query: where does botulinum toxin type h come from

pos: Botulinum toxin Botulinum toxin Botulinum toxin (BTX) is a neurotoxic protein produced by the bacterium "Clostridium botulinum" and related species. It prevents the release of the neurotransmitter acetylcholine from axon endings at the neuromuscular junction and thus causes flaccid paralysis. Infection with the bacterium causes the disease botulism. The toxin is also used commercially in medicine, cosmetics and research. Botulinum is the most acutely lethal toxin known, with an estimated human median lethal dose (LD) of 1.3–2.1 ng/kg intravenously or intramuscularly and 10–13 ng/kg when inhaled. There are eight types of botulinum toxin, named type A–H. Types A and B are capable

pos: Clostridium novyi stages: Initial growth wherein no toxin is produced; vigorous growth wherein toxin is produced; and spore formation wherein endospores are formed and toxin production decreases. It is suggested that type C may be type B that forms spores more readily so does not go through the toxin-production stage. Isolating and identifying "C novyi" is difficult due to its extreme anaerobic nature. Commercial kits may not be adequate. It is also fastidious and difficult to culture, requiring the presence of thiols. The alpha-toxin of "Clostridium botulinum" types C and D, is similar to the "C novyi" beta-toxin. The A and B

pos: Grass sickness mild with CGS), excess salivation, constipation, nasogastric fluid secretion, patchy sweating, muscle tremors and eyelid drooping. The cause remains unknown, however the toxin produced from the bacterium "Clostridium botulinum" type C may be involved. "Clostridium botulinum" is a soil-borne bacterium, which may be better known for producing clinical signs of botulism. It may cause grass sickness when the spores of "C. botulinum" type C are ingested and produce their toxin locally within the intestine. The main risk factor for grass sickness, as the name may suggest, is grass. The disease is almost always seen in grazing animals, although there are

pos: Botulinum toxin new drug names and the approved uses for each. A similar warning was issued by Health Canada in 2009, warning that botulinum toxin products can spread to other parts of the body. Botulinum toxin produced by "Clostridium botulinum" is the cause of botulism. Humans most commonly ingest the toxin from eating improperly-canned foods in which "C. botulinum" has grown. However, the toxin can also be introduced through an infected wound. In infants, the bacteria can sometimes grow in the intestines and produce botulinum toxin within the intestine and can cause a condition known as floppy baby syndrome. In all cases,

pos: Botulinum toxin of "Clostridium botulinum", which makes botulinum toxin. Their reports were later found to be incorrect; no such lab was ever found. Botulinum toxin A is marketed under the brand names Botox and Xeomin. Botulinum toxin B is marketed under the brand name Myobloc. In the United States, botulinum toxin products are manufactured by a variety of companies, for both therapeutic and cosmetic use. A U.S. supplier reported in its company materials in 2011 that it could "supply the world's requirements for 25 indications approved by Government agencies around the world" with less than one gram of raw botulinum toxin. Myobloc

pos: Clostridium botulinum Clostridium botulinum Clostridium botulinum is a Gram-positive, rod-shaped, anaerobic, spore-forming, motile bacterium with the ability to produce the neurotoxin botulinum. The botulinum toxin can cause a severe flaccid paralytic disease in humans and other animals and is the most potent toxin known to mankind, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg in humans. "C. botulinum" is a diverse group of pathogenic bacteria initially grouped together by their ability to produce botulinum toxin and now known as four distinct groups, "C. botulinum" groups I-IV. "C. botulinum" groups I-IV, as well as some strains of "Clostridium butyricum" and "Clostridium

pos: Botulism with the bacteria, which then secrete the toxin into the bloodstream. This has become more common in intravenous drug users since the 1990s, especially people using black tar heroin and those injecting heroin into the skin rather than the veins. Wound botulism accounts for 29% of cases. Isolated cases of botulism have been described after inhalation by laboratory workers. Botulism has occurred after cosmetic use of inappropriate strengths of Botox. The toxin is the protein botulinum toxin produced under anaerobic conditions (where there is no oxygen) by the bacterium "Clostridium botulinum". "Clostridium botulinum" is a large anaerobic Gram-positive bacillus that

pos: Botulism Botulism Botulism is a rare and potentially fatal illness caused by a toxin produced by the bacterium "Clostridium botulinum". The disease begins with weakness, blurred vision, feeling tired, and trouble speaking. This may then be followed by weakness of the arms, chest muscles, and legs. Vomiting, swelling of the abdomen, and diarrhea may also occur. The disease does not usually affect consciousness or cause a fever. Botulism can be spread in several different ways. The bacterial spores which cause it are common in both soil and water. They produce the botulinum toxin when exposed to low oxygen levels and certain

pos: Clostridium botulinum (heptavalent) Types A to G, and 3) BabyBIG®, Botulism Immune Globulin Intravenous (Human) (BIG-IV) for pediatric patients under the age of one year. Outcomes vary between one and three months, but with prompt interventions, mortality from botulism ranges from less than 5 percent to 8 percent. Clostridium botulinum Clostridium botulinum is a Gram-positive, rod-shaped, anaerobic, spore-forming, motile bacterium with the ability to produce the neurotoxin botulinum. The botulinum toxin can cause a severe flaccid paralytic disease in humans and other animals and is the most potent toxin known to mankind, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg

pos: Botulism clinical signs in horses are similar to cattle. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, neck, and head. Death generally occurs 24 to 72 hours after initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs. "Clostridium botulinum" type C toxin has been incriminated as the cause of grass sickness, a condition in horses which occurs in rainy and hot summers in Northern Europe. The main symptom is pharynx paralysis. Domestic dogs may develop systemic toxemia after consuming C. botulinum type C exotoxin

pos: Botulinum toxin somatic and autonomic motor systems, without affecting sensory signals or mental functions. He observed that the toxin develops under anaerobic conditions, and can be lethal in minute doses. His prescience in suggesting that the toxin might be used therapeutically earned him recognition as the pioneer of modern botulinum toxin therapy. In 1895 (seventy-five years later), Émile van Ermengem, professor of bacteriology and a student of Robert Koch, correctly described "Clostridium botulinum" as the bacterial source of the toxin. Thirty-four attendees at a funeral were poisoned by eating partially salted ham, an extract of which was found to cause botulism-like paralysis

pos: Botulinum toxin refrigeration at temperatures below 3 °C (38 °F) retards the growth of "Clostridium botulinum". The organism is also susceptible to high salt, high oxygen, and low pH levels. The toxin itself is rapidly destroyed by heat, such as in thorough cooking. The spores that produce the toxin are heat-tolerant and will survive boiling water for an extended period of time. The botulinum toxin is denatured and thus deactivated at temperatures greater than . As a zinc metalloprotease (see below), the toxin's activity is also susceptible, post-exposure, to inhibition by protease inhibitors, e.g., zinc-coordinating hydroxamates. University-based ophthalmologists in the USA and

pos: Botulinum toxin therapy of strabismus as successful as strabismus surgery for patients with binocular vision and that it is less successful than surgery for those who have no binocular vision. Botulinum toxin is the most acutely lethal toxin that is known. It is produced by the bacterium clostridium botulinum. It acts inside nerve terminals by decreasing the release of acetylcholine, blocking neuromuscular transmission and thereby causing flaccid muscular paralysis. As a result, the muscle is weakened for about 3 to 4 months. For treating strabismus, the toxin is used in much diluted form, and the injection is targeted to reach specific muscles that move the

pos: Neurotoxin in isolating them from a system. As calcium flux is necessary for proper excitability of a cell, any significant inhibition could prevent a large amount of functionality. Significantly, ω-CgTx is capable of long term binding to and inhibition of voltage-dependent calcium channels located in the membranes of neurons but not those of muscle cells. Botulinum Toxin (BTX) is a group of neurotoxins consisting of eight distinct compounds, referred to as BTX-A,B,C,D,E,F,G,H, which are produced by the bacterium "Clostridium botulinum" and lead to muscular paralysis. A notably unique feature of BTX is its relatively common therapeutic use in treating dystonia and

pos: Management of strabismus affected by "muscle length", which determines the degree of stretch in a given eye position. Botulinum toxin paralysis reduces total muscle force by removing, or reducing, the contractile component. Botulinum toxin is a neurotoxin present in the cytoplasm of the anaerobic bacterium "Clostridium botulinum". It binds presynaptically with high affinity to sites on cholinergic nerve terminals, decreasing release of acetylcholine, thereby blocking neuromuscular transmission, and causing flaccid muscle paralysis. Crotoxin appears to act similarly. To weaken an eye muscle, 1 to 12 units (a few nanograms) of toxin are injected directly into it. The treated muscle weakens over 48–72 hours

pos: Clostridium botulinum C3 toxin Clostridium botulinum C3 toxin Clostridium botulinum C3 exoenzyme is a toxin that causes the addition of one or more ADP-ribose moieties to Rho-like proteins. Many bacterial toxins nucleotide-binding modify by ADP-ribosylation proteins involved in essential cell functions, leading to their toxic effects. The molecular basis of the action of these enzymes consists in binding of nicotinamide adenine dinucleotide (NAD), splitting NAD into its ADP-ribose and nicotinamide components, and transferring the ADP-ribose moiety to a specific residue on to a protein substrate, often of eukaryotic origin. All the toxins of this family share a highly conserved glutamate, which is the catalytic

pos: Clostridium botulinum C3 toxin residue critical for the NAD-glycohydrolase activity. ADP-ribosyltransferase toxins have distinct substrate specificities and variable pathophysiological properties and can be subdivided into four subfamilies: diphtheria-like toxins, cholera-like toxins, binary toxins and C3-like exoenzymes. C3-like exoenzymes unlike other ADP-ribosyltransferase toxins do not require a specific cell-surface binding translocation component for cell entry. Their specificity is for the small GTP-binding proteins RhoA, RhoB, and RhoC, which are ADP-ribosylated on an asparagine residue. Clostridium botulinum C3 toxin Clostridium botulinum C3 exoenzyme is a toxin that causes the addition of one or more ADP-ribose moieties to Rho-like proteins. Many bacterial toxins nucleotide-binding modify by ADP-ribosylation

pos: Wrinkle as a natural moisturizer and lubricant between epidermal cells to inhibit the production of matrix metalloproteinases (MMPs). Dermal fillers are injectable products frequently used to correct wrinkles, and other depressions in the skin. They are often a kind of soft tissue designed to enable injection into the skin for purposes of improving the appearance. The most common products are based on hyaluronic acid and calcium hydroxylapatite. Botulinum toxin is a neurotoxin protein produced by the bacterium "Clostridium botulinum". Botox is a specific form of botulinum toxin manufactured by Allergan for both therapeutic and cosmetic use. Besides its cosmetic application, Botox

pos: Flaccid paralysis onset, as might be found with polio. AFP is the most common sign of acute polio, and used for surveillance during polio outbreaks. AFP is also associated with a number of other pathogenic agents including enteroviruses, echoviruses, West Nile virus, and adenoviruses, among others. The "Clostridium botulinum" bacteria are the cause of botulism. Vegetative cells of "C. botulinum" may be ingested. Introduction of the bacteria may also occur via endospores in a wound. When the bacteria are in vivo, they induce flaccid paralysis. This happens because "C. botulinum" produces a toxin which blocks the release of acetylcholine. Botulism toxin blocks

pos: Synaptobrevin tetanus. A related bacterium, "Clostridium botulinum", produces the botulinum toxin. Various botulinum toxin serotypes exist that each cleave specific peptide bonds of specific neuronal SNARE proteins, and synaptobrevin is this target protein for several of the serotypes. SEC22A; SEC22B; SYBL1; VAMP1; VAMP2; VAMP3; VAMP4; VAMP5; VAMP8; YKT6; Synaptobrevin Synaptobrevins ("synaptobrevin isotypes 1-2") are small integral membrane proteins of secretory vesicles with molecular weight of 18 kilodalton (kDa) that are part of the vesicle-associated membrane protein (VAMP) family. Synaptobrevin is one of the SNARE proteins involved in formation of the SNARE complexes. Out of four α-helices of the core SNARE complex

pos: Virulence factor inhibition of certain biochemical pathways in the host. The two most potent known exotoxins are the tetanus toxin (tetanospasmin) secreted by "Clostridium tetani" and the botulinum toxin secreted by "Clostridium botulinum". Exotoxins are also produced by a range of other bacteria including "Escherichia coli"; "Vibrio cholerae" (causative agent of cholera); "Clostridium perfringens" (common causative agent of food poisoning as well as gas gangrene) and "Clostridium difficile" (causative agent of pseudomembranous colitis). A potent three-protein virulence factor produced by "Bacillus anthracis", called anthrax toxin, plays a key role in anthrax pathogenesis. Exotoxins are extremely immunogenic meaning that they trigger the humoral

neg: Clostridium botulinum found in excess to the type F. Similarly, strains producing Ab and Af toxins have been reported. Evidence indicates the neurotoxin genes have been the subject of horizontal gene transfer, possibly from a viral source. This theory is supported by the presence of integration sites flanking the toxin in some strains of "C. botulinum". However, these integrations sites are degraded, indicating that the "C. botulinum" acquired the toxin genes quite far in the evolutionary past. Only botulinum toxin types A, B, E, F and H cause disease in humans. Types A, B, and E are associated with food-borne illness, with

neg: Spasmodic torticollis Drug Administration (FDA) for clinical use in the United States. Some patients experience or develop immunoresistance to botulinum toxin type A and must use botulinum toxin type B. Approximately 4% to 17% of patients develop botulinum toxin type A antibodies. The only botulinum toxin type B accessible in the United States is Myobloc. Treatment using botulinum toxin type B is comparable to type A, with an increased frequency of the side effect dry mouth. Common side effects include pain at the injection site (up to 28%), dysphagia due to the spread to adjacent muscles (11% to 40%), dry mouth (up

neg: Botulinum toxin of causing disease in humans, and are also used commercially and medically. Types C–G are less common; types E and F can cause disease in humans, while the other types cause disease in other animals. Type H is considered the deadliest substance in the world an injection of only 2 ng can cause death to an adult. Botulinum toxin types A and B are used in medicine to treat various muscle spasms and diseases characterized by overactive muscle. Commercial forms are marketed under the brand names Botox and Dysport, among others. Botulinum toxin is used to treat a number of

neg: Clostridium botulinum of which can cause disease in humans. They are resistant to degradation by enzymes found in the gastrointestinal tract. This allows for ingested toxin to be absorbed from the intestines into the bloodstream. However, all types of botulinum toxin are rapidly destroyed by heating to 100 °C for 15 minutes (900 seconds). Most strains produce one type of neurotoxin, but strains producing multiple toxins have been described. "C. botulinum" producing B and F toxin types have been isolated from human botulism cases in New Mexico and California. The toxin type has been designated Bf as the type B toxin was

neg: Clostridium botulinum toxin and "C. baratii" had produced type F toxin. The ability of "C. botulinum" to naturally transfer neurotoxin genes to other clostridia is concerning, especially in the food industry, where preservation systems are designed to destroy or inhibit only "C. botulinum" but not other "Clostridium" species. In the laboratory, "C. botulinum" is usually isolated in tryptose sulfite cycloserine (TSC) growth medium in an anaerobic environment with less than 2% oxygen. This can be achieved by several commercial kits that use a chemical reaction to replace O with CO. "C. botulinum" is a lipase-positive microorganism that grows between pH of 4.8

neg: Botulinum toxin control trials have shown botulinum toxin type A to improve headache symptoms and quality of life when used prophylactically for patients with chronic migraine who exhibit headache characteristics consistent with: pressure perceived from outside source, shorter total duration of chronic migraines (<30 years), "detoxification" of patients with coexisting chronic daily headache due to medication overuse, and no current history of other preventive headache medications. A few small trials have found benefits in people with depression. The drug is under development for the treatment of premature ejaculation. Botulinum toxin Botulinum toxin (BTX) is a neurotoxic protein produced by the bacterium "Clostridium

neg: Spasmodic torticollis The most commonly used treatment for spasmodic torticollis is the use of botulinum toxin injection in the dystonic musculature. Botulinum toxin type A is most often used; it prevents the release of acetylcholine from the presynaptic axon of the motor end plate, paralyzing the dystonic muscle. By disabling the movement of the antagonist muscle, the agonist muscle is allowed to move freely. With botulinum toxin injections, patients experience relief from spasmodic torticollis for approximately 12 to 16 weeks. There are several type A preparations available worldwide; however Botox and Dysport are the only preparations approved by the U.S. Food and

neg: Botulinum toxin or Neurobloc, a botulinum toxin type B product, is produced by Solstice Neurosciences, a subsidiary of US WorldMeds. AbobotulinumtoxinA), a therapeutic formulation of the type A toxin manufactured by Galderma in the United Kingdom, is licensed for the treatment of focal dystonias and certain cosmetic uses in the U.S. and other countries. Besides the three primary U.S. manufacturers, there are numerous other botulinum toxin producers. Xeomin, manufactured in Germany by Merz, is also available for both therapeutic and cosmetic use in the U.S. Lanzhou Institute of Biological Products in China manufactures a BTX-A product; as of 2014 it was the

neg: Clostridium botulinum is related to food, such as honey, problems generally begin within 18 to 36 hours after the toxin enters the baby's body. Signs and symptoms include: Beneficial effects of botulinum toxin: Purified botulinum toxin is diluted by a physician for treatment: Adult intestinal toxemia: A very rare form of botulism that occurs by the same route as infant botulism but is among adults. Occurs rarely and sporadically. Signs and symptoms include: A number of quantitative surveys for "C. botulinum" spores in the environment have suggested a prevalence of specific toxin types in given geographic areas, which remain unexplained. Type A

neg: Botulism to remove the source of the toxin-producing bacteria. Botulinum antitoxin consists of antibodies that neutralize botulinum toxin in the circulatory system by passive immunization. This prevents additional toxin from binding to the neuromuscular junction, but does not reverse any already inflicted paralysis. In adults, a trivalent antitoxin containing antibodies raised against botulinum toxin types A, B, and E is used most commonly, however a heptavalent botulism antitoxin has also been developed and was approved by the U.S. FDA in 2013. In infants, horse-derived antitoxin is sometimes avoided for fear of infants developing serum sickness or lasting hypersensitivity to horse-derived proteins.

neg: Botulinum toxin reportedly been observed by a number of independent groups (Brin, and the Columbia University group under Monte Keen.) After formal trials, on April 12, 2002, the FDA announced regulatory approval of botulinum toxin type A (Botox Cosmetic) to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines). Subsequently, cosmetic use of botulinum toxin type A has become widespread. The results of Botox Cosmetic can last up to four months and may vary with each patient. The US Food and Drug Administration approved an alternative product-safety testing method in response to increasing public concern that LD50 testing

neg: Clostridium botulinum "mouse bioassay" test determines the type of "C. botulinum" toxin present using monoclonal antibodies. An enzyme-linked immunosorbent assay (ELISA) with digoxigenin-labeled antibodies can also be used to detect the toxin, and quantitative PCR can detect the toxin genes in the organism. "C. botulinum" is a soil bacterium. The spores can survive in most environments and are very hard to kill. They can survive the temperature of boiling water at sea level, thus many foods are canned with a pressurized boil that achieves even higher temperatures, sufficient to kill the spores. "C. botulinum" is an obligate anaerobe that is widely distributed

neg: Iraqi Armed Forces program) under Saddam Hussein until the end of 1991 Gulf War. By the time Iraqis were testing biological warheads (containing anthrax and botulinum toxin) in Iraq's deserts, the 1980 to 1988 Iran–Iraq war had come to an end. In December 1990 the Iraqis had filled 100 R-400 bombs with botulinum toxin, 50 with anthrax, and 16 with aflatoxin. In addition, 13 Al Hussein missile warheads were filled with botulinum toxin, 10 with anthrax, and 2 with aflatoxin. These weapons were deployed in January 1991 to four locations for use against Coalition forces only as "weapons of last resort" in case

neg: Botulinum toxin the outbreak of World War II, weaponization of botulinum toxin was investigated at Fort Detrick in Maryland. Carl Lamanna and James Duff developed the concentration and crystallization techniques that Edward J. Schantz used to create the first clinical product. When the Army’s Chemical Corps was disbanded, Schantz moved to the Food Research Institute in Wisconsin, where he manufactured toxin for experimental use and generously provided it to the academic community. The mechanism of botulinum toxin action – blocking the release from nerve endings of the neurotransmitter acetylcholine – was elucidated in the mid-1900s, and remains an important research topic. Nearly

neg: Clostridium botulinum type E specifically associated with fish products. Type C produces limber-neck in birds and type D causes botulism in other mammals. No disease is associated with type G. The "gold standard" for determining toxin type is a mouse bioassay, but the genes for types A, B, E, and F can now be readily differentiated using quantitative PCR. As no antitoxin to type H is yet available, discovered in 2013 and by far the deadliest, details are kept under shroud. A few strains from organisms genetically identified as other "Clostridium" species have caused human botulism: "C. butyricum" has produced type E

neg: Clostridium butyricum 588 (as active agent). CBM 588 does not establish permanently in the gut, in common with other orally administered probiotic bacteria. CBM 588 for clinical use is produced by submerged anaerobic fermentation followed by centrifugation, drying, blending and packaging. The MIYAIRI 588 strain of "C. butyricum" does not carry any genes encoding any toxins and virulence factors associated with "Clostridium" or other enteropathogens. Absence of neurotoxin production has been demonstrated by polymerase chain reaction (PCR) and Southern blot hybridisation for type E botulinum toxin gene. The absence of genes encoding botulinum neurotoxin A,B,F and genes encoding non-toxic haemagglutinin (NTNH) and

neg: Botulinum toxin maximally visible two weeks following injection. The treated muscles gradually regain function, and generally return to their former appearance three to four months after treatment. Muscles can be treated repeatedly to maintain the smoothed appearance. Botulinum toxin is also used to treat disorders of hyperactive nerves including excessive sweating, neuropathic pain, and some allergy symptoms. In addition to these uses, botulinum toxin is being evaluated for use in treating chronic pain. While botulinum toxin is generally considered safe in a clinical setting, there can be serious side effects from its use. Most commonly, botulinum toxin can be injected into the

neg: Botulinum toxin therapy of strabismus causing postsurgical strabismus as a complication of cataract surgery due to the myotoxicity of the local anaesthetic drug bupivaine when inadvertently injected into an extraocular muscle. Botulinum toxin therapy of strabismus Botulinum toxin therapy of strabismus is a medical technique used sometimes in the management of strabismus, in which botulinum toxin is injected into selected extraocular muscles in order to reduce the misalignment of the eyes. The injection of the toxin to treat strabismus, reported upon in 1981, is considered to be the first ever use of botulinum toxin for therapeutic purposes. Today, the injection of botulinum toxin into the

neg: Botulinum toxin therapy of strabismus Botulinum toxin therapy of strabismus Botulinum toxin therapy of strabismus is a medical technique used sometimes in the management of strabismus, in which botulinum toxin is injected into selected extraocular muscles in order to reduce the misalignment of the eyes. The injection of the toxin to treat strabismus, reported upon in 1981, is considered to be the first ever use of botulinum toxin for therapeutic purposes. Today, the injection of botulinum toxin into the muscles that surround the eyes is one of the available options in the management of strabismus. Other options for strabismus management are vision therapy and occlusion

neg: Botulinum toxin therapy of strabismus successful than surgery for those who have no binocular vision. One study found that botulinum toxin therapy had similar long-term success rates for treating infantile esotropia with botulinum toxin A before the age of 12 months as would have been expected from strabismus surgery. Another study reported similar long-term success rates for infantile esotropia treated before 24 months of age by either strabismus surgery or botulinum toxin treatment. Botulinum toxin has also been used postoperatively for improving the alignment in patients with over- or undercorrection after strabismus surgery, leading to rapid elimination of postoperative diplopia but possibly requiring repeated injections

neg: Botulinum toxin a time. Botulinum toxin type B (BTX-B) received FDA approval for treatment of cervical dystonia on December 21, 2000. Trade names for BTX-B are Myobloc in the United States, and Neurobloc in the European Union. Onabotulinumtoxin A (trade name Botox) received FDA approval for treatment of chronic migraines on October 15, 2010. The toxin is injected into the head and neck to treat these chronic headaches. Approval followed evidence presented to the agency from two studies funded by Allergan showing a very slight improvement in incidence of chronic migraines for migraine sufferers undergoing the Botox treatment. Since then, several randomized

neg: Neurogenic bladder dysfunction botulinum toxin type A than with type B. This use of botulinum toxin is discussed at length in the French medical literature. Neurogenic bladder dysfunction Neurogenic bladder dysfunction, sometimes simply referred to as neurogenic bladder, is a dysfunction of the urinary bladder due to disease of the central nervous system or peripheral nerves involved in the control of micturition (urination). Neurogenic bladder usually causes difficulty - or full inability - to pass urine without use of a catheter or other method. Any condition that impairs bladder and bladder outlet afferent and efferent signaling can cause neurogenic bladder. It is often

neg: Botulinum toxin distributor of botulinum toxin, was unable to obtain product liability insurance, and could no longer supply the drug. As supplies became exhausted, patients who had come to rely on periodic injections became desperate. For 4 months, as liability issues were resolved, American blepharospasm patients traveled to Canadian eye centers for their injections. Based on data from thousands of patients collected by 240 investigators, Allergan received FDA approval in 1989 to market Oculinum for clinical use in the United States to treat adult strabismus and blepharospasm, using the trademark Botox. This was under the 1983 US Orphan Drug Act. Richard Clark,

neg: Management of chronic headaches found that the headache frequency over a 28-day period lowered for chronic headache patients on topiramate. Another medication to prevent headaches is botulinum toxin type A (BoNTA or BOTOX), which is given by injection instead of being taken orally. In a clinical study of botulinum toxin type A, patients participating in the 9-month treatment period with three treatments experienced headache frequency decreases up to 50%. As with all medications, the preventative medications may have side effects. Since different people respond to drugs differently, chronic headache sufferers may have to go through a "trial-and-error" period to find the right medications. The

neg: Clostridium botulinum baratii", are the bacteria responsible for producing botulinum toxin. "C. botulinum" is responsible for foodborne botulism (ingestion of preformed toxin), infant botulism (intestinal infection with toxin-forming "C. botulinum"), and wound botulism (infection of a wound with "C. botulinum"). "C. botulinum" produces heat-resistant endospores that are commonly found in soil and are able to survive under adverse conditions. "C. botulinum" is commonly associated with bulging canned food; bulging, misshapen cans are due to an internal increase in pressure caused by gas produced by the bacteria. "C. botulinum "is a Gram-positive, rod-shaped, spore-forming bacterium. It is an obligate anaerobe, meaning that oxygen

neg: Clostridia of the genus "Clostridium" are saprophytic organisms found in many places in the environment, most notably the soil. However, the genus does contain some human pathogens (outlined below). The toxins produced by certain members of the genus "Clostridium" are among the most dangerous known. Examples are tetanus toxin (known as tetanospasmin) produced by "C. tetani" and botulinum toxin produced by "C. botulinum". Some species have been isolated from women with bacterial vaginosis. Notable species of this class include: Heliobacteria and "Christensenella" are also members of the class Clostridia. Some of the enzymes produced by this group are used in bioremediation.

neg: Clostridium botulinum was restricted to aerobic spore-forming rods. Since 1959, all species producing the botulinum neurotoxins (types A-G) have been designated "C. botulinum". Substantial phenotypic and genotypic evidence exists to demonstrate heterogeneity within the species. This has led to the reclassification of "C. botulinum" type G strains as a new species, "C. argentinense". Group I "C. botulinum" strains that do not produce a botulin toxin are referred to as "C. sporogenes". The complete genome of "C. botulinum" has been sequenced at Wellcome Trust Sanger Institute in 2007. Botulism poisoning can occur due to preserved or home-canned, low-acid food that was not processed

neg: Whiplash (medicine) disorders grade 1–3 may include non-narcotic analgesics. Non-steroidal anti-inflammatory drugs may also be prescribed in the case of WAD 2 and WAD 3, but their use should be limited to a maximum of three weeks. Botulinum toxin A is used to treat involuntary muscle contraction and spasms. Botulinum toxin type-A is only temporary and repeated injections need to take place in order to feel the effects. According to a year long follow-up study in 2008 on 186 patients, the WAD-classification and Quebec Task Force regimen were not linked to better clinical outcomes. The consequences of whiplash range from mild pain

neg: Notalgia paresthetica of botulinum toxin type A (Botox) have been tried with some success. Even though botulinum normally wears off in three to six months, the treatment appears to be long term, and it has been theorised that botulinum type A effects lasting change in pain signaling. Unfortunately, repeated injections have been associated with diminished movement ability of the upper back and arms and its recommendation as a treatment has therefore become less popular. Notalgia paresthetica Notalgia paraesthetica (NP) or notalgia paresthetica (also known as "Hereditary localized pruritus", "Posterior pigmented pruritic patch", and "Subscapular pruritus") is a chronic sensory neuropathy. Notalgia paraesthetica

neg: Botulinum toxin absorbed through the eyes, mucous membranes, respiratory tract, or non-intact skin. The effects of botulinum toxin are different from those of nerve agents involved insofar in that botulism symptoms develop relatively slowly (over several days), while nerve agent effects are generally much more rapid and can be instantaneous. Evidence suggests that nerve exposure (simulated by injection of atropine and pralidoxime) will increase mortality by enhancing botulinum toxin's mechanism of toxicity. With regard to detection, current protocols using NBC detection equipment (such as M-8 paper or the ICAM) will not indicate a "positive" when samples containing botulinum toxin are tested. To

neg: Botulinum toxin therapy of strabismus relief from diplopia. For patients who have had healthy vision heretofore until a small, horizontal deviation set in suddenly, the injection of botulinum toxin may allow them to maintain the binocular vision skills that had been acquired earlier. Some consider botulinum injections to be a treatment option for children with small- to moderate-angle infantile esotropia. Studies have provided indications that performing injections into both medial rectus muscles may be more effective than an injection into one medial rectus muscle alone. Botulinum toxin therapy has been reported to be similarly successful as strabismus surgery for patients with binocular vision and less

neg: Botulinum toxin BTX-A has since been approved for the treatment of severe primary axillary hyperhidrosis (excessive underarm sweating of unknown cause), which cannot be managed by topical agents. In 2010, the FDA approved intramuscular botulinum toxin injections for prophylactic treatment of chronic migraine headache. In cosmetic applications, botulinum toxin is considered safe and effective for reduction of facial wrinkles, especially in the uppermost third of the face. Injection of botulinum toxin into the muscles under facial wrinkles causes relaxation of those muscles, resulting in the smoothing of the overlying skin. Smoothing of wrinkles is usually visible three days after treatment and is

neg: Botulinum toxin confirm a diagnosis of botulinum toxin poisoning, therapeutically or to provide evidence in death investigations, botulinum toxin may be quantitated by immunoassay of human biological fluids; serum levels of 12–24 mouse LD units per milliliter have been detected in poisoned patients. The Japanese doomsday cult Aum Shinrikyo produced botulinum toxin and spread it as an aerosol in downtown Tokyo during the 1990s, but the attacks caused no fatalities. During the early 1980s, the German and French newspapers reported that the police had raided a Baader-Meinhof gang safe house in Paris and had found a makeshift laboratory that contained flasks full

neg: Botulinum toxin problems. Botulinum toxin is used to treat a number of disorders characterized by overactive muscle movement, including post-stroke spasticity, post-spinal cord injury spasticity, spasms of the head and neck, eyelid, vagina, limbs, jaw, and vocal cords. Similarly, botulinum toxin is used to relax clenching of muscles, including those of the oesophagus, jaw, lower urinary tract and bladder, or clenching of the anus which can exacerbate anal fissure. It may also be used for improper eye alignment. Botulinum toxin appears to be effective for refractory overactive bladder. Strabismus is caused by imbalances in the actions of muscles that rotate the eyes,

neg: Botulinum toxin therapy of strabismus of botulinum toxin therapy. As stated in a review article of 2007, its use for strabismus "varies enormously in different cities and countries for no apparent reason." In a small-scale study, adults whose reading difficulties due to convergence insufficiency had been unsuccessfully addressed by convergence exercises, base-in prism glasses or strabismus surgery showed improved reading after botulinum toxin therapy, maintaining improved reading remaining also after six months. Botulinum toxin is considered a useful alternative to surgery in particular cases, for example for persons unfit for general anaesthesia, in evolving or unstable clinical conditions, after unsuccessful surgery, or to provide short-term

neg: Clostridium botulinum the antigenicity of the botulinum toxin produced. The classification into groups is based on the ability of the organism to digest complex proteins. Studies at the DNA and rRNA level support the subdivision of the species into groups I-IV. Most outbreaks of human botulism are caused by group I (proteolytic) or II (non-proteolytic) "C. botulinum". Group III organisms mainly cause diseases in animals. Group IV "C. botulinum" has not been shown to cause human or animal disease. Neurotoxin production is the unifying feature of the species. Eight types of toxins have been identified that are allocated a letter (A–H), several

neg: Neuromuscular junction this area. Botulinum toxin (aka botulinum neurotoxin, BoNT, and sold under the trade name Botox) inhibits the release of acetylcholine at the neuromuscular junction by interfering with SNARE proteins. This toxin crosses into the nerve terminal through the process of endocytosis and subsequently interferes with SNARE proteins, which are necessary for ACh release. By doing so, it induces a transient flaccid paralysis and chemical denervation localized to the striated muscle that it has affected. The inhibition of the ACh release does not set in until approximately two weeks after the injection is made. Three months after the inhibition occurs, neuronal

neg: Management of strabismus guidance generally provides more effective injections, but is only suitable for alert, cooperative adults. Because injection treatment does not result in the scaring that is often a troublesome consequence of conventional strabismus surgery, if therapeutic goals are not achieved with one injection, additional injections or surgical treatments can readily be given. Replacement of strabismus surgery with less invasive procedures began in Alan B Scott’s San Francisco lab with his development of botulinum toxin injection treatment. Some forms of strabismus can be corrected by weakening an extraocular muscle. Botulinum toxin blocks the neuromuscular transmission and thus paralyzes injected muscles. Paralysis is

neg: Ricin undenatured ricin toxin.<ref name="http://www.ansci.cornell.edu/plants/toxicagents/ricin.html"></ref> Ricin is several orders of magnitude less toxic than botulinum or tetanus toxin, but the latter are harder to come by. Compared to botulinum or anthrax as biological weapons or chemical weapons, the quantity of ricin required to achieve LD over a large geographic area is significantly more than an agent such as anthrax (tons of ricin vs. only kilogram quantities of anthrax). Ricin is easy to produce, but is not as practical or likely to cause as many casualties as other agents. Ricin is easily denatured by temperatures over meaning many methods of deploying ricin

neg: Cerebral palsy need for high quality research. A 2013 systematic review found that many of the therapies used to treat CP have no good evidence base; the treatments with the best evidence are medications (anticonvulsants, botulinum toxin, bisphosphonates, diazepam), therapy (bimanual training, casting, constraint-induced movement therapy, context-focused therapy, fitness training, goal-directed training, hip surveillance, home programmes, occupational therapy after botulinum toxin, pressure care) and surgery. Surgical intervention in CP children mainly includes orthopaedic surgery and neurosurgery (selective dorsal rhizotomy). CP is not a progressive disorder (meaning the brain damage does not worsen), but the symptoms can become more severe over time. A

neg: Synaptic vesicle botulinum and tetanus toxins. The botulinum toxin has protease activity which degrades the SNAP-25 protein. The SNAP-25 protein is required for vesicle fusion that releases neurotransmitters, in particular acetylcholine. Botulinum toxin essentially cleaves these SNARE proteins, and in doing so, prevents synaptic vesicles from fusing with the cellular synaptic membrane and releasing their neurotransmitters. Tetanus toxin follows a similar pathway, but instead attacks the protein synaptobrevin on the synaptic vesicle. In turn, these neurotoxins prevent synaptic vesicles from completing full collapse fusion. Without this mechanism in effect, muscle spasms, paralysis, and death can occur. The second mechanism by which synaptic

neg: Botulinum toxin is derived from equine antibodies which have been altered to make them less immunogenic. This antitoxin is effective against all known strains of botulism. Botulinum toxin exerts its effect by cleaving key proteins required for nerve activation. First, the toxin binds specifically to nerves which use the neurotransmitter acetylcholine. Once bound to the nerve terminal, the neuron takes up the toxin into a vesicle. As the vesicle moves farther into the cell, it acidifies, activating a portion of the toxin which triggers it to push across the vesicle membrane and into the cell cytoplasm. Once inside the cytoplasm, the toxin

neg: Botulinum toxin a plastic surgeon from Sacramento (CA), was the first to document a cosmetic use for botulinum toxin. He treated forehead asymmetry caused by left sided forehead nerve paralysis that occurred during a cosmetic facelift. Since the injured nerve could possibly regenerate by 24 months, a two-year waiting period was necessary before definitive surgical treatment could be done. Clark realized that botulinum toxin, which had been previously used only for cross eyed babies and facial tics, could also be injected to smooth the wrinkles of the right forehead to match her paralyzed left. He received FDA approval for this cosmetic application

neg: Botulinum toxin unintended muscle groups, especially when used for treating muscle spasticity in children treated for cerebral palsy. In 2009, the FDA announced that boxed warnings would be added to available botulinum toxin products, warning of their ability to spread from the injection site. Additionally, the FDA announced name changes to several botulinum toxin products, meant to emphasize that the products are not interchangeable and require different doses for proper use. Botox and Botox Cosmetic were renamed "onabotulinumtoxinA", Myobloc was renamed "rimabotulinumtoxinB", and Dysport name renamed "abobotulinumtoxinA". In conjunction with this, the FDA issued a communication to health care professionals reiterating the

neg: Botulinum toxin therapy of strabismus of the intervention is one to two minutes if the person performing the procedure has sufficient experience. The dosage to be used cannot be determined with precision, as no reliable relation between dose and effect could be established so far. The toxicity of botulinum toxin varies from one lot to the next; furthermore, the body may show an immunoreaction by which the efficacy of subsequent treatments is reduced. Botulinum toxin is considered as an alternative to surgery in certain clinical situations. A study performed in the 1980s found outcomes of surgery to be "more predictable and longer lasting" than those

neg: Botulinum toxin therapy of strabismus been demonstrated by means of magnetic resonance imaging and by means of ultrasonography. Bupivacaine injection is therefore being investigated as a further possibility of treating strabismus. In some interventions bupivacaine has been used alone. In others, a botulinum toxin injection into an extraocular muscle is accompanied by a bupivacaine injection into the antagonist muscle. Alan B. Scott first injected botulinum toxin into extraocular muscles since the early 1970s and published his results 1981, giving rise to a wide scope of clinical research on the use of the toxin. The effect of bupivaine injection on extraocular muscles was first known as

neg: Botulinum toxin therapy of strabismus eye, thereby temporarily weakening the selected muscles. After local or general anaesthesia has been applied, the botulinum toxin is injected directly into the selected eye muscles using a specially designed needle electrode that is connected to an electromyography (EMG) apparatus as well as to a syringe containing the botulinum toxin solution. When under local anaesthesia, the patient is asked to move the eyes just before the toxin is injected. This results in an EMG signal which provides instant feedback on the correct placement of the needle. If the patient is a young child, general anaesthesia is always used. The duration

neg: Management of strabismus can stabilize eye alignment. Botulinum A toxin (introduced as Oculinum), now called Botox, is the principal drug used to temporarily paralyze extraocular muscles, and is widely accepted as an alternative to surgery for many types of strabismus. "Crotoxin", a snake neurotoxin, is being developed in Belo Horizonte, Brazil as a potential alternative. Botulinum toxin injection is commonly used for small and moderate degrees of infantile "esotropia", acquired adult strabismus, and where it is a consequence of retinal detachment surgery, that is, in cases where there is good potential for binocular vision, so that the corrected alignment can be stabilized by

neg: Hemifacial spasm remain highly effective. Whilst the toxin is expensive, the cost of even prolonged courses of injections compares favourably with the cost of surgery. Patients with HFS should be offered a number of treatment options. Very mild cases or those who are reluctant to have surgery or Botulinum toxin injections can be offered medical treatment, sometimes as a temporary measure. In young and fit patients microsurgical decompression and Botulinum injections should be discussed as alternative procedures. In the majority of cases, and especially in the elderly and the unfit, Botulinum toxin injection is the treatment of first choice. Imaging procedures should

neg: Botulinum toxin in the United States, according to the American Society of Plastic Surgeons. Qualifications for Botox injectors vary by county, state and country. Botox cosmetic providers include dermatologists, plastic surgeons, aesthetic spa physicians, dentists, nurse practitioners, nurses and physician assistants. The global market for botulinum toxin products, driven by their cosmetic applications, is forecast to reach $2.9 billion by 2018. The facial aesthetics market, of which they are a component, is forecast to reach $4.7 billion ($2 billion in the U.S.) in the same timeframe. Botulinum toxin has been recognized as a potential agent for use in bioterrorism. It can be

neg: Botulinum toxin target visible to both, can stabilize the corrected alignment. In January 2014, botulinum toxin was approved by UK's Medicines and Healthcare Products Regulatory Agency (MHRA) for treatment of restricted ankle motion due to lower limb spasticity associated with stroke in adults. On July 29, 2016, Food and Drug Administration (FDA), of the United States of America approved abobotulinumtoxinA for injection for the treatment of lower limb spasticity in pediatric patients two years of age and older. AbobotulinumtoxinA is the first and only FDA-approved botulinum toxin for the treatment of pediatric lower limb spasticity. In the United States of America, the

neg: Botulism This can lead to a variety of autonomic signs and symptoms described above. In all cases, illness is caused by the botulinum toxin produced by the bacterium "C. botulinum" in anaerobic conditions and not by the bacterium itself. The pattern of damage occurs because the toxin affects nerves that fire (depolarize) at a higher frequency first. Mechanisms of entry into the human body for botulinum toxin are described below. The most common form in Western countries is infant botulism. This occurs in infants who are colonized with the bacterium in the small intestine during the early stages of their lives.

neg: Tetanospasmin Tetanospasmin Tetanus toxin is an extremely potent neurotoxin produced by the vegetative cell of "Clostridium tetani" in anaerobic conditions, causing tetanus. It has no known function for clostridia in the soil environment where they are normally encountered. It is also called spasmogenic toxin, or TeNT. The LD of this toxin has been measured to be approximately 2.5-3 ng/kg, making it second only to botulinum toxin (LD 2 ng/kg) as the deadliest toxin in the world. However, these tests are conducted solely on mice, which may react to the toxin differently from humans and other animals. "C. tetani" also produces the

neg: Heptavalent botulism antitoxin only product available for treating botulism in adults, and for botulism in infants caused by botulinum toxins other than types A and B. "HBAT" has been used to treat a case of type F infant botulism and, on a case-by-case basis, may be used for future cases of non-type A and non-type B infant botulism. Early administration of "HBAT" is considered critical as the antitoxin can neutralize only circulating toxin, not toxin that has become bound to nerve terminals. One vial (20 mL) of "HBAT" is administered to a patient as an intravenous infusion. It must be diluted with 0.9%

neg: Botulism forms subterminal endospores. There are eight serological varieties of the bacterium denoted by the letters A to H. The toxin from all of these acts in the same way and produces similar symptoms: the motor nerve endings are prevented from releasing acetylcholine, causing flaccid paralysis and symptoms of blurred vision, ptosis, nausea, vomiting, diarrhea or constipation, cramps, and respiratory difficulty. Botulinum toxin is broken into 8 neurotoxins (labeled as types A, B, C [C1, C2], D, E, F, and G), which are antigenically and serologically distinct but structurally similar. Human botulism is caused mainly by types A, B, E, and

neg: Iraqi biological weapons program systems including aerial spray tanks and drone aircraft. The Iraqi government had weaponized 6,000 liters of "B. anthracis" spores and 12,000 liters of botulinum toxin in aerial bombs, rockets, and missile warheads before the outbreak of war in 1991. These bio-weapons were deployed but never used. After Kamel's defection, it became known that in December 1990 the Iraqis had filled 100 R-400 bombs with botulinum toxin, 50 with anthrax, and 16 with aflatoxin. In addition, 13 Al Hussein (SCUD) warheads were filled with botulinum toxin, 10 with anthrax, and 2 with aflatoxin. These weapons were deployed in January 1991 to

neg: Botulinum toxin cosmetic use. These can arise from paralysis of critical muscle groups and can include arrhythmia, heart attack, and in some cases seizures, respiratory arrest, and death. Additionally, side effects which are common in cosmetic use are also common in therapeutic use, including trouble swallowing, muscle weakness, allergic reactions, and flu-like syndromes. In response to the occurrence of these side effects, in 2008 the U.S. Food and Drug Administration notified the public of the potential dangers of the botulinum toxin as a therapeutic. Namely, they warned that the toxin can spread to areas distant from the site of injection and paralyze

neg: Clostridium botulinum It has other "off-label" medical purposes, such as treating severe facial pain, such as that caused by trigeminal neuralgia. Botulinum toxin produced by "C. botulinum" is often believed to be a potential bioweapon as it is so potent that it takes about 75 nanograms to kill a person ( of 1 ng/kg, assuming an average person weighs ~75 kg); 1 kilogram of it would be enough to kill the entire human population. For comparative purposes, a quarter of a typical grain of sand's weight (350 ng) of botulinum toxin would constitute a lethal dose for humans. A "mouse protection" or

neg: Tension headache few times in a week at most. Analgesic/sedative combinations are widely used (e.g., analgesic/antihistamine combinations like Syndol, Mersyndol and Percogesic, analgesic/barbiturate combinations such as Fiorinal). Frequent use of analgesics may, however, lead to medication overuse headache. Botulinum toxin does not appear to be helpful. Current evidence for acupuncture is slight. A 2016 systematic review suggests better evidence among those with frequent tension headaches, but concludes that further trials comparing acupuncture with other treatment options are needed. People with tension-type headache often use spinal manipulation, soft tissue therapy, and myofascial trigger point treatment. Studies of effectiveness are mixed. A 2006 systematic

neg: Botulinum toxin use in the stability and potency testing of Botox in response to increasing public concern that LD50 testing was required for each batch sold in the market. William J. Binder reported in 2000 that patients who had cosmetic injections around the face reported relief from chronic headache. This was initially thought to be an indirect effect of reduced muscle tension, but it is now known that the toxin inhibits release of peripheral nociceptive neurotransmitters, suppressing the central pain processing systems responsible for migraine headache. As of 2013, botulinum toxin injections are the most common cosmetic operation, with 6.3 million procedures

neg: Tokyo subway sarin attack the outside world made during the election campaign) and defected, an attitude among the remaining members that 'the unenlightened' did not deserve salvation became accepted. Attempts to stockpile botulinum toxin proved unsuccessful. Seiichi Endo - one of the members tasked with acquiring botulinum toxin - collected soil samples from the Ishikari River, and attempted to produce the toxin using three 10,000 litre capacity fermenters. In total, around 50 batches of 9,000 litres of a crude broth were produced – however, the cult did not attempt to purify the broth (which mostly would have consisted of bacterial cultivation media; one member

neg: Migraine treatment perception. Biofeedback to induce muscle relaxation is widely used in migraine prevention. OnabotulinumtoxinA (trade name Botox) received FDA approval for treatment of chronic migraines (occurring more than 15 days per month) in 2010. The toxin is injected into the muscles of head and neck. Approval followed evidence presented to the agency from two studies funded by Allergan, Inc. showing a very slight improvement in incidence of chronic migraines for migraine sufferers undergoing the Botox treatment. Since then, several randomized control trials have shown Botulinum Toxin Type A to improve headache symptoms and quality of life when used prophylactically for patients

neg: Botulinum toxin all toxin treatments are based on this effect in various body tissues. Ophthalmologists specializing in eye muscle disorders (strabismus) had developed the method of EMG-guided injection (using the electromyogram, the electrical signal from an activated muscle, to guide injection) of local anesthetics as a diagnostic technique for evaluating an individual muscle’s contribution to an eye movement. Because strabismus surgery frequently needed repeating, a search was undertaken for non-surgical, injection treatments using various anesthetics, alcohols, enzymes, enzyme blockers, and snake neurotoxins. Finally, inspired by Daniel Drachman’s work with chicks at Johns Hopkins, Alan B. Scott and colleagues injected botulinum toxin into

neg: Botulinum toxin infected material may be removed surgically. Botulinum antitoxin is available and may be used to prevent the worsening of symptoms, though it will not reverse existing nerve damage. In severe cases, mechanical respiration may be used to support patients suffering from respiratory failure. The nerve damage heals over time, generally over weeks to months. With proper treatment, the case fatality rate for botulinum poisoning can be greatly reduced. Two preparations of botulinum antitoxins are available for treatment of botulism. Trivalent (A,B,E) botulinum antitoxin is derived from equine sources using whole antibodies. The second antitoxin is Heptavalent (A,B,C,D,E,F,G) botulinum antitoxin, which

neg: Botulinum toxin cytoplasm as the vacuole acidifies. The light chain is a zinc metalloprotease and is the active part of the toxin. It is translocated into the host cell cytoplasm where it cleaves the host protein SNAP-25, a member of the SNARE protein family which is responsible for fusion. The cleaved SNAP-25 is unable to mediate fusion of vesicles with the host cell membrane, thus preventing the release of the neurotransmitter acetylcholine from axon endings. This blockage is slowly reversed as the toxin loses activity and the SNARE proteins are slowly regenerated by the affected cell. The seven toxin types (A-G) have

neg: Enrico Fazzini Parkinson's symptoms. Dr. Enrico Fazzini completed his neurology training at Boston University in 1987 and his fellowship in Movement Disorders at Columbia Presbyterian in 1989 where he was instrumental in the development of botulinum toxin type A for use in dystonia. In addition to being a neurologist, Dr. Fazzini has a Ph.D. in Behavioral Neuroscience from Boston University and is an expert on the diagnosis and treatment of patients with traumatic brain injuries. Dr. Fazzini was consulted by the Vatican for the treatment of John Paul II. He confirmed the competency of then Attorney-General Janet Reno after she was diagnosed

neg: Botulinum toxin of the toxin and successfully treated the person and published the case study in 1989. Marrying ophthalmology to dermatology, Jean and Alistair Carruthers observed that blepharospasm patients who received injections around the eyes and upper face also enjoyed diminished facial glabellar lines (“frown lines” between the eyebrows), thereby initiating the highly-popular cosmetic use of the toxin. Brin, and a group at Columbia University under Monte Keen made similar reports. In 2002, following clinical trials, the FDA approved Botox Cosmetic, botulinum A toxin to temporarily improve the appearance of moderate-to-severe glabellar lines. The FDA approved a fully "in vitro" assay for

neg: Botulinum toxin therapy of strabismus therapy, corrective glasses (or contact lenses) and prism glasses, and strabismus surgery. The effects that are due only to the toxin itself (including the side effects) generally wear off within 3 to 4 months. In contrast, improvements in alignment may be long-lasting, particularly in two circumstances. First, if the "antagonist" muscle (the muscle pulling in the opposite direction) is active, the injected muscle will be stretched, and may permanently lengthen by adding tissue during the period of toxin paresis. Second, if binocular vision has been achieved and stabilized, alignment may "lock in". There are indications that botulinum toxin therapy is

neg: Management of cerebral palsy management methods. Botulinum toxin injections are given into muscles that are spastic or sometimes dystonic, the aim being to reduce the muscle hypertonus that can be painful. A reduction in muscle tone can also facilitate bracing and the use of orthotics. Most often lower extremity muscles are injected. Botulinum toxin is focal treatment, meaning that a limited number of muscles can be injected at the same time. The effect of the toxin is reversible and a reinjection is needed every 4–6 months. In children it decreases spasticity and improve range of motion and thus has become commonly used. Botulin toxin

neg: Botulinum toxin spores, where exposure to an anaerobic environment allows the spores to germinate, after which the bacteria can multiply and produce toxin. Critically, "it is ingestion of toxin rather than spores or vegetative bacteria" that causes botulism. Botulism is nevertheless known to be transmitted through canned foods not cooked correctly before canning or after can opening, and so is preventable. Infant botulism cases arise chiefly as a result of environmental exposure and are therefore more difficult to prevent. Infant botulism arising from consumption of honey can be prevented by eliminating honey from diets of children less than 12 months old. Proper

neg: Canning canned non-acidic food substances that have not received a strong enough thermal heat treatment. "C. botulinum" prefers low oxygen environments and is a poor competitor to other bacteria, but its spores are resistant to thermal treatments. When a canned food is sterilized insufficiently, most other bacteria besides the "C. botulinum" spores are killed, and the spores can germinate and produce botulism toxin. Botulism is a rare but serious paralytic illness, leading to paralysis that typically starts with the muscles of the face and then spreads towards the limbs. The botulinum toxin is extremely dangerous because it cannot be detected by

neg: Botulinum toxin in laboratory animals. Van Ermengem isolated and grew the bacterium, and described its toxin, which was later purified by P Tessmer Snipe and Hermann Sommer. Over the next three decades, 1895-1925, as food canning was approaching a billion-dollar-a-year industry, botulism was becoming a public health hazard. Karl Friedrich Meyer, a prodigiously productive Swiss-American veterinary scientist created a center at the Hooper Foundation in San Francisco, where he developed techniques for growing the organism and extracting the toxin, and conversely, for preventing organism growth and toxin production, and inactivating the toxin by heating. The California canning industry was thereby preserved. With

neg: Botulinum toxin monkey extraocular muscles. The result was remarkable: a few picograms induced paralysis that was confined to the target muscle, long in duration, and without side-effects. After working out techniques for freeze-drying, buffering with albumin, and assuring sterility, potency, and safety, Scott applied to the FDA for investigational drug use, and began manufacturing botulinum type A neurotoxin in his San Francisco lab. He injected the first strabismus patients in 1977, reported its clinical utility in 1980, and had soon trained hundreds of ophthalmologists in EMG-guided injection of the drug he named "Oculinum" ("eye aligner"). In 1986, Oculinum Inc, Scott's micromanufacturer and

neg: Botulinum toxin FDA approves the text of the labels of prescription medicines. The FDA approves which medical conditions the drug manufacturer may sell the drug for. However, those approved by the FDA to prescribe these drugs may freely prescribe them for any condition they wish, called off-label use. Botulinum toxins have been used off-label for several pediatric conditions, including infantile esotropia. Khalaf Bushara and David Park were the first to demonstrate a nonmuscular use of BTX-A while treating patients with hemifacial spasm in England in 1993, showing that botulinum toxin injections inhibit sweating, and so are useful in treating hyperhidrosis (excessive sweating).

neg: Fish sauce fish sauce, called the "base". The dregs are then mixed with water and salt and again fermented for three to four months. This yields a second-grade fish sauce, mostly used in cooking. In 2014, the US Food and Drug Administration (FDA) banned the import of Thai fish sauces due to lack of information about tests for botulinum toxin. The toxin can cause death if more than 0.5 microgram is consumed. The Thai Office of Food Safety and Quality then tested 48 brands of fish sauce to determine the content of botulinum toxin in the products. Of 48 brands tested, 28

neg: Botulism these other conditions. These tests may include a brain scan, cerebrospinal fluid examination, nerve conduction test (electromyography, or EMG), and an edrophonium chloride (Tensilon) test for myasthenia gravis. A definite diagnosis can be made if botulinum toxin is identified in the food, stomach or intestinal contents, vomit or feces. The toxin is occasionally found in the blood in peracute cases. Botulinum toxin can be detected by a variety of techniques, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests and mouse inoculation or feeding trials. The toxins can be typed with neutralization tests in mice. In toxicoinfectious botulism, the organism can

neg: Synaptopathy botulinum toxin affect neurotransmitter release. Tetanus toxin can enter the body via a wound, and botulinum toxin can be ingested or administered therapeutically to alleviate dystonia or as cosmetic treatment. Another example of synaptopathy occurs in the auditory system. This cochlear synaptopathy has been seen after prolonged noise exposure in both primate and non-primate models. Two possible reasons for this neuronal death are both glutamate-mediated excitotoxicity in the postsynaptic terminal, and presynaptic ribbon damage which occurs by an unknown mechanism. Synaptopathies are attracting research interest because they provide an insight into fundamental mechanisms of synaptic transmission and because an improved

neg: Median toxic dose substance's TD. Examples of these toxic endpoints include cancer, blindness, anemia, birth defects, etc. Median toxic dose In toxicology, the median toxic dose (TD) of a drug or toxin is the dose at which toxicity occurs in 50% of cases. The "type" of toxicity should be specified for this value to have meaning for practical purposes. The median toxic dose encompasses the category of toxicity that is greater than half maximum effective concentration (ED) but less than the median lethal dose (LD). However, for some highly potent toxins (ex. lofentanil, botulinum toxin) the difference between the ED50 and TD50 is

neg: Median toxic dose Median toxic dose In toxicology, the median toxic dose (TD) of a drug or toxin is the dose at which toxicity occurs in 50% of cases. The "type" of toxicity should be specified for this value to have meaning for practical purposes. The median toxic dose encompasses the category of toxicity that is greater than half maximum effective concentration (ED) but less than the median lethal dose (LD). However, for some highly potent toxins (ex. lofentanil, botulinum toxin) the difference between the ED50 and TD50 is so minute that the values assigned to them may be approximated to equal doses.