document_title: Serotonin

question_text: where are serotonin receptors located in the body

text: Serotonin

text: Functions[edit]

text: Serotonin is a neurotransmitter and is found in all bilateral animals including insects.[18] Serotonin is also present in plants (phytoserotonin).[19]

text: Perception of resource availability[edit]

text: Serotonin mediates the animal's perceptions of resource; In less complex animals, such as some invertebrates, resources simply mean food availability.[20] In plants serotonin synthesis seems to be associated with stress signals.[19] In more complex animals, such as arthropods and vertebrates, resources also can mean social dominance.[21] In response to the perceived abundance or scarcity of resources, an animal's growth, reproduction or mood may be elevated or lowered. This may somewhat depend on how much serotonin the organism has at its disposal.[citation needed]

text: Cellular effects[edit]

text: Receptors[edit]

text: The 5-HT receptors, the receptors for serotonin, are located on the cell membrane of nerve cells and other cell types in animals, and mediate the effects of serotonin as the endogenous ligand and of a broad range of pharmaceutical and hallucinogenic drugs. Except for the 5-HT3 receptor, a ligand-gated ion channel, all other 5-HT receptors are G-protein-coupled receptors (also called seven-transmembrane, or heptahelical receptors) that activate an intracellular second messenger cascade.[22]

text: Termination[edit]

text: Serotonergic action is terminated primarily via uptake of 5-HT from the synapse. This is accomplished through the specific monoamine transporter for 5-HT, SERT, on the presynaptic neuron. Various agents can inhibit 5-HT reuptake, including cocaine, dextromethorphan (an antitussive), tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs). A 2006 study conducted by the University of Washington suggested that a newly discovered monoamine transporter, known as PMAT, may account for "a significant percentage of 5-HT clearance".[23]

text: Contrasting with the high-affinity SERT, the PMAT has been identified as a low-affinity transporter, with an apparent Km of 114 micromoles/l for serotonin; approximately 230 times higher than that of SERT. However, the PMAT, despite its relatively low serotonergic affinity, has a considerably higher transport 'capacity' than SERT, "resulting in roughly comparable uptake efficiencies to SERT in heterologous expression systems."[this quote needs a citation] The study also suggests some SSRIs, such as fluoxetine and sertraline anti-depressants, inhibit PMAT but at IC50 values which surpass the therapeutic plasma concentrations by up to four orders of magnitude. Therefore, SSRI monotherapy is "ineffective" in PMAT inhibition. At present, no known pharmaceuticals are known to appreciably inhibit PMAT at normal therapeutic doses. The PMAT also suggestively transports dopamine and norepinephrine, albeit at Km values even higher than that of 5-HT (330–15,000 μmoles/L).[citation needed]

text: Serotonylation[edit]

text: Serotonin can also signal through a nonreceptor mechanism called serotonylation, in which serotonin modifies proteins.[24] This process underlies serotonin's effects upon platelet-forming cells (thrombocytes) in which it links to the modification of signaling enzymes called GTPases that then trigger the release of vesicle contents by exocytosis.[25] A similar process underlies the pancreatic release of insulin.[24]

text: The effects of serotonin upon vascular smooth muscle tone (this is the biological function from which serotonin originally got its name) depend upon the serotonylation of proteins involved in the contractile apparatus of muscle cells.[26]

text:
Binding profile of serotonin

Receptor
Ki (nM)[27]
Receptor function[Note 1]

5-HT1 receptor family signals via Gi/o inhibition of adenylyl cyclase.

5-HT1A
3.17
Memory[vague] (agonists ↓); learning[vague] (agonists ↓); anxiety (agonists ↓); depression (agonists ↓); positive, negative, and cognitive symptoms of schizophrenia (partial agonists ↓); analgesia (agonists ↑); aggression (agonists ↓); dopamine release in the prefrontal cortex (agonists ↑); serotonin release and synthesis (agonists ↓)

5-HT1B
4.32
Vasoconstriction (agonists ↑); aggression (agonists ↓); bone mass (↓). Serotonin autoreceptor.

5-HT1D
5.03
Vasoconstriction (agonists ↑)

5-HT1E
7.53

5-HT1F
10

5-HT2 receptor family signals via Gq activation of phospholipase C.

5-HT2A
11.55
Psychedelia (agonists ↑); depression (agonists & antagonists ↓); anxiety (antagonists ↓); positive and negative symptoms of schizophrenia (antagonists ↓); norepinephrine release from the locus coeruleus (antagonists ↑); glutamate release in the prefrontal cortex (agonists ↑); urinary bladder contractions (agonists ↑)[28]

5-HT2B
8.71
Cardiovascular functioning (agonists increase risk of pulmonary hypertension), empathy (via the spindle neurons or Von Economo neurons[29])

5-HT2C
5.02
Dopamine release into the mesocorticolimbic pathway (agonists ↓); acetylcholine release in the prefrontal cortex (agonists ↑); appetite (agonists ↓); antipsychotic effects (agonists ↑); antidepressant effects (agonists & antagonists ↑)

Other 5-HT receptors

5-HT3
593
Emesis (agonists ↑); anxiolysis (antagonists ↑).

5-HT4
125.89
Movement of food across the GI tract (agonists ↑); memory & learning (agonists ↑); antidepressant effects (agonists ↑). Signalling via Gαs activation of adenylyl cyclase.

5-HT5A
251.2
Memory consolidation.[30] Signals via Gi/o inhibition of adenylyl cyclase.

5-HT6
98.41
Cognition (antagonists ↑); antidepressant effects (agonists & antagonists ↑); anxiogenic effects (antagonists ↑[31]). Gs signalling via activating adenylyl cyclase.

5-HT7
8.11
Cognition (antagonists ↑); antidepressant effects (antagonists ↑). Acts by Gs signalling via activating adenylyl cyclase.

text: Nervous system[edit]

text: The neurons of the raphe nuclei are the principal source of 5-HT release in the brain.[32] There are nine raphe nuclei, designated B1-B9, which contain the majority of serotonin-containing neurons (some scientists chose to group the nuclei raphes lineares into one nucleus), all of which are located along the midline of the brainstem, and centered on the reticular formation.[33][34] Axons from the neurons of the raphe nuclei form a neurotransmitter system reaching almost every part of the central nervous system. Axons of neurons in the lower raphe nuclei terminate in the cerebellum and spinal cord, while the axons of the higher nuclei spread out in the entire brain.

text: Ultrastructure and Function[edit]

text: The serotonin nuclei may also be divided into two main groups, the rostral and caudal containing three and four nuclei respectively. The rostral group consists of the caudal linear nuclei (B8), the dorsal raphe nuclei (B6 and B7) and the median raphe nuclei (B5, B8 and B9), that project into multiple cortical and subcortical structures. The caudal group consists of the nucleus raphe magnus (B3), raphe obscurus nucleus (B2), raphe pallidus nucleus (B1), and lateral medullary reticular formation, that project into the brainstem.[35]

text: Serotonergic pathway are involved in sensorimotor function, with pathways projecting both into cortical (Dorsal and Median Raphe Nuclei), subcortical, and spinal areas involved in motor activity. Pharmacological manipulation suggest that serotonergic activity increases with motor activity, while firing rates of serotonergic neurons increase with intense visual stimuli. The descending projections form a pathway that inhibits pain called the "descending inhibitory pathway" that may be relevant to disorder such as fibromyalgia, migraine and other pain disorders, and the efficacy of antidepressants in them.[36]

text: Serotonergic projections from the caudal nuclei are involved in regulating mood, emotion and hypo[37] or hyperserotonergic[38] states may be involved in depression and sickness behavior.

text: Microanatomy[edit]

text: Serotonin is released into the synapse, or space between neurons, and diffuses over a relatively wide gap (>20 µm) to activate 5-HT receptors located on the dendrites, cell bodies and presynaptic terminals of adjacent neurons.

text: When humans smell food, dopamine is released to increase the appetite. But, unlike in worms, serotonin does not increase anticipatory behaviour in humans; instead, the serotonin released while consuming activates 5-HT2C receptors on dopamine-producing cells. This halts their dopamine release, and thereby serotonin decreases appetite. Drugs that block 5-HT2C receptors make the body unable to recognize when it is no longer hungry or otherwise in need of nutrients, and are associated with weight gain,[39] especially in people with a low number of receptors.[40] The expression of 5-HT2C receptors in the hippocampus follows a diurnal rhythm,[41] just as the serotonin release in the ventromedial nucleus, which is characterised by a peak at morning when the motivation to eat is strongest.[42]

text: The amount of food that an animal acquires depends not only on food availability but also on the animal's ability to compete with others. This is especially true for social animals, where the stronger individuals might steal food from the weaker (this is not to say some non-social animals do not concern themselves with the needs of others or steal food from others[citation needed]). Thus, serotonin is involved not only in the perception of food availability but also in social rank.

text: In macaques, alpha males have twice the level of serotonin released in the brain than subordinate males and females (as measured by the levels of 5-Hydroxyindoleacetic acid (5-HIAA) in the cerebro-spinal fluid). Dominance status and cerebro-serotonin levels appear to be positively correlated. When dominant males were removed from such groups, subordinate males begin competing for dominance. Once new dominance hierarchies were established, serotonin levels of the new dominant individuals also increased to double those in subordinate males and females. The reason why serotonin levels are only high in dominant males but not dominant females has not yet been established.[43]

text: In humans, levels of 5-HT1A receptor activation in the brain show negative correlation with aggression,[44] and a mutation in the gene that codes for the 5-HT2A receptor may double the risk of suicide for those with that genotype.[45] Serotonin in the brain is not usually degraded after use, but is collected by serotonergic neurons by serotonin transporters on their cell surfaces. Studies have revealed nearly 10% of total variance in anxiety-related personality depends on variations in the description of where, when and how many serotonin transporters the neurons should deploy.[46]

text: Psychological influences[edit]

text: Serotonin has been implicated in cognition, mood, anxiety and psychosis, but strong clarity has not been achieved.[47][48]

text: Outside the nervous system[edit]

text: In the digestive tract (emetic)[edit]

text: The gut is surrounded by enterochromaffin cells, which release serotonin in response to food in the lumen. This makes the gut contract around the food. Platelets in the veins draining the gut collect excess serotonin.

text: If irritants are present in the food, the enterochromaffin cells release more serotonin to make the gut move faster, i.e., to cause diarrhea, so the gut is emptied of the noxious substance. If serotonin is released in the blood faster than the platelets can absorb it, the level of free serotonin in the blood is increased. This activates 5-HT3 receptors in the chemoreceptor trigger zone that stimulate vomiting.[49] The enterochromaffin cells not only react to bad food but are also very sensitive to irradiation and cancer chemotherapy. Drugs that block 5HT3 are very effective in controlling the nausea and vomiting produced by cancer treatment, and are considered the gold standard for this purpose.[50]

text: Bone metabolism[edit]

text: In mice and humans, alterations in serotonin levels and signalling have been shown to regulate bone mass.[51][52][53][54] Mice that lack brain serotonin have osteopenia, while mice that lack gut serotonin have high bone density. In humans, increased blood serotonin levels have been shown to be significant negative predictor of low bone density. Serotonin can also be synthesized, albeit at very low levels, in the bone cells. It mediates its actions on bone cells using three different receptors. Through 5-HT1B receptors, it negatively regulates bone mass, while it does so positively through 5-HT2B receptors and 5-HT2C receptors. There is very delicate balance between physiological role of gut serotonin and its pathology. Increase in the extracellular content of serotonin results in a complex relay of signals in the osteoblasts culminating in FoxO1/ Creb and ATF4 dependent transcriptional events.[55] These studies have opened a new area of research in bone metabolism that can be potentially harnessed to treat bone mass disorders.[56]

text: Organ development[edit]

text: Since serotonin signals resource availability it is not surprising that it affects organ development. Many human and animal studies have shown that nutrition in early life can influence, in adulthood, such things as body fatness, blood lipids, blood pressure, atherosclerosis, behavior, learning and longevity.[57][58][59] Rodent experiment shows that neonatal exposure to SSRI's makes persistent changes in the serotonergic transmission of the brain resulting in behavioral changes,[60][61] which are reversed by treatment with antidepressants.[62] By treating normal and knockout mice lacking the serotonin transporter with fluoxetine scientists showed that normal emotional reactions in adulthood, like a short latency to escape foot shocks and inclination to explore new environments were dependent on active serotonin transporters during the neonatal period.[63][64]

text: Human serotonin can also act as a growth factor directly. Liver damage increases cellular expression of 5-HT2A and 5-HT2B receptors, mediating liver compensatory regrowth (see Liver § Regeneration and transplantation)[65] Serotonin present in the blood then stimulates cellular growth to repair liver damage.[66] 5HT2B receptors also activate osteocytes, which build up bone[67] However, serotonin also inhibits osteoblasts, through 5-HT1B receptors.[68]

text: Cardiovascular growth factor[edit]

text: Serotonin, in addition, evokes endothelial nitric oxide synthase activation and stimulates, through a 5-HT1B receptor-mediated mechanism, the phosphorylation of p44/p42 mitogen-activated protein kinase activation in bovine aortic endothelial cell cultures.[69] In blood, serotonin is collected from plasma by platelets, which store it. It is thus active wherever platelets bind in damaged tissue, as a vasoconstrictor to stop bleeding, and also as a fibrocyte mitotic (growth factor), to aid healing.[70]

text: Pharmacology[edit]

text: Several classes of drugs target the 5-HT system, including some antidepressants, antipsychotics, anxiolytics, antiemetics, and antimigraine drugs, as well as the psychedelic drugs and empathogens.

text: Psychedelic drugs[edit]

text: The psychedelic drugs psilocin/psilocybin, DMT, mescaline, psychedelic mushroom and LSD are agonists, primarily at 5HT2A/2C receptors.[71][72][73] The empathogen-entactogen MDMA releases serotonin from synaptic vesicles of neurons.[74]

text: Antidepressants[edit]

text: Drugs that alter serotonin levels are used in treating depression, generalized anxiety disorder and social phobia. Monoamine oxidase inhibitors (MAOIs) prevent the breakdown of monoamine neurotransmitters (including serotonin), and therefore increase concentrations of the neurotransmitter in the brain. MAOI therapy is associated with many adverse drug reactions, and patients are at risk of hypertensive emergency triggered by foods with high tyramine content, and certain drugs. Some drugs inhibit the re-uptake of serotonin, making it stay in the synaptic cleft longer. The tricyclic antidepressants (TCAs) inhibit the reuptake of both serotonin and norepinephrine. The newer selective serotonin reuptake inhibitors (SSRIs) have fewer side-effects and fewer interactions with other drugs.[75]

text: Certain SSRI medications have been shown to lower serotonin levels below the baseline after chronic use, despite initial increases.[76] The 5-HTTLPR gene codes for the number of serotonin transporters in the brain, with more serotonin transporters causing decreased duration and magnitude of serotonergic signaling.[77] The 5-HTTLPR polymorphism (l/l) causing more serotonin transporters to be formed is also found to be more resilient against depression and anxiety.[78][79]

text: Serotonin syndrome[edit]

text: Extremely high levels of serotonin can cause a condition known as serotonin syndrome, with toxic and potentially fatal effects. In practice, such toxic levels are essentially impossible to reach through an overdose of a single antidepressant drug, but require a combination of serotonergic agents, such as an SSRI with an MAOI.[80] The intensity of the symptoms of serotonin syndrome vary over a wide spectrum, and the milder forms are seen even at nontoxic levels.[81]

text: Antiemetics[edit]

text: Some 5-HT3 antagonists, such as ondansetron, granisetron, and tropisetron, are important antiemetic agents. They are particularly important in treating the nausea and vomiting that occur during anticancer chemotherapy using cytotoxic drugs. Another application is in the treatment of postoperative nausea and vomiting.

text: Other[edit]

text: Some serotonergic agonist drugs cause fibrosis anywhere in the body, particularly the syndrome of retroperitoneal fibrosis, as well as cardiac valve fibrosis.[82] In the past, three groups of serotonergic drugs have been epidemiologically linked with these syndromes. These are the serotonergic vasoconstrictive antimigraine drugs (ergotamine and methysergide),[82] the serotonergic appetite suppressant drugs (fenfluramine, chlorphentermine, and aminorex), and certain anti-Parkinsonian dopaminergic agonists, which also stimulate serotonergic 5-HT2B receptors. These include pergolide and cabergoline, but not the more dopamine-specific lisuride.[83]

text: As with fenfluramine, some of these drugs have been withdrawn from the market after groups taking them showed a statistical increase of one or more of the side effects described. An example is pergolide. The drug was declining in use since it was reported in 2003 to be associated with cardiac fibrosis.[84]

text: Two independent studies published in the New England Journal of Medicine in January 2007, implicated pergolide, along with cabergoline, in causing valvular heart disease.[85][86] As a result of this, the FDA removed pergolide from the United States market in March 2007.[87] (Since cabergoline is not approved in the United States for Parkinson's Disease, but for hyperprolactinemia, the drug remains on the market. Treatment for hyperprolactinemia requires lower doses than that for Parkinson's Disease, diminishing the risk of valvular heart disease).[88]

text: Methyl-tryptamines and hallucinogens[edit]

text: Several plants contain serotonin together with a family of related tryptamines that are methylated at the amino (NH2) and (OH) groups, are N-oxides, or miss the OH group. These compounds do reach the brain, although some portion of them are metabolized by monoamine oxidase enzymes (mainly MAO-A) in the liver. Examples are plants from the Anadenanthera genus that are used in the hallucinogenic yopo snuff. These compounds are widely present in the leaves of many plants, and may serve as deterrents for animal ingestion. Serotonin occurs in several mushrooms of the genus Panaeolus.[89]

text: Comparative biology and evolution[edit]

text: Unicellular organisms[edit]

text: Serotonin is used by a variety of single-cell organisms for various purposes. SSRIs have been found to be toxic to algae.[90] The gastrointestinal parasite Entamoeba histolytica secretes serotonin, causing a sustained secretory diarrhea in some people.[16][91] Patients infected with E. histolytica have been found to have highly elevated serum serotonin levels, which returned to normal following resolution of the infection.[92] E. histolytica also responds to the presence of serotonin by becoming more virulent.[93] This means serotonin secretion not only serves to increase the spread of enteamoebas by giving the host diarrhea but also serves to coordinate their behaviour according to their population density, a phenomenon known as quorum sensing. Outside the gut of a host, there is nothing that the entoamoebas provoke to release serotonin, hence the serotonin concentration is very low. Low serotonin signals to the entoamoebas they are outside a host and they become less virulent to conserve energy. When they enter a new host, they multiply in the gut, and become more virulent as the enterochromaffine cells get provoked by them and the serotonin concentration increases.

text: Plants[edit]

text: In drying seeds, serotonin production is a way to get rid of the buildup of poisonous ammonia. The ammonia is collected and placed in the indole part of L-tryptophan, which is then decarboxylated by tryptophan decarboxylase to give tryptamine, which is then hydroxylated by a cytochrome P450 monooxygenase, yielding serotonin.[94]

text: However, since serotonin is a major gastrointestinal tract modulator, it may be produced by plants in fruits as a way of speeding the passage of seeds through the digestive tract, in the same way as many well-known seed and fruit associated laxatives. Serotonin is found in mushrooms, fruits and vegetables. The highest values of 25–400 mg/kg have been found in nuts of the walnut (Juglans) and hickory (Carya) genera. Serotonin concentrations of 3–30 mg/kg have been found in plantains, pineapples, banana, kiwifruit, plums, and tomatoes. Moderate levels from 0.1–3 mg/kg have been found in a wide range of tested vegetables.[17]

text: Serotonin is one compound of the poison contained in stinging nettles (Urtica dioica), where it causes pain on injection in the same manner as its presence in insect venoms (see below). It is also naturally found in Paramuricea clavata, or the Red Sea Fan.[95]

text: Serotonin and tryptophan have been found in chocolate with varying cocoa contents. The highest serotonin content (2.93 µg/g) was found in chocolate with 85% cocoa, and the highest tryptophan content (13.27–13.34 µg/g) was found in 70–85% cocoa. The intermediate in the synthesis from tryptophan to serotonin, 5-hydroxytryptophan, was not found.[96]

text: Invertebrates[edit]

text: Serotonin functions as a neurotransmitter in the nervous systems of most animals. For example, in the roundworm Caenorhabditis elegans, which feeds on bacteria, serotonin is released as a signal in response to positive events, such as finding a new source of food or in male animals finding a female with which to mate.[97] When a well-fed worm feels bacteria on its cuticle, dopamine is released, which slows it down; if it is starved, serotonin also is released, which slows the animal down further. This mechanism increases the amount of time animals spend in the presence of food.[98] The released serotonin activates the muscles used for feeding, while octopamine suppresses them.[99] Serotonin diffuses to serotonin-sensitive neurons, which control the animal's perception of nutrient availability.

text: If lobsters are injected with serotonin, they behave like dominant individuals whereas octopamine causes subordinate behavior.[21] A crayfish that is frightened may flip its tail to flee, and the effect of serotonin on this behavior depends largely on the animal's social status. Serotonin inhibits the fleeing reaction in subordinates, but enhances it in socially dominant or isolated individuals. The reason for this is social experience alters the proportion between serotonin receptors (5-HT receptors) that have opposing effects on the fight-or-flight response.[clarification needed] The effect of 5-HT1 receptors predominates in subordinate animals, while 5-HT2 receptors predominates in dominants.[100]

text: Insects[edit]

text: Serotonin is evolutionary conserved and appears across the animal kingdom. It is seen in insect processes in roles similar to in the human central nervous system, such as memory, appetite, sleep, and behavior.[101][18] Locust swarming is mediated by serotonin, by transforming social preference from aversion to a gregarious state that enables coherent groups.[102] Learning in flies and honeybees is affected by the presence of serotonin.[103][104] Insect 5-HT receptors have similar sequences to the vertebrate versions, but pharmacological differences have been seen. Invertebrate drug response has been far less characterized than mammalian pharmacology and the potential for species selective insecticides has been discussed.[105]

text: Wasps and hornets have serotonin in their venom,[106] which causes pain and inflammation.[15] as do scorpions.[107]

text: If flies are fed serotonin, they are more aggressive; flies depleted of serotonin still exhibit aggression, but they do so much less frequently.[108]

text: Growth and reproduction[edit]

text: In the nematode C. elegans, artificial depletion of serotonin or the increase of octopamine cues behavior typical of a low-food environment: C. elegans becomes more active, and mating and egg-laying are suppressed, while the opposite occurs if serotonin is increased or octopamine is decreased in this animal.[20] Serotonin is necessary for normal nematode male mating behavior,[109] and the inclination to leave food to search for a mate.[110] The serotonergic signaling used to adapt the worm's behaviour to fast changes in the environment affects insulin-like signaling and the TGF beta signaling pathway,[111] which control long-term adaption.

text: In the fruit fly insulin both regulates blood sugar as well as acting as a growth factor. Thus, in the fruit fly, serotonergic neurons regulate the adult body size by affecting insulin secretion.[112][113] Serotonin has also been identified as the trigger for swarm behavior in locusts.[114] In humans, though insulin regulates blood sugar and IGF regulates growth, serotonin controls the release of both hormones, modulating insulin release from the beta cells in the pancreas through serotonylation of GTPase signaling proteins.[24] Exposure to SSRIs during Pregnancy reduces fetal growth.[115]

text: Genetically altered C. elegans worms that lack serotonin have an increased reproductive lifespan, may become obese, and sometimes present with arrested development at a dormant larval state.[116][117]

text: Aging and age-related phenotypes[edit]

text: Serotonin is known to regulate aging, learning and memory. The first evidence comes from the study of longevity in C. elegans.[118] During early phase of aging[vague], the level of serotonin increases, which alters locomotory behaviors and associative memory.[119] The effect is restored by mutations and drugs (including mianserin and methiothepin) that inhibit serotonin receptors. The observation does not contradict with the notion that the serotonin level goes down in mammals and humans, which is typically seen in late but not early[vague] phase of aging.

text: Biochemical mechanisms[edit]

text: Biosynthesis[edit]

text: In animals including humans, serotonin is synthesized from the amino acid L-tryptophan by a short metabolic pathway consisting of two enzymes: tryptophan hydroxylase (TPH), aromatic amino acid decarboxylase (DDC) and the coenzyme pyridoxal phosphate. The TPH-mediated reaction is the rate-limiting step in the pathway. TPH has been shown to exist in two forms: TPH1, found in several tissues, and TPH2, which is a neuron-specific isoform.[120]

text: Serotonin can be synthesized from tryptophan in the lab using Aspergillus niger and Psilocybe coprophila as catalysts. The first phase to 5-hydroxytryptophan would require letting tryptophan sit in ethanol and water for 7 days, then mixing in enough HCl (or other acid) to bring the pH to 3, and then adding NaOH to make a pH of 13 for 1 hour. Asperigillus niger would be the catalyst for this first phase. The second phase to synthesizing tryptophan itself from the 5-hydroxytryptophan intermediate would require adding ethanol and water, and letting sit for 30 days this time. The next two steps would be the same as the first phase: adding HCl to make the pH = 3, and then adding NaOH to make the pH very basic at 13 for 1 hour. This phase uses the Psilocybe coprophila as the catalyst for the reaction.[121]

text: Serotonin taken orally does not pass into the serotonergic pathways of the central nervous system, because it does not cross the blood–brain barrier.[122] However, tryptophan and its metabolite 5-hydroxytryptophan (5-HTP), from which serotonin is synthesized, does cross the blood–brain barrier. These agents are available as dietary supplements, and may be effective serotonergic agents. One product of serotonin breakdown is 5-hydroxyindoleacetic acid (5-HIAA), which is excreted in the urine. Serotonin and 5-HIAA are sometimes produced in excess amounts by certain tumors or cancers, and levels of these substances may be measured in the urine to test for these tumors.

text: Effects of food content[edit]

text: Consuming purified tryptophan increases brain serotonin whereas eating foods containing tryptophan does not.[123] This is because the transport system which brings tryptophan across the blood-brain barrier is also selective for the other amino acids contained in protein sources.[122] High plasma levels of other large neutral amino acids compete for transport and prevent the elevated plasma tryptophan from increasing serotonin synthesis.

text: History and etymology[edit]

text: In 1935, Italian Vittorio Erspamer showed an extract from enterochromaffin cells made intestines contract. Some believed it contained adrenaline, but two years later, Erspamer was able to show it was a previously unknown amine, which he named "enteramine".[124] In 1948, Maurice M. Rapport, Arda Green, and Irvine Page of the Cleveland Clinic discovered a vasoconstrictor substance in blood serum, and since it was a serum agent affecting vascular tone, they named it serotonin.[125]

text: In 1952, enteramine was shown to be the same substance as serotonin, and as the broad range of physiological roles was elucidated, the abbreviation 5-HT of the proper chemical name 5-hydroxytryptamine became the preferred name in the pharmacological field.[126] Synonyms of serotonin include: 5-hydroxytriptamine, thrombotin, enteramin, substance DS, and 3-(β-Aminoethyl)-5-hydroxyindole.[127] In 1953, Betty Twarog and Page discovered serotonin in the central nervous system.[128]


document_title: Nicky, Ricky, Dicky & Dawn

question_text: nicky ricky dicky & dawn mae real name

question_tokens: nicky ricky dicky & dawn mae real name

root

text: Nicky, Ricky, Dicky & Dawn

text: Premise[edit]

text: The series focuses on quadruplets Nicky, Ricky, Dicky, and Dawn Harper, 10-years-old at the start of the series,[1] who have nothing in common and often fight, but must work together to solve everyday situations.

tag: p

text: Episodes[edit]

text: SeasonEpisodesOriginally airedFirst airedLast aired120September 13, 2014 (2014-09-13)March 24, 2015 (2015-03-24)225May 23, 2015 (2015-05-23)August 6, 2016 (2016-08-06)323January 7, 2017 (2017-01-07)August 5, 2017 (2017-08-05)414January 6, 2018 (2018-01-06)August 4, 2018 (2018-08-04)

tag: table

text: Cast and characters[edit]

text:
Brian Stepanek as Tom, the father of the quadruplets. It is a running gag in the series that he cares more about his possessions than his children, but he loves his family and is a kid at heart.
Allison Munn as Anne, the mother of the quadruplets who usually gets caught up in Tom's new obsessions.
Aidan Gallagher as Nicky, the youngest of the quadruplets. He is shown to be quite comedic, quirky, and easily confused.
Casey Simpson as Ricky, is the second oldest of the quadruplets. He is the smart one of the group, always seen carrying a book or doing his homework. He is also a neat freak and a bit of a goody two-shoes, though he occasionally tries to prove to Dawn and his brothers that he can bend rules as well.
Mace Coronel as Dicky, the third oldest and easy-going quadruplet who cares a great deal about his appearance. He always takes the easy way out. He ships himself to Australia in "Quadcodile Dundee".
Lizzy Greene as Dawn, the oldest of the quadruplets. Although she's always seen bothering her brothers, she does care about them deeply. There is a consistent rivalry for the leader spot of the quads between her and Ricky.
Gabrielle Elyse as Josie, a worker at Tom's sporting shop and babysitter for Nicky, Ricky, Dicky and Dawn. She only appears in the first season.
Kyla-Drew Simmons as Mae, the quads' friend and Dawn's best friend. She once called herself "the fifth quad". In the first two seasons, she is a recurring character, but she is promoted to a main character in the third season.

tag: ul

text: Production[edit]

text: The series was originally picked up for 13 episodes on March 13, 2014, but was later increased to 20 episodes.[2] The series premiered on September 13, 2014. On November 18, 2014, the series was renewed for a second season.[3] The second season premiered on May 23, 2015. On February 9, 2016, Nickelodeon renewed Nicky, Ricky, Dicky & Dawn for a third season of 14 episodes. It was also confirmed that Matt Fleckenstein would step down as show runner.[4] Actress Lizzy Greene announced on her Twitter account that production for season three started on April 26, 2016.[5] The third season premiered on January 7, 2017. The series was renewed for a fourth season and had its episode order for the third season increased from 14 to 24 by Nickelodeon on March 20, 2017.[6] On October 4, 2017, it was announced that Mace Coronel would be leaving both Nicky, Ricky, Dicky & Dawn, about five episodes before the end of the fourth season, and Nickelodeon.[7] On November 15, 2017, Nickelodeon announced that the fourth season would be the last.[8]

text: Reception[edit]

text: Ratings[edit]

text:
Season

Episodes

First aired

Last aired
Avg. viewers(millions)

Date

Viewers(millions)

Date

Viewers(millions)

1

20

September 13, 2014 (2014-09-13)

1.60[9]

March 24, 2015 (2015-03-24)

1.75[10]
1.75

2

25

May 23, 2015 (2015-05-23)

1.11[11]

August 6, 2016 (2016-08-06)

1.31[12]
1.46

3

23

January 7, 2017 (2017-01-07)

1.58[13]

August 5, 2017 (2017-08-05)

2.00[14]
1.47

4

14

January 6, 2018 (2018-01-06)

1.08[15]

August 4, 2018 (2018-08-04)

0.84[16]
0.95

text: Awards and nominations[edit]

text: This section does not cite any sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (March 2017) (Learn how and when to remove this template message)

text:
Year

Award

Category

Result

Refs

2015

Nickelodeon Kids' Choice Awards

Favorite TV Show

Nominated

[17][18]

2017

Nickelodeon Kids' Choice Awards

Favorite TV Show – Kids' Show

Nominated

[19]


document_title: Non-cooperation movement

question_text: who was the first leader arrested in the non corporation movement

text: Non-cooperation movement

text: Factors leading to the movement[edit]

text: The Non-cooperation movement was a reaction to the oppressive policies of the British Indian government such as the Rowlatt Act and the Jallianwala Bagh massacre. A meeting of civilians held at Jallianwala Bagh near the Golden Temple in Amritsar was fired upon by soldiers under the command of Brigadier-General Reginald Dyer, killing 379 protesters and injuring thousands. The outcry generated by the massacre led to thousands of unrests and more deaths at the hands of the police. The massacre became the most infamous event of British rule in India.

text: Gandhi was horrified. He lost all faith in the goodness of the British government and declared that it would be a "sin" to cooperate with the "satanic" government.

text: Indian Muslims who had participated in the Khilafat movement to restore the status of the Caliph gave their support to the non-cooperation movement. In response to the Jallianwala Bagh Massacre and other violence in Punjab, the movement sought to secure Swaraj, independence for India. Gandhi promised Swaraj in one year if his Non-Cooperation programme was fully implemented. The other reason to start the non-cooperation movement was that Gandhi lost faith in constitutional methods and turned from cooperator of British rule to non-cooperator.

text: Other causes include economic hardships to the common man, which the nationalists attributed to the flow of Indian wealth to Britain, the ruin of Indian artisans due to British factory-made goods replacing handmade goods, and resentment with the British government over Indian soldiers dying in World War I while fighting as part of the British Army.

text: The calls of early political leaders like Bal Gangadhar Tilak (Congress Extremists) were called major public meetings. They resulted in disorder or obstruction of government services. The British took them very seriously and imprisoned him in mandale in Burma and V.O.Chidambaram Pillai Got 40 years imprisonment . The non-cooperation movement aimed to challenge the colonial economic and power structure, and British authorities would be forced to take notice of the demands of the independence movement .

text: Satyagraha[edit]

text: Satyagraha is a Sanskrit term which is a compound of two words: satya ("truth") and agraha ("holding firmly to" or "force"). Gandhi's call was for a nationwide protest against the Rowlatt Act. All offices and factories would be closed. Indians would be encouraged to withdraw from Raj-sponsored schools, police services, the military, and the civil service, and lawyers were asked to leave the Raj's courts. Public transportation and English-manufactured goods, especially clothing, was boycotted.

text: Veterans like Bal Gangadhar Tilak, Bipin Chandra Pal, Mohammad Ali Jinnah, Annie Besant, and Sammed Akiwate opposed the idea outright. The All India Muslim League also criticized the idea. But the younger generation of Indian nationalists were thrilled, and backed Gandhi. The Congress Party adopted his plans, and he received extensive support from Muslim leaders like Maulana Azad, Mukhtar Ahmed Ansari, Hakim Ajmal Khan, Abbas Tyabji, Maulana Muhammad Ali and Maulana Shaukat Ali.

text: The eminent Hindi writer, poet, play-wright, journalist, and nationalist Rambriksh Benipuri, who spent more than eight years in prison fighting for India's independence, wrote:

text: When I recall Non-Cooperation era of 1921, the image of a storm confronts my eyes. From the time I became aware, I have witnessed numerous movements, however, I can assert that no other movement upturned the foundations of Indian society to the extent that the Non-Cooperation movement did. From the most humble huts to the high places, from villages to cities, everywhere there was a ferment, a loud echo.[1]

text: Success and suspension[edit]

text: The success of the revolt was a total shock to British authorities and a massive encouragement to millions of Indian nationalists. On 5th February,1922 a clash took place at Chauri Chaura, a small town in the district of Gorakhpur, Uttar Pradesh. A police officer had beaten some volunteers picketing a liquor shop. A whole crowd of peasants that had gathered there went to the police chowki (pron.-chau key) (station). The mob set fire to the police chowki with some 22 police men inside it.

text: Mahatma Gandhi felt that the revolt was veering off-course, and was disappointed that the revolt had lost its non-violent nature. He did not want the movement to degenerate into a contest of violence, with police and angry mobs attacking each other back and forth, victimizing civilians in between. Gandhi appealed to the Indian public for all resistance to end, went on a fast lasting 3 weeks, and called off the non-cooperation movement.

text: End of non-cooperation[edit]

text: The non-cooperation movement was withdrawn because of the Chauri Chaura incident. Although he had stopped the national revolt single-handedly, on March 10, 1922, Gandhi was arrested. On March 18, 1922, he was imprisoned for six years for publishing seditious materials. This led to suppression of the movement and was followed by the arrest of other leaders.

text: Although most Congress leaders remained firmly behind Gandhi, the determined broke away. The Ali brothers would soon become fierce critics. Motilal Nehru and Chittaranjan Das formed the Swaraj Party, rejecting Gandhi's leadership. Many nationalists had felt that the non-cooperation movement should not have been stopped due to isolated incidents of violence, and most nationalists, while retaining confidence in Gandhi, were discouraged.

text: Contemporary historians and critics suggest that the movement was successful enough to break the back of British rule, and possibly even the catalyst for the movement that lead to independence in 1947.

text: But many historians and Indian leaders of the time also defended Gandhi's judgment. However, there have been claims that Gandhi called off the movement in an attempt to salvage his own personal image, which would have been tarnished had he been blamed for the Chauri Chaura incident, although a similar type of movement was introduced in 1930, the civil disobedience movement. The main difference was the introduction of a policy of violating the law.

text: Savings[edit]

text: Gandhi's commitment to non-violence was redeemed when, between 1930 and 1934, tens of millions again revolted in the Salt Satyagraha which made India's cause famous worldwide for its unerring adherence to non-violence. The Satyagraha ended in success: the demands of Indians were met, and the Congress Party was recognized as a representative of the Indian people. The Government of India Act 1935 also gave India its first taste in democratic self-governance.


document_title: MIDI beat clock

question_text: what is the rate of midi clock in ppqn

question_tokens: what is the rate of midi clock in ppqn

text: MIDI beat clock

text: MIDI beat clock (also known as MIDI timing clock or simply MIDI clock) is a clock signal that is broadcast via MIDI to ensure that several MIDI-enabled devices such as a synthesizer or music sequencer stay in synchronization. It is not MIDI timecode.

text: Unlike MIDI timecode, the MIDI beat clock is tempo-dependent. Clock events are sent at a rate of 24 ppqn (pulses per quarter note). Those pulses are used to maintain a synchronized tempo for synthesizers that have BPM-dependent voices and also for arpeggiator synchronization. Location information can be specified using MIDI Song Position Pointer (SPP, see below), although many simple MIDI devices ignore this message.

text: Because of limitations in MIDI and synthesizers, devices driven by MIDI beatclock are often subject to clock drift.[citation needed]

text: MIDI beat clock defines the following real time messages:

text:
clock (decimal 248, hex 0xF8)
start (decimal 250, hex 0xFA)
continue (decimal 251, hex 0xFB)
stop (decimal 252, hex 0xFC)

text: MIDI also specifies a System Common message called Song Position Pointer (SPP). SPP can be used in conjunction with the above realtime messages for complete sync. This message consists of 3 bytes; a status byte (decimal 242, hex 0xF2), followed by two 7-bit data bytes (least significant byte first) forming a 14-bit value which specifies the number of "MIDI beats" (1 MIDI beat = a 16th note = 6 clock pulses) since the start of the song. This message only needs to be sent once if a jump to a different position in the song is needed. Thereafter only realtime clock messages need to be sent to advance the song position one tick at a time.


document_title: Ryan Michelle Bathe

question_text: who is ryan michelle bathe on this is us

text: Ryan Michelle Bathe

text: Personal life[edit]

text: Bathe grew up in Stamford, Connecticut. She graduated from Stanford University, and she received a Master of Fine Arts from New York University.[1] She is a member of Delta Sigma Theta Sorority, Incorporated. In June 2007, Ryan Michelle Bathe married fellow actor (and Stanford alum) Sterling K. Brown. They have two sons.[2][3]

text: Career[edit]

text: Bathe has had guest starring roles in a number of television shows, include ER, Half & Half, Girlfriends, Brothers & Sisters, and How I Met Your Mother. She was regular cast member during the second season of the ABC legal drama series Boston Legal playing attorney Sara Holt.[4] From 2009 to 2010, she had a recurring role on the short-lived NBC medical drama Trauma, and in 2011 had starring role in the TV Land sitcom Retired at 35.[5] She had main roles in the independent films All About Us and April Moon.

text: In 2012, Bathe co-starred opposite Katherine Heigl in the crime comedy film One for the Money. Later that year, she had a recurring role opposite her real life husband Sterling K. Brown in the Lifetime drama series Army Wives.[6] In 2014, she was a female lead opposite Kevin Hart in the ABC comedy pilot Keep It Together.[7] In 2016, Bathe was cast in a recurring role in the NBC drama series, This Is Us, also starring Brown.[8]

text: Selected filmography[edit]

text:
Empire as Celeste (2018)
This Is Us as Yvette (Season 1) (2016)
Army Wives as Charlie (Season 6 recurring character) (2012)
One for the Money as Jackie (hooker) (2011)
Retired at 35 as Jessica (Season 1 main cast member) (2011)
Private Practice (2010)
Trauma (2009)
Leaving Barstow (2008)
How I Met Your Mother (April 2008) as Lily's friend Michelle
Boston Legal as Sara Holt (2005–2006)
Good Fences (2003)
Bones (2009)


document_title: Squealer (Animal Farm)

question_text: who does squealer in animal farm represent in the russian revolution

text: Squealer (Animal Farm)

text: Allusion[edit]

text: Throughout the novel Squealer is highly skilled at making speeches to the animals. He is also one of the leaders of the farm. Under the rule of Napoleon, Squealer does things to manipulate the animals. Squealer represents Vyacheslav Molotov who was Stalin's protégé and head of Communist propaganda.

text: It is also possible that Squealer represents the Soviet newspaper, Pravda. This paper was Stalin's key to propaganda in the communist times, and was very powerful to proletarians of the time (proletarians being Boxer, the horse).

text: Squealer's Arguments[edit]

text: Squealer takes the central role in making announcements to the animals, as Napoleon appears less and less often as the book progresses. Near the start of the book, it is said that he was very convincing and could turn "black into white". This is foreshadowing several euphemisms he uses to maintain the control of the barn through difficult times. He is Napoleon's (Stalin's) key to propaganda for the farm (Soviet Union).

text: Breaking the Commandments and Telling Lies[edit]

text: Throughout the book, Napoleon and Squealer broke the Seven Commandments, the tenets on which governance of the farm is based. To prevent the animals from suspecting them, Squealer preys on the animals' confusion and alters the Commandments from time to time as the need arises. Squealer falls off a ladder while trying to change one of the commandments in the night. A few days later it is discovered that Squealer was altering the commandment regarding alcohol which suggests the reason he fell off the ladder was because he was drunk at the time. Orwell uses Squealer mainly to show how the increasingly totalitarian and corrupt regime uses propaganda and deceit to get its ideas accepted and implemented by the people. In the end, Squealer reduces the Seven Commandments into one commandment, that "All animals are equal, but some animals are more equal than others".

text: A point is made by how Napoleon dismisses the education of the mature animals as a lost case while Snowball attempts to educate them all (he does focus on the key ideals of Animalism, but nevertheless) and starts many committees which are apparently for the good of the entire Farm — Napoleon is explicitly stated to have 'no interest' in these committees, instead snatching up newborn dogs to educate them in seclusion. He takes advantage of their malleable minds and molds them to his liking — the dogs show up later as a secret police. Meanwhile, Snowball's programs are generally failures. As the newer generations are brought up with propaganda and the old generations are ignored, Squealer begins making changes to the Seven Commandments. The animals experience a vague feeling of unease, and when Clover and Muriel ponder the changes, they are told that they have simply forgotten — and they accept this easily, which is helped along by the growling dogs that accompany the pigs everywhere. Benjamin alone appears to understand what is happening, though he never acts. If asked, he says that donkeys live a long time, and that "none of you has ever seen a dead donkey". True to his cynical nature, he continues to believe that life never gets better. He is briefly outraged by Boxer's death, but becomes ever more cynical when Squealer again convinces the denizens of the Farm that Boxer was only taken to a hospital.

text: In the end, this works out to Squealer's advantage. Terror and silver-tongued oration fool nearly everyone, and the sole animal who sees through these fronts, Benjamin, is simply too cynical to do anything.

text: This reflected Orwell's view that events in Russia following the Revolution of 1917 had followed an unwelcome path, and that the egalitarian socialism he believed in had there become a brutal dictatorship built around a cult of personality and enforced by terror and lies. Orwell wrote, "All people who are morally sound have known since about 1931 that the Russian régime stinks".[1] Squealer as the chief propagandist of the regime is early prominent in the story and Orwell delineates the path down which small lies lead to bigger lies. Orwell regarded propaganda as a feature of all modern governments but especially prominent in totalitarian regimes, which depended on it. In The Prevention of Literature (1946) he described 'organised lying' as a crucial element of totalitarian states.[2]


document_title: Destroy All Humans!

question_text: who owns the rights to destroy all humans

text: Destroy All Humans!

text: Setting[edit]

text: The games take place mostly on Earth where the Furon Cryptosporidium, also known as Crypto, is tasked by his superiors to gather Furon DNA locked inside human brain stems in order to save his race from cloning themselves into extinction. In Destroy All Humans!, Crypto's objectives also include investigating what happened to his previous clone. Destroy All Humans! 2 features Crypto hunting for revenge, after the KGB try to assassinate him and successfully destroy the mothership and his mission officer, Orthopox, as well as exterminating the Furons' enemy from the Martian War, the Blisk. Destroy All Humans! Big Willy Unleashed involves Crypto protecting Pox's new fast food chain using a giant robot mech disguised as the restaurant's mascot, called "Big Willy". Destroy All Humans! Path of the Furon is available on Xbox 360 (and PlayStation 3 only in Australia and Europe), and involves Crypto seeking enlightenment to help him stop a conspiracy that threatens the Furon empire. Destroy All Humans! takes place in 1959; Destroy All Humans! 2 takes place in 1969; Destroy All Humans! Big Willy Unleashed takes place in 1975; Destroy All Humans! Path of the Furon takes place in 1979.

text: Games[edit]

text:
Aggregate review scoresAs of June 2, 2013.

Game

GameRankings

Metacritic

Destroy All Humans!

(Xbox) 76.98%[2](PS2) 76.04%[3]

(Xbox) 76[4](PS2) 74[5]

Destroy All Humans! 2

(Xbox) 76.61%[6](PS2) 75.75%[7]

(Xbox) 74[8](PS2) 74[9]

Destroy All Humans! Big Willy Unleashed

(Wii) 53.42%[10]

(Wii) 53[11]

Destroy All Humans! Path of the Furon

(X360) 38.41%[12](PS3) 26.50%[13]

(X360) 34[14]

text: Destroy All Humans![edit]

text: In 1959, Cryptosporidium 137 first arrived on Earth to investigate the planet and search for his predecessor clone, Cryptosporidium-136, who disappeared in 1947 after Orthopox 13 sent him to Earth on a similar mission. Pox sends Crypto on a mission to harvest human brain stems (which contain Furon DNA due to an encounter between Furon warriors and humans in ancient times) to prevent his species from going extinct. To accomplish his mission, he must defeat Majestic, a shadowy government organization led by a black-clad figure named Silhouette. After accomplishing this, Crypto takes over the United States by posing as the President.

text: Destroy All Humans! 2[edit]

text: Ten years have gone by since Crypto defeated Majestic and took over the American government. Orthropox 13 has died after a Soviet nuclear missile destroyed the Furon mothership. Pox has downloaded his consciousness into a personal holographic projector designed to communicate between Furons on Motherships and planet surfaces. Pox's unit, dubbed a HoloPox, allows him to communicate with, advise, and vex Crypto down on Earth. Crypto 137 has died of unknown causes, but appears in Big Willy Unleashed and Crypto 138, a clone with pure Furon DNA harvested from human brains, has taken his place as the President. Crypto 138 is the first Furon in millennia to possess genitalia, as his pure DNA has not been corrupted by radiation. When the KGB destroy the mothership and Pox, Crypto must find a way to stop them from destroying what he has worked so hard to achieve. Along the way, he is supported by Natalya Ivanova, a rogue KGB agent whom he constantly hits on. He also comes across the Blisk, the dreaded enemy that the Furons thought they defeated in the Martian War.

text: Destroy All Humans! Big Willy Unleashed[edit]

text: Big Willy Unleashed takes place after Destroy All Humans! 2 and before Path of the Furon. Crypto and Pox start a fast food restaurant that serves human meat from all the people Crypto has killed harvesting more Furon DNA. Later, their rival restaurant, Colonel Kluckin' (a parody of Colonel Sanders), discovers their secret, where upon Crypto must protect the restaurant with the Big Willy mascot mech.

text: Destroy All Humans! Path of the Furon[edit]

text: Using the money earned from the Big Willy fast food franchise that Orthopox started, Pox and his destructive Furon warrior minion Crypto have opened a "family friendly" casino with which they use to obtain a steady financial income and human DNA. Crypto has lost his motivation because the death of Natalya, and has forgotten what it means to destroy humans. He drinks too much alcohol, watches too much television, and has ultimately become lazy. Later Crypto is attacked by mysterious cyborgs called Nexosporidium Warriors, who arrive from his own planet, which frightens both Crypto and his commander Pox. Soon Crypto finds himself face to face with a conspiracy from his own homeworld that, if not stopped, could destroy his entire race. In the midst of all the chaos, Crypto hears a voice in his head, telling him to go to the city of Shen Long. Later, Crypto, while in Sunnywood, is shot in the neck, faints, and then wakes up in a Kung Fu monastery where he is greeted by a Furon martial arts expert known as The Master. The Master beseeches him to submit to his tutelage, and train in mind and firepower, to help him defeat these new threats. Now Crypto is about to go down the path to enlightenment, shape his own destiny, uncover who is behind this frightening conspiracy, and ultimately be able to destroy all humans.

text: Future[edit]

text: The franchise intellectual property (IP) holder, THQ, went bankrupt in late 2012. During this, many IPs of THQ were sold off. On April 22, 2013, it was announced that in a $4.9 million deal with THQ, Nordic Games purchased the rights to Destroy All Humans! among other IPs.[15] On their official Twitter account the company claimed: "We are thinking about what to do next with it."[16] In June 2016, Reihard Pollice, Nordic Games' product development director and executive producer, stated, "there are a few options we are evaluating now. Hope to get started on one of these soon."[17] In late 2016, Destroy All Humans! and Destroy All Humans! 2 were ported to PlayStation 4 upsized to 1080p.[1][18].  In 2018, Destroy All Humans! was ported to Xbox One in their backward compatibility catalog.[19]


document_title: Canon PowerShot S

question_text: when did the canon powershot sx530 come out

text: Canon PowerShot S

text: G-series in a compact body[edit]

text: From the PowerShot S90 onwards the S-series continues a line of Canon compact digital cameras that commenced with the Ixus 900Ti and feature the Digic image processors and larger than average sensors as fitted to the advanced PowerShot G-series cameras. The Ixus / S-series and the equivalent G-series models are listed below:

text:
Ixus 900Ti(SD900)* / PowerShot G7 / Digic III / 10MP 3648 × 2736 1/1.8″ CCD.
Ixus 960IS(SD950IS)* / PowerShot G9 / Digic III / 12.1MP 4000 × 3000 1/1.7″ CCD.
Ixus 980IS(SD990IS) / PowerShot G10 / Digic 4 / 14.7MP 4416 × 3312 1/1.7″ CCD.
PowerShot S90, S95, S200 / PowerShot G11, G12 / Digic 4 / 10MP 3648 × 2736 1/1.7″ CCD (S200 features Digic 5).
PowerShot S100, S110 / PowerShot G15 / Digic 5 / 12.1MP 4000×3000 1/1.7" CMOS.
Powershot S120 / PowerShot G16 / Digic 6 / 12.1MP 4000×3000 1/1.7" CMOS.

text: (* The Ixus 900Ti and 960IS feature a titanium body.)

text: Models[edit]

text: Compact S series[edit]

text: The Sxx series is made up of two sub-series. The S10 and S20 were compact point-and-shoot cameras, while the S30-onwards were prosumer digital cameras that were the de-contented, lower-cost alternative to the equivalent G-series camera at the time.

text:
Model
Release
date
Sensor
resolution, size, type
Lens (35 mm equiv)
zoom, aperture
Image processor
LCD screen
size, pixels
Card
Size
W×H×D
(mm)
Weight
(body, g)
Photo
Notes

Point-and-Shoot

S10
October 1999
2.1 MP
1600×1200
1/2" CCD
35–70 mm (2×)
f/2.8–4.0

1.8"
CF
105.4 × 69.4 × 33.8
270

Smallest true zoom 2 MP camera when released[1]

S20
March 2000
3.3 MP
2048×1536
1/1.8" CCD
32–64 mm (2×)
f/2.9–4.0

[2]

Prosumer

S30
September 2001
3.2 MP
2048×1536
1/1.8" CCD
35–105 mm (3×)
f/2.8–4.9

1.8"
CF
112 × 58 × 42
260

New larger body shape, addition of manual controls, added RAW support[3]

S40
October 2001
4.1 MP
2272×1704
1/1.8" CCD

[4]

S45
October 2002
DIGIC

[5]

S50
March 2003
5.0 MP
2592×1944
1/1.8" CCD

[6]

S60
June 2004
28–100 mm (3.6×)
f/2.8–5.3
114.0 × 56.5 × 38.8
230

First to use wide-angle lens, supports conversion lenses, smaller and lighter body with re-arranged rear panel[7]

S70
September 2004
7.1 MP
3072×2304
1/1.8" CCD

[8]

S80
October 2005
8.0 MP
3264×2448
1/1.8" CCD
DIGIC II
2.5"
115,000
SD, MMC
104.0 × 57.0 × 38.8
225

Redesigned smaller and lighter body, no RAW support. Includes new 4:3 HD Movie (1024x768) Mode[9]
Bears similarity to later Powershot G series models such as G10 & G11[10]

S90
September 2009
10.0 MP
3648×2736
1/1.7" CCD
28–105 mm (3.8×)
f/2.0–4.9
DIGIC 4
3.0"
461,000
SD, SDHC, MMC, MMC+, HC MMC+
100.0 × 58.4 × 30.9
175

New High Sensitivity System and higher ISO speeds, f/2.0 lens, image stabilization. HD movie feature removed.[11] Bears similarity to earlier Powershot SD series models[10]

S95
August 2010
99.8 × 58.4 × 29.5
170

Hybrid IS, 720p HD video.[12]

S100
September 2011
12.1 MP
4000×3000
1/1.7" CMOS
24–120 mm (5×)
f/2.0–5.9
DIGIC 5
SD, SDHC, SDXC, Eye-Fi
98.9 × 59.8 × 26.7
173

GPS, 1080p HD video.[13] Not to be confused with the older S100, the first Digital IXUS/ELPH camera.

S110
September 2012
3.0" 461,000 touch screen
98.8 × 59.0 × 26.9

No GPS, 1080p HD video. IS. Wifi. Touch screen.

S120
August 2013
12.1 MP
4000×3000
1/1.7" BSI-CMOS
24–120 mm (5×)
f/1.8–5.7
DIGIC 6
3.0" 922,000 touch screen
SD, SDHC, SDXC
100.2 × 59.0 × 29.0
193

WiFi. Touch screen. Maximum aperture 1.8.

S200
February 2014
10.0 MP
3648x2736
1/1.7" CCD
24–120 mm (5×)
f/2.0–5.9
DIGIC 5
3.0" 461,000
SD, SDHC, SDXC
100 × 59 × 26
181

WiFi. No RAW. 720p HD video.

text: Super Zoom S/SX series[edit]

text: The S1 to SX60 series consists of ultra-zoom cameras, having longer zoom ranges and a more extensive list of features. The SX100 and later SX models are a more compact, affordable spin-off. The "SX" stands for "Super Zoom." All S and SX models feature image stabilization and most have full manual controls.

text:
Model
Release
date
Sensor
resolution, size, type
Lens (35 mm equiv)
zoom, aperture
Image processor
LCD screen
size, pixels
Card
Size
W×H×D
(mm)
Weight
(body, g)
Photo
Notes

Sx / SXx series

S1 IS
March 2004
3.2 MP
2048×1536
1/2.7" CCD
38–380 (10×)
f/2.8–3.1
DIGIC
1.5" vari-angle
114,000
CF
111.0 × 78.0 × 66.1
370

First in the series[14]

S2 IS
June 2005
5.0 MP
2592×1944
1/2.5" CCD
36–432 (12×)
f/2.7–3.5
DIGIC II
1.8" vari-angle
115,000
SD
113 × 78.0 × 75.5
405

[15]

S3 IS
February 2006
6.0 MP
2816×2112
1/2.5" CCD
2.0" vari-angle
115,000
SD, SDHC, MMC
113.4 × 78.0 × 75.5
410

[16]

S5 IS
June 2007
8.0 MP
3264x2448
1/2.5" CCD
DIGIC III
2.5" vari-angle
207,000
117.0 × 80.0 × 77.7
450

First S series with hotshoe[17]

SX1 IS
December 2008
10 MP
3648×2736
1/2.3" CMOS
28–560 (20×)
f/2.8–5.7
DIGIC 4
2.8" vari-angle
230,000
SD, SDHC, MMC, MMC+, HC MMC+
128 × 88 × 88
585

Replaces S5 IS, first PowerShot to use CMOS, firmware update allows shooting in RAW, and full HD 1080p recording support[18]

SX10 IS
October 2008
10 MP
3648×2736
1/2.3" CCD
2.5" vari-angle
230,000
124 × 88 × 87
560

Replaces S5 IS[19]

SX20 IS
August 2009
12 MP
4000×3000
1/2.3" CCD

Replaces SX10 IS[20]

SX30 IS
September 2010
14.1 MP
4320×3240
1/2.3" CCD
24-840 (35x)
f/2.7-5.8
2.7" vari-angle
230,000
122.9 × 92.4 × 107.7
601

Replaces SX20 IS[21]

SX40 HS
September 2011
12.1 MP
4000×3000
1/2.3" CMOS
DIGIC 5
2.7" vari-angle
230,000
122.9 × 92.4 × 107.7
600

Replaces SX1/SX30 IS[22]

SX50 HS
September 2012
12.1 MP
4000×3000
1/2.3" CMOS
24-1200 (50x)
f/3.4-6.5
2.8" vari-angle
461,000
SD, SDHC, SDXC
122.5 × 87.3 × 105.5
595

Replaces SX40 HS[23]

SX60 HS
September 2014
16.1 MP
4608 x 3456
1/2.3" CMOS
21-1365 (65x)
f/3.4-6.5
DIGIC 6
3.0" vari-angle
922,000
SD, SDHC, SDXC
127 x 91 x 114 mm
649

Replaces SX50 HS[24]

SX100 series (2007-2013, economic superzooms)

SX100 IS
August 2007
8.0 MP
3264×2448
1/2.5" CCD
36–360 (10×)
f/2.8–4.3
DIGIC III
2.5" fixed
172,000
SD, SDHC, MMC, MMC+, HC MMC+
108.7 × 71.4 × 46.7
265

Smaller spin-off of SX series[25]

SX110 IS
September 2008
9.0 MP
3456×2592
1/2.3" CCD
3.0" fixed
230,000
111 × 71 × 45

[26]

SX120 IS
August 2009
10.0 MP
3648×2736
1/2.5" CCD
DIGIC 4
111 × 71 × 45
245

[27]

SX130 IS
September 2010
12.1 MP
4000x3000
1/2.3" CCD
28-336mm (12x)
f/3.4-5.6
113.3 x 73.2 x 45.8
260

Replaces SX120 IS[28]

SX150 IS
August 2011
14.1 MP
4320 x 3240
1/2.3" CCD
SD, SDHC, SDXC, MMC, MMC+, HC MMC+, Eye-Fi
258

Replaces SX130 IS[29]

SX160 IS
September 2012
16.0 MP
4608 x 3456
1/2.3" CCD
28-448mm (16x)
f/3.4-5.9
111.0 x 72.5 x 44.1
291

Replaces SX150 IS

SX170 IS
2013
16.0 MP
4608 x 3456
1/2.3" CCD
28-448mm (16x)
f/3.5-5.9
108.0 x 71 x 43.9
228

The only one in SX100-series that uses a Li-Ion battery

SX200 series (2009-2013, advanced pocketable superzooms)

SX200 IS
March 2009
12.1 MP
4000x3000
1/2.3" CCD
28–336 (12x)
f/3.4–5.3
DIGIC 4
3.0" fixed
230,000
SD, SDHC, MMC, MMC+, HC MMC+
103 × 61 × 38
220

Adds HD video[30]

SX210 IS
March 2010
14.1 MP
4320×3240
1/2.3" CCD
28–392 (14×)
f/3.1–5.9
SD, SDHC, SDXC, MMC, MMC+, HC MMC+
106 × 59 × 32
215

[31]

SX220 HS
February 2011
12.1 MP
4000x3000
1/2.3" CMOS
3.0" fixed
461,000
SD, SDHC, SDXC, MMC, MMC+, HC MMC+, Eye-Fi
106 x 59 x 33

No GPS[32]

SX230 HS

Adds GPS[32]

SX240 HS
February 2012
25–500 (20×)
f/3.5–6.8
DIGIC 5
SD, SDHC, SDXC, Eye-Fi
106 x 61 x 33
224

No GPS.[33] Not sold in North America; the GPS-equipped SX260 HS, otherwise identical to this model, is sold there instead.[34]

SX260 HS
231

Adds GPS[33]

SX270 HS
April 2013
DIGIC 6
SD, SDHC, SDXC
106.4 x 61.1 x 32.6
227

With GPS. There is also Wi-Fi. But not sold in North America; the GPS- is also equipped in SX280 HS and it is sold there instead.

SX280 HS
106.4 x 62.8 x 32.6
233

With GPS and Wi-fi

SX400 series (2014-, cheaper alternative to the SX500-series, no manual controls, CCD-sensors)

SX400 IS
October 2014
16.0 MP
4608x3456
1/2.3" CCD
24-720 (30x) f/3.4-5.8
DIGIC 4+
3.0" fixed
230,000
SD, SDHC, SDXC
104.4 x 69.1 x 80.1
313

No Wi-Fi or GPS, Very similar to SX500 IS

SX410 IS
February 2015
20.0 MP
5152x3864
1/2.3" CCD
24-960 (40x) f/3.5-6.3
104.4 x 69.1 x 85.1
325

No Wi-Fi or GPS

SX420 IS
January 2016
24-1008 (42x) f/3.5-6.6
104 x 69 x 85
325

WiFI

SX430 IS
January 2017
24-1080 (45x) f/3.5-6.8
104.4 x 69.1 x 85.1
323

WiFi

SX500 series (2012-, cheaper and lighter alternative to SXx series)

SX500 IS
April 2012
16.0 MP
4608x3456
1/2.3" CCD
24-720 (30x) f/3.4-5.8
DIGIC 4
3.0" fixed
461,000
SD, SDHC, SDXC
104.0 x 69.5 x 80.2
341

Improved Autofocus (AF). Not compatible for SD/SDHC Memory cards exceeding 8 GB capacity.

SX510 HS
August 2013
12.1 MP
4000x3000
1/2.3" CMOS
349

Adds Wi-Fi

SX520 HS
2014
16.0 MP
4608x3456
1/2.3" CMOS
24-1008 (42x) f/3.4-5.8
DIGIC 4+
119.0 x 81.0 x 91.0
442

No Wi-Fi

SX530 HS
January 2015
24-1200 (50x) f/3.4-6.5
120.0 x 81.7 x 91.9
442

Wi-Fi but no GPS. GPS via linked compatible smartphone ("camera connect").

SX540 HS
January 2016
20.2 MP
5184x3888
1/2.3" CMOS
DIGIC 6
120.0 x 81.7 x 91.9
442

Wi-Fi but no GPS. GPS via linked compatible smartphone ("camera connect").

SX600 series (2014-, cheaper alternative to the SX700 series, no manual controls)

SX600 HS
2014
16.0 MP
4608x3456
1/2.3" CMOS
25-450 (18x) f/3.8-6.9
DIGIC 4+
3.0" fixed
461,000
SD, SDHC, SDXC
103.8 x 61.0 x 26.0
188

SX610 HS
January 2015
20.2 MP
5184x3888
1/2.3" CMOS
3.0" fixed
922,000
105.3 x 61.0 x 26.7
191

SX620 HS
May 2016
25-625 (25x)
f/3.2-6.6

96.9 x
56.9 x
27.9

182

SX700 series (2014-, successor to the SX200-series)

SX700 HS
2014
16.0 MP
4608x3456
1/2.3" CMOS
25-750 (30x) f/3.2-6.9
DIGIC 6
3.0" fixed
922,000
SD, SDHC, SDXC
112.7 x 65.8 x 34.8
245

Remote shooting through WiFi

SX710 HS
January 2015
20.2 MP
5184x3888
1/2.3" CMOS
269

SX720 HS
February 2016
24-960 (40x)
f/3.3-6.9

109.7 x
63.8 x
35.7

270

SX730 HS
April 2017
3.0" tilting
922,000

110.1 x
63.8 x
39.9

300


document_title: 2014 FIFA World Cup statistics

question_text: who conceded the most goals in world cup 2014

text: 2014 FIFA World Cup statistics

text: Goalscorers[edit]

text: The winner of the Golden Boot was James Rodríguez.

text: James Rodríguez

text: Thomas Müller

text:
Lionel Messi
 Neymar
 Robin van Persie

text:
Enner Valencia
 Karim Benzema
 André Schürrle
 Arjen Robben
 Xherdan Shaqiri

text:
Abdelmoumene Djabou
 Islam Slimani
 Tim Cahill
 David Luiz
 Oscar
 Alexis Sánchez
 Jackson Martínez
 Bryan Ruiz
 Mario Mandžukić
 Ivan Perišić
 Mario Götze
 Mats Hummels
 Miroslav Klose
 Toni Kroos
 André Ayew
 Asamoah Gyan
 Wilfried Bony
 Gervinho
 Memphis Depay
 Ahmed Musa
 Clint Dempsey
 Luis Suárez

text:
Yacine Brahimi
 Sofiane Feghouli
 Rafik Halliche
 Ángel Di María
 Gonzalo Higuaín
 Marcos Rojo
 Mile Jedinak
 Kevin De Bruyne
 Marouane Fellaini
 Romelu Lukaku
 Dries Mertens
 Divock Origi
 Jan Vertonghen
 Edin Džeko
 Vedad Ibišević
 Miralem Pjanić
 Avdija Vršajević
 Fernandinho
 Fred
 Thiago Silva
 Joël Matip
 Charles Aránguiz
 Jean Beausejour
 Jorge Valdivia
 Eduardo Vargas
 Pablo Armero
 Juan Cuadrado
 Teófilo Gutiérrez
 Juan Quintero
 Joel Campbell
 Óscar Duarte
 Marco Ureña
 Ivica Olić
 Wayne Rooney
 Daniel Sturridge
 Olivier Giroud
 Blaise Matuidi
 Paul Pogba
 Moussa Sissoko
 Mathieu Valbuena
 Sami Khedira
 Mesut Özil
 Sokratis Papastathopoulos
 Georgios Samaras
 Andreas Samaris
 Carlo Costly
 Reza Ghoochannejhad
 Mario Balotelli
 Claudio Marchisio
 Keisuke Honda
 Shinji Okazaki
 Giovani dos Santos
 Andrés Guardado
 Javier Hernández
 Rafael Márquez
 Oribe Peralta
 Daley Blind
 Stefan de Vrij
 Leroy Fer
 Klaas-Jan Huntelaar
 Wesley Sneijder
 Georginio Wijnaldum
 Peter Odemwingie
 Cristiano Ronaldo
 Nani
 Silvestre Varela
 Aleksandr Kerzhakov
 Aleksandr Kokorin
 Koo Ja-cheol
 Lee Keun-ho
 Son Heung-min
 Xabi Alonso
 Juan Mata
 Fernando Torres
 David Villa
 Blerim Džemaili
 Admir Mehmedi
 Haris Seferović
 Granit Xhaka
 John Brooks
 Julian Green
 Jermaine Jones
 Edinson Cavani
 Diego Godín

text:
Sead Kolašinac (against Argentina)
 Marcelo (against Croatia)
 John Boye (against Portugal)
 Noel Valladares (against France)
 Joseph Yobo (against France)

text: Source: FIFA[1]

text: Assists[edit]

text: Juan Cuadrado and Toni Kroos topped the assists table with four assists during the tournament.

text:
Juan Cuadrado
 Toni Kroos

text:
Karim Benzema
 André Schürrle

text:
Kevin De Bruyne
 Eden Hazard
 Alexis Sánchez
 Abel Aguilar
 James Rodríguez
 Christian Bolaños
 Walter Ayoví
 Mathieu Valbuena
 Philipp Lahm
 Thomas Müller
 Mesut Özil
 Serge Aurier
 Daley Blind
 Daryl Janmaat
 Josip Drmić
 Graham Zusi

text:
Yacine Brahimi
 Abdelmoumene Djabou
 Sofiane Feghouli
 Carl Medjani
 Islam Slimani
 Ángel Di María
 Ezequiel Garay
 Gonzalo Higuaín
 Lionel Messi
 Marcos Rojo
 Ryan McGowan
 Tommy Oar
 Romelu Lukaku
 Divock Origi
 Edin Džeko
 Senad Lulić
 Miralem Pjanić
 Tino-Sven Sušić
 Dante
 David Luiz
 Luiz Gustavo
 Marcelo
 Neymar
 Oscar
 Thiago Silva
 Allan Nyom
 Charles Aránguiz
 Mauricio Pinilla
 Jorge Valdivia
 Eduardo Vargas
 Teófilo Gutiérrez
 Adrián Ramos
 Joel Campbell
 Júnior Díaz
 Cristian Gamboa
 Eduardo
 Nikica Jelavić
 Ivan Perišić
 Danijel Pranjić
 Ivan Rakitić
 Juan Carlos Paredes
 Glen Johnson
 Wayne Rooney
 Mathieu Debuchy
 Paul Pogba
 Benedikt Höwedes
 Sami Khedira
 Kwadwo Asamoah
 John Boye
 Asamoah Gyan
 Sulley Muntari
 Theofanis Gekas
 Georgios Samaras
 Brayan Beckeles
 Javad Nekounam
 Antonio Candreva
 Andrea Pirlo
 Gervinho
 Keisuke Honda
 Yuto Nagatomo
 Giovani dos Santos
 Héctor Herrera
 Rafael Márquez
 Memphis Depay
 Klaas-Jan Huntelaar
 Arjen Robben
 Wesley Sneijder
 Michel Babatunde
 Emmanuel Emenike
 Cristiano Ronaldo
 Miguel Veloso
 Dmitri Kombarov
 Lee Keun-ho
 Yun Suk-young
 Cesc Fàbregas
 Andrés Iniesta
 Juanfran
 Gökhan Inler
 Admir Mehmedi
 Ricardo Rodríguez
 Michael Bradley
 Edinson Cavani
 Fernando Muslera
 Gastón Ramírez

text: Source: UEFA[2]

text: Scoring[edit]

text:
Total number of goals scored: 171
Average goals per match: 2.67
Total number of braces: 14  Karim Benzema, Toni Kroos, Mario Mandžukić, Jackson Martínez, Lionel Messi, Ahmed Musa, Neymar (2), Robin van Persie, Arjen Robben, James Rodríguez, André Schürrle, Luis Suárez, Enner Valencia
Total number of hat-tricks: 2  Thomas Müller, Xherdan Shaqiri
Total number of penalty kicks awarded: 13
Total number of penalty kicks scored: 12  Xabi Alonso, Karim Benzema, Edinson Cavani, Juan Cuadrado, Sofiane Feghouli, Klaas-Jan Huntelaar, Mile Jedinak, Thomas Müller, Neymar, Robin van Persie, James Rodríguez, Georgios Samaras
Total number of penalty kicks missed or saved: 1  Karim Benzema
Penalty kick success rate: 7001923100000000000♠92.31%
Own goals scored: 5  John Boye, Sead Kolašinac, Marcelo, Noel Valladares, Joseph Yobo

text:
First goal of the tournament: Marcelo (own goal) for Croatia against Brazil
First brace of the tournament: Neymar for Brazil against Croatia
First hat-trick of the tournament: Thomas Müller for Germany against Portugal
Last goal of the tournament: Mario Götze for Germany against Argentina
Last brace of the tournament: André Schürrle for Germany against Brazil
Last hat-trick of the tournament: Xherdan Shaqiri for Switzerland against Honduras
Fastest goal in a match from kickoff: 1st minute (0:30) Clint Dempsey for United States - MS against Ghana
Fastest goal in a match after coming on as a substitute: 2 minutes  Marco Ureña for Costa Rica against Uruguay (introduced in the 83rd minute), Admir Mehmedi for Switzerland against Ecuador (introduced in the 46th minute), Miroslav Klose for Germany against Ghana (introduced in the 69th minute), Leroy Fer for Netherlands against Chile (introduced in the 75th minute), Julian Green for United States - MS against Belgium (introduced in the 105+2nd minute)
Latest goal in a match without extra time: 90+5th minute  Silvestre Varela for Portugal against United States - MS
Latest goal in a match with extra time: 120+1st minute  Abdelmoumene Djabou for Algeria against Germany
Latest winning goal in a match without extra time: 90+4th minute  Klaas-Jan Huntelaar for Netherlands against Mexico
Latest winning goal in a match with extra time: 118th minute  Ángel Di María for Argentina against Switzerland
Shortest time difference between two goals scored by the same team in a match: 2 minutes  (1:06) Olivier Giroud and Blaise Matuidi for France against Switzerland

text:
Most goals scored by a team: 18  Germany
Fewest goals scored by a team: 1  Cameroon, Honduras, Iran
Most goals conceded by a team: 14  Brazil
Fewest goals conceded by a team: 2  Costa Rica
Best goal difference: +14  Germany
Worst goal difference: -8  Cameroon
Most goals scored in a match by both teams: 8  Brazil 1–7 Germany
Most goals scored in a match by one team: 7  Germany against Brazil
Most goals scored in a match by the losing team: 2  Australia against Netherlands, Switzerland against France, South Korea against Algeria, Nigeria against Argentina
Biggest margin of victory: 6 goals  Brazil 1–7 Germany
Most clean sheets achieved by a team: 4  Argentina, Germany, Netherlands
Fewest clean sheets achieved by a team: 0  Algeria, Australia, Bosnia and Herzegovina, Cameroon, Ghana, Honduras, Italy, Ivory Coast, Portugal, Russia, South Korea, United States
Most clean sheets given by an opposing team: 2  Argentina, Brazil, Cameroon, Costa Rica, France, Greece, Honduras, Iran, Italy, Netherlands, Nigeria
Fewest clean sheets given by an opposing team: 0  Algeria, Colombia, Croatia, Germany, Ghana, Ivory Coast
Most consecutive clean sheets achieved by a team: 3  Argentina, Netherlands
Most consecutive clean sheets given by an opposing team: 2  Argentina, Cameroon, Greece, Iran, Italy, Netherlands

text:
Most goals scored by an individual: 6  James Rodríguez
Most assists provided by an individual: 4  Juan Cuadrado, Toni Kroos
Most goals and assists produced by an individual: 8  James Rodríguez (6 goals, 2 assists), Thomas Müller (5 goals, 3 assists)
Most clean sheets achieved by a goalkeeper: 4  Jasper Cillessen, Manuel Neuer, Sergio Romero
Fewest clean sheets achieved by a goalkeeper: 0  Igor Akinfeev, Boubacar Barry, Asmir Begović, Beto, Gianluigi Buffon, Iker Casillas, Fatau Dauda, Panagiotis Glykos, Joe Hart, Tim Howard, Charles Itandje, Jung Sung-ryong, Kim Seung-gyu, Adam Kwarasey, Raïs M'Bolhi, Rui Patrício, Mathew Ryan, Salvatore Sirigu, Noel Valladares
Most consecutive clean sheets achieved by a goalkeeper: 3  Jasper Cillessen, Sergio Romero
Most goals scored by one player in a match: 3  Thomas Müller for Germany against Portugal, Xherdan Shaqiri for Switzerland against Honduras
Oldest goal scorer: 37 years and 43 days[3]  Noel Valladares (own goal) for France against Honduras
Youngest goal scorer: 19 years and 25 days[3]  Julian Green for United States - MS against Belgium

text: Wins and losses[edit]

text:
Most wins: 6 – Germany
Fewest wins: 0 – Australia, Cameroon, England, Ghana, Honduras, Iran, Japan, Russia, South Korea
Most losses: 3 – Australia, Cameroon, Honduras
Fewest losses: 0 – Costa Rica, Germany, Netherlands
Most draws: 3 – Costa Rica
Fewest draws: 0 – Australia, Belgium, Bosnia and Herzegovina, Cameroon, Colombia, Croatia, Honduras, Italy, Ivory Coast, Spain, Switzerland, Uruguay
Most points in the group stage: 9 – Argentina, Belgium, Colombia, Netherlands
Fewest points in the group stage: 0 – Australia, Cameroon, Honduras

text: Match awards[edit]

text: Man of the Match[edit]

text:
Rank

Name
Team

Opponent

Awards

1

Lionel Messi
 Argentina

Bosnia and Herzegovina (GS), Iran (GS),  Nigeria (GS), Switzerland (R16)

4

2

Keylor Navas
 Costa Rica

England (GS), Greece (R16), Netherlands (QF)

3

Arjen Robben
 Netherlands

Australia (GS), Chile (GS), Brazil (TP)

James Rodríguez
 Colombia

Greece (GS), Ivory Coast (GS), Uruguay (R16)

5

Karim Benzema
 France

Honduras (GS), Switzerland (GS)

2

Mario Götze
 Germany

Ghana (GS), Argentina (F)

Tim Howard
 United States

Portugal (GS), Belgium (R16)

Thomas Müller
 Germany

Portugal (GS), United States (GS)

 Neymar
 Brazil

Croatia (GS), Cameroon (GS)

Guillermo Ochoa
 Mexico

Brazil (GS), Netherlands (R16)

Xherdan Shaqiri
  Switzerland

Ecuador (GS), Honduras (GS)

Islam Slimani
 Algeria

South Korea (GS), Russia (GS)

13

Mario Balotelli
 Italy

England (GS)

1

Gianluigi Buffon
 Italy

Uruguay (GS)

Joel Campbell
 Costa Rica

Uruguay (GS)

 Júlio César
 Brazil

Chile (R16)

Kevin De Bruyne
 Belgium

Algeria (GS)

Clint Dempsey
 United States

Ghana (GS)

 Cristiano Ronaldo
 Portugal

Ghana (GS)

Alexander Domínguez
 Ecuador

France (GS)

Edin Džeko
 Bosnia and Herzegovina

Iran (GS)

Eden Hazard
 Belgium

Russia (GS)

Gonzalo Higuaín
 Argentina

Belgium (QF)

Keisuke Honda
 Japan

Greece (GS)

Mats Hummels
 Germany

France (QF)

Toni Kroos
 Germany

Brazil (SF)

 David Luiz
 Brazil

Colombia (QF)

Raïs M'Bolhi
 Algeria

Germany (R16)

Mario Mandžukić
 Croatia

Cameroon (GS)

Rafael Márquez
 Mexico

Croatia (GS)

Jackson Martínez
 Colombia

Japan (GS)

John Obi Mikel
 Nigeria

Iran (GS)

Peter Odemwingie
 Nigeria

Bosnia and Herzegovina (GS)

Robin van Persie
 Netherlands

Spain (GS)

Paul Pogba
 France

Nigeria (R16)

Sergio Romero
 Argentina

Netherlands (SF)

Bryan Ruiz
 Costa Rica

Italy (GS)

Georgios Samaras
 Greece

Ivory Coast (GS)

Alexis Sánchez
 Chile

Australia (GS)

Giovani dos Santos
 Mexico

Cameroon (GS)

Son Heung-min
 South Korea

Russia (GS)

Luis Suárez
 Uruguay

England (GS)

Yaya Touré
 Ivory Coast

Japan (GS)

Enner Valencia
 Ecuador

Honduras (GS)

Eduardo Vargas
 Chile

Spain (GS)

Jan Vertonghen
 Belgium

South Korea (GS)

David Villa
 Spain

Australia (GS)

text: Clean sheets[edit]

text: The winner of the Golden Glove was Manuel Neuer.

text:
Rank

Name
Team

Opponent

Awards

1

Jasper Cillessen
 Netherlands

Chile (GS), Costa Rica (QF), Argentina (SF), Brazil (TP)

4

Manuel Neuer
 Germany

Portugal (GS), United States (GS), France (QF), Argentina (F)

Sergio Romero
 Argentina

Iran (GS), Switzerland (R16), Belgium (QF), Netherlands (SF)

4

Hugo Lloris
 France

Honduras (GS), Ecuador (GS), Nigeria (R16)

3

Keylor Navas
 Costa Rica

Italy (GS), England (GS), Netherlands (QF)

6

Thibaut Courtois
 Belgium

Russia (GS), South Korea (GS)

2

Vincent Enyeama
 Nigeria

Iran (GS), Bosnia and Herzegovina (GS)

Orestis Karnezis
 Greece

Japan (GS), Ivory Coast (GS)

Guillermo Ochoa
 Mexico

Cameroon (GS), Brazil (GS)

David Ospina
 Colombia

Greece (GS), Uruguay (R16)

11

Diego Benaglio
  Switzerland

Honduras (GS)

1

Claudio Bravo
 Chile

Spain (GS)

 Júlio César
 Brazil

Mexico (GS)

Alexander Domínguez
 Ecuador

France (GS)

 Eduardo
 Portugal

Ghana (GS)

Ben Foster
 England

Costa Rica (GS)

Alireza Haghighi
 Iran

Nigeria (GS)

Eiji Kawashima
 Japan

Greece (GS)

Tim Krul
 Netherlands

Costa Rica (QF)

Faryd Mondragón
 Colombia

Japan (GS)

Fernando Muslera
 Uruguay

Italy (GS)

Stipe Pletikosa
 Croatia

Cameroon (GS)

Pepe Reina
 Spain

Australia (GS)

Michel Vorm
 Netherlands

Brazil (TP)

text: Discipline[edit]

text:
Total number of yellow cards: 187
Average yellow cards per match: 2.92
Total number of red cards: 10
Average red cards per match: 0.16
First yellow card of the tournament:Neymar for Brazil against Croatia
First red card of the tournament:Maxi Pereira for Uruguay against Costa Rica
Fastest yellow card from kick off: 2 minutes  Thiago Silva for Brazil against Netherlands
Fastest yellow card after coming on as a substitute: 3 minutes  José Miguel Cubero for Costa Rica against Italy (introduced in the 68th minute)
Latest yellow card in a match without extra time: 90+4 minutes  João Moutinho for Portugal against Ghana
Latest yellow card in a match with extra time: 120+4 minutes  Ezequiel Garay for Argentina against Switzerland
Fastest dismissal from kick off: 37 minutes  Pepe for Portugal against Germany
Fastest dismissal of a substitute: 20 minutes  Ante Rebić for Croatia against Mexico (introduced in the 69th minute)
Latest dismissal in a match without extra time: 90+4 minutes  Maxi Pereira for Uruguay against Costa Rica
Shortest time difference between two yellow cards given to the same player: 11 minutes  Kostas Katsouranis for Greece against Japan (booked in the 27th minute and again in the 38th minute)
Most yellow cards (team): 14  Brazil
Most red cards (team): 1  Belgium, Cameroon, Costa Rica, Croatia, Ecuador, Greece, Honduras, Italy, Portugal, Uruguay
Fewest yellow cards (team): 2  Portugal
Most yellow cards (player): 3  Thiago Silva
Most red cards (player): 1  Steven Defour, Óscar Duarte, Kostas Katsouranis, Claudio Marchisio, Wilson Palacios, Pepe, Maxi Pereira, Ante Rebić, Alex Song, Antonio Valencia
Most yellow cards (match): 8  Costa Rica vs Greece
Most red cards (match): 1  Uruguay vs Costa Rica, France vs Honduras, Germany vs Portugal, Cameroon vs Croatia, Japan vs Greece, Croatia vs Mexico, Italy vs Uruguay, Ecuador vs France, South Korea vs Belgium, Costa Rica vs Greece
Fewest yellow cards (match): 1  England vs Italy, Iran vs Nigeria, Switzerland vs France, Germany vs Ghana, United States vs Portugal, Honduras vs Switzerland, Ecuador vs France, France vs Nigeria, Brazil vs Germany
Most cards in one match: 1 red card, 8 yellow cards  Costa Rica vs Greece

text: Multiple World Cups[edit]

text:
Name

 2002

 2006

 2010

 2014

Total goals

Goals
Against

Goals
Against

Goals
Against

Goals
Against

 Miroslav Klose

5
KSA (3), IRL, CMR

5
CRC (2), ECU (2), ARG

4
AUS, ENG, ARG (2)

2
GHA, BRA

16

text:
Name

 2002

 2006

 2010

 2014

Total goals

Goals
Against

Goals
Against

Goals
Against

Goals
Against

 Tim Cahill

N/A

2
JPN (2)

1
SRB

2
CHI, NED

5

 Clint Dempsey

N/A

1
GHA

1
ENG

2
GHA, POR

4

 Asamoah Gyan

N/A

1
CZE

3
SRB, AUS, USA

2
GER, POR

6

 Rafael Márquez

0
N/A

1
ARG

1
RSA

1
CRO

3

 Robin van Persie

N/A

1
CIV

1
CMR

4
ESP (2), AUS, BRA

6

 Arjen Robben

N/A

1
SCG

2
SVK, URU

3
ESP (2), AUS

6

 Cristiano Ronaldo

N/A

1
IRN

1
PRK

1
GHA

3

 David Villa

N/A

3
UKR (2), FRA

5
HON (2), CHI, POR, PAR

1
AUS

9

text:
Ronaldo went on to score at a fourth World Cup, in 2018.
Márquez played in 2002 but did not score. He also went on to play in 2018 but did not score either.
Cahill went on to play in 2018 too but did not score either.

text:
Name

 1998

 2002

 2006

 2010

 2014

Total

Apps
Against

Apps
Against

Apps
Against

Apps
Against

Apps
Against

 DaMarcus Beasley

N/A

3
POR, KOR, POL

3
CZE, ITA, GHA

1
ALG

4
GHA, POR, GER, BEL

11

 Gianluigi Buffon

0
N/A

4
ECU, CRO, MEX, KOR

7
GHA, USA, CZE, AUS, UKR, GER, FRA

1
PAR

2
CRC, URU

14

 Iker Casillas

N/A

5
SVN, PAR, RSA, IRL, KOR

3
UKR, TUN, FRA

7
SUI, HON, CHI, POR, PAR, GER, NED

2
NED, CHI

17

 Samuel Eto'o

1
ITA

3
IRL, KSA, GER

N/A

3
JPN, DEN, NED

1
MEX

8

 Miroslav Klose

N/A

7
KSA, IRL, CMR, PAR, USA, KOR, BRA

7
CRC, POL, ECU, SWE, ARG, ITA, POR

5
AUS, SRB, ENG, ARG, ESP

5
GHA, USA, FRA, BRA, ARG

24

 Rafael Márquez

N/A

4
CRO, ECU, ITA, USA

4
IRN, ANG, POR, ARG

4
RSA, FRA, URU, ARG

4
CMR, BRA, CRO, NED

16

 Xavi

N/A

3
PAR, RSA, KOR

3
UKR, TUN, FRA

7
SUI, HON, CHI, POR, PAR, GER, NED

1
NED

14

text:
Buffon attended the 1998 World Cup as an unused substitute.
Eto'o's Cameroon failed to qualify for the 2006 World Cup.
Márquez became the first player to captain his team in four different World Cups. He went on to play and captain the team in a fifth World Cup, in 2018.

text: Overall results[edit]

text: Bold numbers indicate the maximum values in each column.

text: By team[edit]

text: The Netherlands was the only team that used all 23 players during the tournament, making it the first team in World Cup history to ever use all of its squad players.[4]

text:
Team

Pld

W

D

L

Pts

APts

GF

AGF

GA

AGA

GD

AGD

CS

ACS

YC

AYC

RC

ARC

 Algeria

4

1

1

2

4

1.00

7
1.75

7
1.75

0
0.00

0

0.00

6

1.50

0

0.00

 Argentina

7

5

1

1

16

2.29

8
1.14

4
0.57

+4
0.57

4

0.57

8

1.14

0

0.00

 Australia

3

0

0

3

0

0.00

3
1.00

9
3.00

-6
-2.00

0

0.00

6

2.00

0

0.00

 Belgium

5

4

0

1

12

2.40

6
1.20

3
0.60

+3
0.60

2

0.40

7

1.40

1

0.20

 Bosnia & Herz.

3

1

0

2

3

1.00

4
1.33

4
1.33

0
0.00

0

0.00

3

1.00

0

0.00

 Brazil

7

3

2

2

11

1.57

11
1.57

14
2.00

-3
-0.43

1

0.14

14

2.00

0

0.00

 Cameroon

3

0

0

3

0

0.00

1
0.33

9
3.00

-8
-2.67

0

0.00

4

1.33

1

0.33

 Chile

4

2

1

1

7

1.75

6
1.50

4
1.00

+2
0.50

1

0.25

7

1.75

0

0.00

 Colombia

5

4

0

1

12

2.40

12
2.40

4
0.80

+8
1.60

2

0.40

5

1.00

0

0.00

 Costa Rica

5

2

3

0

9

1.80

5
1.00

2
0.40

+3
0.60

3

0.60

12

2.40

1

0.20

 Croatia

3

1

0

2

3

1.00

6
2.00

6
2.00

0
0.00

1

0.33

4

1.33

1

0.33

 Ecuador

3

1

1

1

4

1.33

3
1.00

3
1.00

0
0.00

1

0.33

5

1.67

1

0.33

 England

3

0

1

2

1

0.33

2
0.67

4
1.33

-2
-0.67

1

0.33

4

1.33

0

0.00

 France

5

3

1

1

10

2.00

10
2.00

3
0.60

+7
1.40

3

0.60

5

1.00

0

0.00

 Germany

7

6

1

0

19

2.71

18
2.57

4
0.57

+14
2.00

4

0.57

6

0.86

0

0.00

 Ghana

3

0

1

2

1

0.33

4
1.33

6
2.00

-2
-0.67

0

0.00

6

2.00

0

0.00

 Greece

4

1

2

1

5

1.25

3
0.75

5
1.25

-2
-0.50

1

0.25

8

2.00

1

0.25

 Honduras

3

0

0

3

0

0.00

1
0.33

8
2.67

-7
-2.33

0

0.00

7

2.33

1

0.33

 Iran

3

0

1

2

1

0.33

1
0.33

4
1.33

-3
-1.00

1

0.33

4

1.33

0

0.00

 Italy

3

1

0

2

3

1.00

2
0.67

3
1.00

-1
-0.33

0

0.00

3

1.00

1

0.33

 Ivory Coast

3

1

0

2

3

1.00

4
1.33

5
1.67

-1
-0.33

0

0.00

7

2.33

0

0.00

 Japan

3

0

1

2

1

0.33

2
0.67

6
2.00

-4
-1.33

1

0.33

4

1.33

0

0.00

 Mexico

4

2

1

1

7

1.75

5
1.25

3
0.75

+2
0.50

2

0.50

8

2.00

0

0.00

 Netherlands

7

5

2

0

17

2.43

15
2.14

4
0.57

+11
1.57

4

0.57

11

1.57

0

0.00

 Nigeria

4

1

1

2

4

1.00

3
0.75

5
1.25

-2
-0.50

2

0.50

3

0.75

0

0.00

 Portugal

3

1

1

1

4

1.33

4
1.33

7
2.33

-3
-1.00

0

0.00

2

0.67

1

0.33

 Russia

3

0

2

1

2

0.67

2
0.67

3
1.00

-1
-0.33

0

0.00

4

1.33

0

0.00

 South Korea

3

0

1

2

1

0.33

3
1.00

6
2.00

-3
-1.00

0

0.00

6

2.00

0

0.00

 Spain

3

1

0

2

3

1.00

4
1.33

7
2.33

-3
-1.00

1

0.33

3

1.00

0

0.00

  Switzerland

4

2

0

2

6

1.50

7
1.75

7
1.75

0
0.00

1

0.25

3

0.75

0

0.00

 United States

4

1

1

2

4

1.00

5
1.25

6
1.50

-1
-0.25

0

0.00

4

1.00

0

0.00

 Uruguay

4

2

0

2

6

1.50

4
1.00

6
1.50

-2
-0.50

1

0.25

8

2.00

1

0.25

Total

64(1)

51

13(2)

51

179

1.40

171

1.34

171

1.34

0

0.00

37

0.29

187

1.46

10

0.08

text: Team(s) rendered in italics represent(s) the host nation(s). The competition's winning team is rendered in bold.(1) – Total games lost not counted in total games played (total games lost = total games won)(2) – Total number of games drawn (tied) for all teams = Total number of games drawn (tied) ÷ 2 (both teams involved)(3) – As per statistical convention in football, matches decided in extra time are counted as wins and losses, while matches decided by penalty shoot-outs are counted as draws.

text: By confederation[edit]

text:
Confederation

T

Pld

W

D

L

Pts

APts

Pts/T

AFC
4
12
0
3
9
3
0.25
0.75

CAF
5
17
3
3
11
12
0.71
2.40

CONCACAF
4
16
5
5
6
20
1.25
5.00

CONMEBOL
6
30
17
5
8
56
1.87
9.33

UEFA
13
53
26
10
17
88
1.66
6.77

Total

32

64(1)

51

13(2)

51

179

1.40

5.59

text: Host nation(s) are situated in the region(s) rendered in italics.(1) – Total games lost not counted in total games played (total games lost = total games won)(2) – Total number of games drawn (tied) for all teams = Total number of games drawn (tied) ÷ 2 (both teams involved)(3) – As per statistical convention in football, matches decided in extra time are counted as wins and losses, while matches decided by penalty shoot-outs are counted as draws.

text: Stadiums[edit]

text:
Stadium

City

Capacity

Elevation[5]

Matchesplayed

Totalattendance

Averageattendanceper match

Averageattendanceas % of capacity

Totalgoalsscored

Averagegoals scoredper match

Arena da Amazônia

Manaus

40,549[6]

72 m

4

160,227

40,057

98.79%

14

3.50

Arena da Baixada

Curitiba

39,631[7]

920 m

4

156,991

39,248

99.03%

8

2.00

Arena das Dunas

Natal

39,971[8]

45 m

4

158,167

39,542

98.93%

5

1.25

Arena de São Paulo

São Paulo

63,321[9]

792 m

6

375,593

62,599

98.86%

11

1.83

Arena Fonte Nova

Salvador

51,900[10]

0 m

6

300,674

50,112

96.56%

24

4.00

Arena Pantanal

Cuiabá

41,112[11]

165 m

4

158,717

39,679

96.52%

12

3.00

Arena Pernambuco

Recife

42,610[12]

0 m

5

204,882

40,976

96.17%

11

2.20

Estádio Beira-Rio

Porto Alegre

43,394[13]

47 m

5

214,969

42,994

99.08%

22

4.40

Estádio Castelão

Fortaleza

60,342[14]

0 m

6

356,896

59,483

98.58%

17

2.83

Estádio do Maracanã

Rio de Janeiro

74,738[15]

0 m

7

519,189

74,170

99.24%

10

1.43

Estádio Mineirão

Belo Horizonte

58,170[16]

800 m

6

345,350

57,558

98.95%

17

2.13

Estádio Nacional

Brasília

69,349[17]

1172 m

7

478,218

68,317

98.51%

20

2.86


document_title: Glossary

question_text: where do you put the glossary in a report

text: Glossary

text: A glossary, also known as a vocabulary or clavis, is an alphabetical list of terms in a particular domain of knowledge with the definitions for those terms. Traditionally, a glossary appears at the end of a book and includes terms within that book that are either newly introduced, uncommon, or specialized. While glossaries are most commonly associated with non-fiction books, in some cases, fiction novels may come with a glossary for unfamiliar terms.

text: A bilingual glossary is a list of terms in one language defined in a second language or glossed by synonyms (or at least near-synonyms) in another language.

text: In a general sense, a glossary contains explanations of concepts relevant to a certain field of study or action. In this sense, the term is related to the notion of ontology. Automatic methods have been also provided that transform a glossary into an ontology[1] or a computational lexicon.[2]

text: Core glossary[edit]

text: A core glossary is a simple glossary or defining dictionary that enables definition of other concepts, especially for newcomers to a language or field of study. It contains a small working vocabulary and definitions for important or frequently encountered concepts, usually including idioms or metaphors useful in a culture.

text: Automatic extraction of glossaries[edit]

text: Computational approaches to the automated extraction of glossaries from corpora[3] or the Web[4][5] have been developed in the recent years. These methods typically start from domain terminology and extract one or more glosses for each term of interest. Glosses can then be analyzed to extract hypernyms of the defined term and other lexical and semantic relations.