johnson
1994–1998
2005–2006
68
46
28
18
0
1,036
1,670
62.0
11,098
65
48
82
82.5
139
368
2
28
[15]

Cunningham, RandallRandall Cunningham
1997–1999
27
23
16
7
0
427
713
59.9
5,680
48
23
67
94.2
61
317
1
28
[16]

George, JeffJeff George
1999
12
10
8
2
0
191
329
58.1
2,816
23
12
80
94.2
16
41
0
17
[17]

Culpepper, DaunteDaunte Culpepper
1999–2005
81
80
38
42
0
1,678
2,607
64.4
20,162
135
86
82
91.5
454
2,476
29
42
[18]

Bouman, ToddTodd Bouman
2001–2002
6
3
1
2
0
54
95
56.8
880
8
4
80
98.6
10
70
0
21
[68]

Wynn, SpergonSpergon Wynn
2001
3
2
0
2
0
48
98
49.0
418
1
6
47
38.6
8
61
0
14
[69]

Frerotte, GusGus Frerotte
2003–2004
2008
43
13
10
3
0
216
367
58.9
2,847
19
17
99
81.4
31
5
1
5
[20]

Jackson, TarvarisTarvaris Jackson
2006–2010
36
20
10
10
0
354
603
58.7
3,984
24
22
71
76.6
119
535
4
33
[19]

Holcomb, KellyKelly Holcomb
2007
3
3
0
3
0
42
83
50.6
515
2
1
40
73.1
0
0
0
0
[76]

Bollinger, BrooksBrooks Bollinger
2006–2007
7
1
0
1
0
46
68
67.6
537
1
2
50
84.0
5
18
0
10
[77]

Favre, BrettBrett Favre
2009–2010
29
29
17
12
0
580
889
65.2
6,711
44
26
63
92.2
26
15
0
10
[21]

Webb, JoeJoe Webb
2010–2013
17
2
1
1
0
88
152
57.9
853
3
5
46
66.6
41
273
4
65
[81]

McNabb, DonovanDonovan McNabb
2011
6
6
1
5
0
94
156
60.3
1,026
4
2
60
82.9
14
59
1
23
[83]

Ponder, ChristianChristian Ponder
2011–2014
38
36
14
21
1
632
1,057
59.8
6,658
38
36
72
75.9
126
639
7
29
[84]

Cassel, MattMatt Cassel
2013–2014
12
9
4
5
0
194
325
59.7
2,232
14
13
79
78.1
27
75
1
13
[87]

Freeman, JoshJosh Freeman
2013
1
1
0
1
0
20
53
37.7
190
0
1
22
40.6
0
0
0
0
[88]

Bridgewater, TeddyTeddy Bridgewater
2014–2017
30
28
17
11
0
551
851
64.7
6,150
28
22
87
86.3
94
398
4
19
[89]

Hill, ShaunShaun Hill
2016
7
1
1
0
0
21
42
50.0
257
0
0
33
69.2
11
–2
0
9
[91]

Bradford, SamSam Bradford
2016–2017
17
17
9
8
0
427
595
71.8
4,259
23
5
71
101.1
22
50
0
24
[90]

Keenum, CaseCase Keenum
2017
15
14
11
3
0
325
481
67.6
3,547
22
7
65
98.3
40
160
1
22
[92]