Alternatively, batroxobin is also used as a topical hemostatic by its rapid local clot-expansion action. Nolan C, Hall LS, ... Itoh N, Tanaka N, Funakoshi I, Kawasaki T, Mihashi S, Yamashina I (June 1988). "Organization of the gene for batroxobin, a ... Vu, TT; Stafford, AR; Leslie, BA; Kim, PY; Fredenburgh, JC; Weitz, JI (7 June 2013). "Batroxobin binds fibrin with higher ... Examples include ancrod and batroxobin, two serine proteases from snakes that have been used in medical preparations. Venombin ...
Batroxobin has a similar action to thrombin but unlike thrombin it is not inhibited by heparin. Normal values for thrombin time ... If batroxobin is used, the time should be between 15 and 20 seconds. Thrombin time can be prolonged by heparin, fibrin ... In blood samples containing heparin, a substance derived from snake venom called batroxobin (formerly reptilase) is used ...
Batroxobin, another medical snake venom serine protease ""Eye On" report: Neurobiological Technologies, Inc" (PDF). Prohost ...
Batroxobin, a toxin from a snake venom, clots platelet-rich plasma without affecting platelet functions (lyses fibrinogen). ...
Batroxobin from B atrox is used as a drug called "Reptilase" that is used to stop bleeding, while batroxobin from B moojeni is ... Batroxobin, is a serine protease found in snake venom produced by Bothrops atrox and Bothrops moojeni, venomous species of pit ... It is also used in a system called "Vivostat", where a person's blood is taken just before surgery and exposed to batroxobin; ...
Coagulation factor X B02BD14 Susoctocog alfa B02BD30 Thrombin B02BX01 Etamsylate B02BX02 Carbazochrome B02BX03 Batroxobin ...
... batroxobin), derived from this snake's venom, is used in modern medical laboratories to measure fibrinogen levels and blood ...
... batroxobin MeSH D08.811.277.656.300.775 - streptokinase MeSH D08.811.277.656.300.775.075 - anistreplase MeSH D08.811.277.656. ...
... batroxobin MeSH D20.888.850.960.200.210 - crotoxin MeSH D20.944.380 - hazardous waste MeSH D20.944.380.638 - radioactive waste ...
... batroxobin MeSH D23.946.833.850.960.200.210 - crotoxin MeSH D23.946.896.980 - virulence factors, bordetella MeSH D23.946. ...
Batroxobin (INN) Bavisant (INN, (USAN) Bavituximab (USAN, INN) Baxitozine (INN) Baycol BayGam BayHep B Baypress BayRab BayTet ...
... also has a high Kd value for binding both forms yA/yA and yA/y'. The bindings sites of batroxobin and thrombin ... The venom batroxobin also induces clots, but does this with or without tissue damage. This is because batroxobin isn't ... Batroxobin is excreted by the liver, kidney and spleen. The excretion of batroxobin can be detected by small metabolite ... Batroxobin is a protein of the serine protease family. Batroxobin is closely related in physiological function and molecular ...
... a is the activated form of the coagulation factor thrombokinase, known eponymously as Stuart-Prower factor. Factor X is an enzyme, a serine endopeptidase, which plays a key role at several stages of the coagulation system. Factor X is synthesized in the liver. The most commonly used anticoagulants in clinical practice, warfarin and the heparin series of anticoagulants and fondaparinux, act to inhibit the action of Factor Xa in various degrees. Traditional models of coagulation developed in the 1960s envisaged two separate cascades, the extrinsic (tissue factor (TF)) pathway and the intrinsic pathway. These pathways converge to a common point, the formation of the Factor Xa/Va complex which together with calcium and bound on a phospholipids surface generate thrombin (Factor IIa) from prothrombin (Factor II). A new model, the cell-based model of anticoagulation appears to explain more fully the steps in coagulation. This model has three stages: 1) initiation of coagulation on TF-bearing ...
Symptoms of mild cinchonism (which may occur from standard therapeutic doses of quinine) include flushed and sweaty skin, ringing of the ears (tinnitus), blurred vision, impaired hearing, confusion, reversible high-frequency hearing loss, headache, abdominal pain, rashes, drug-induced lichenoid reaction (lichenoid photosensitivity),[1] vertigo, dizziness, dysphoria, nausea, vomiting and diarrhea. Large doses of quinine may lead to severe (but reversible) symptoms of cinchonism: skin rashes, deafness, somnolence, diminished visual acuity or blindness, anaphylactic shock, and disturbances in heart rhythm or conduction, and death from cardiotoxicity (damage to the heart). Quinine may also trigger a rare form of hypersensitivity reaction in malaria patients, termed blackwater fever, that results in massive hemolysis, hemoglobinemia, hemoglobinuria, and kidney failure.[citation needed] Most symptoms of cinchonism (except in severe cases) are reversible and disappear once quinine is withdrawn. ...
Luo C, Thielens NM, Gagnon J, Gal P, Sarvari M, Tseng Y, Tosi M, Zavodszky P, Arlaud GJ, Schumaker VN (May 1992). "Recombinant human complement subcomponent C1s lacking beta-hydroxyasparagine, sialic acid, and one of its two carbohydrate chains still reassembles with C1q and C1r to form a functional C1 complex". Biochemistry. 31 (17): 4254-62. doi:10.1021/bi00132a015. PMID 1533159 ...
In other less formal contexts, an alcohol is often called with the name of the corresponding alkyl group followed by the word "alcohol", e.g., methyl alcohol, ethyl alcohol. Propyl alcohol may be n-propyl alcohol or isopropyl alcohol, depending on whether the hydroxyl group is bonded to the end or middle carbon on the straight propane chain. As described under systematic naming, if another group on the molecule takes priority, the alcohol moiety is often indicated using the "hydroxy-" prefix.[17] Alcohols are then classified into primary, secondary (sec-, s-), and tertiary (tert-, t-), based upon the number of carbon atoms connected to the carbon atom that bears the hydroxyl functional group. (The respective numeric shorthands 1°, 2°, and 3° are also sometimes used in informal settings.[18]) The primary alcohols have general formulas RCH2OH. The simplest primary alcohol is methanol (CH3OH), for which R=H, and the next is ethanol, for which R=CH3, the methyl group. Secondary alcohols are those ...
... is a condition or a process in which an organism becomes chemically harmed severely (poisoned) by a toxic substance or venom of an animal.[1] Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the degree of exposure. Absorption of a poison is necessary for systemic poisoning (that is, in the blood throughout the body). In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, toxicity and poisoning can be caused by less dangerous substances than those legally classified as a poison. Toxicology is the study and practice of the symptoms, mechanisms, diagnosis, and treatment of poisoning. Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not ...
... (TXA) is a medication used to treat or prevent excessive blood loss from major trauma, post partum bleeding, surgery, tooth removal, nose bleeds, and heavy menstruation.[1][2] It is also used for hereditary angioedema.[1][3] It is taken either by mouth or injection into a vein.[1]. Side effects are rare.[3] Some include changes in color vision, blood clots and allergic reactions.[3] Greater caution is recommended in people with kidney disease.[4] Tranexamic appears to be safe for use during pregnancy and breastfeeding.[3][5] Tranexamic acid is in the antifibrinolytic family of medications.[4]. Tranexamic acid was discovered in 1962 by Utako Okamoto.[6] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[7] Tranexamic acid is available as a generic medication.[8] The wholesale cost in the developing world is about 4.38 to 4.89 USD for a course of treatment.[9] In the United States a course of ...
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... can be measured by its effects on the target (organism, organ, tissue or cell). Because individuals typically have different levels of response to the same dose of a toxic substance, a population-level measure of toxicity is often used which relates the probabilities of an outcome for a given individual in a population. One such measure is the LD50. When such data does not exist, estimates are made by comparison to known similar toxic things, or to similar exposures in similar organisms. Then, "safety factors" are added to account for uncertainties in data and evaluation processes. For example, if a dose of a toxic substance is safe for a laboratory rat, one might assume that one tenth that dose would be safe for a human, allowing a safety factor of 10 to allow for interspecies differences between two mammals; if the data are from fish, one might use a factor of 100 to account for the greater difference between two chordate classes (fish and mammals). Similarly, an extra protection ...
More than 64,000 Americans died from drug overdoses in 2016.[1] Since 2000, the US drug overdose death rate has gone from 6.2 per 100,000 people in 2000 to 14.7 per 100,000 in 2014.[17] The National Center for Health Statistics report that 19,250 people died of accidental poisoning in the U.S. in the year 2004 (8 deaths per 100,000 population).[18] In 2008 testimony before a Senate subcommittee, Leonard J. Paulozzi,[19] a medical epidemiologist at the Centers for Disease Control and Prevention stated that in 2005 more than 22,000 American lives were lost due to overdoses, and the number is growing rapidly. Paulozzi also testified that all available evidence suggests that unintentional overdose deaths are related to the increasing use of prescription drugs, especially opioid painkillers.[20] However, the vast majority of overdoses are also attributable to alcohol. It is very rare for a victim of an overdose to have consumed just one drug. Most overdoses occur when drugs are ingested in ...
Protein HtrA2, also known as Omi, is a mitochondrially-located serine protease. The human protein Serine protease HTRA2, mitochondrial is 49kDa in size and composed of 458 amino acids. The peptide fragment of 1-31 amino acid is the mitochondrial transition sequence, fragment 32-133 amino acid is propertied, and 134-458 is the mature protein Serine protease HTRA2, mitochondrial, and its theoretical pI of this protein is 6.12.[10] HtrA2 shows similarities with DegS, a bacterial protease present in the periplasm of gram-negative bacteria. Structurally, HtrA2 is a trimeric molecule with central protease domains and a carboxy-terminal PDZ domain, which is characteristic of the HtrA family. The PDZ domain preferentially binds C-terminus of the protein substrate and modulate the proteolytic activity of the trypsin-like protease domain.[11] ...
In biology, poisons are substances that cause disturbances in organisms, usually by chemical reaction or other activity on the molecular scale, when an organism absorbs a sufficient quantity.[1][2] The fields of medicine (particularly veterinary) and zoology often distinguish a poison from a toxin, and from a venom. Toxins are poisons produced by organisms in nature, and venoms are toxins injected by a bite or sting (this is exclusive to animals). The difference between venom and other poisons is the delivery method. Industry, agriculture, and other sectors employ poisonous substances for reasons other than their toxicity. Most poisonous industrial compounds have associated material safety data sheets and are classed as hazardous substances. Hazardous substances are subject to extensive regulation on production, procurement and use in overlapping domains of occupational safety and health, public health, drinking water quality standards, air pollution and environmental protection. Due to the ...
Seol JH, Woo SK, Jung EM, Yoo SJ, Lee CS, Kim KJ, Tanaka K, Ichihara A, Ha DB, Chung CH (April 1991). "Protease Do is essential for survival of Escherichia coli at high temperatures: its identity with the htrA gene product". Biochemical and Biophysical Research Communications. 176 (2): 730-6. doi:10.1016/s0006-291x(05)80245-1. PMID 2025286 ...
... is believed to be due to toxins found in the tick's saliva that enter the bloodstream while the tick is feeding. The two ticks most commonly associated with North American tick paralysis are the Rocky Mountain wood tick (Dermacentor andersoni) and the American dog tick (Dermacentor variabilis); however, 43 tick species have been implicated in human disease around the world.[1] Most North American cases of tick paralysis occur from April to June, when adult Dermacentor ticks emerge from hibernation and actively seek hosts.[2] In Australia, tick paralysis is caused by the tick Ixodes holocyclus. Prior to 1989, 20 fatal cases were reported in Australia.[3] Although tick paralysis is of concern in domestic animals and livestock in the United States as well, human cases are rare and usually occur in children under the age of 10. Tick paralysis occurs when an engorged and gravid (egg-laden) female tick produces a neurotoxin in its salivary glands and transmits it to its host during ...
... includes four (4) syndromes that share some common features and are primarily associated with bivalve molluscs (such as mussels, clams, oysters and scallops.)[1] These shellfish are filter feeders and, therefore, accumulate toxins produced by microscopic algae, such as cyanobacteria, diatoms and dinoflagellates. ...
... (DSP) is one of the four recognized symptom types of shellfish poisoning, the others being paralytic shellfish poisoning, neurotoxic shellfish poisoning and amnesic shellfish poisoning. As the name suggests, this syndrome manifests itself as intense diarrhea and severe abdominal pains. Nausea and vomiting may sometimes occur too. DSP and its symptoms usually set in within about half an hour of ingesting infected shellfish, and last for about one day. A recent case in France, though, with 20 people consuming oysters manifested itself after 36 hours. The causative poison is okadaic acid, which inhibits intestinal cellular de-phosphorylation.[1] This causes the cells to become very permeable to water and causes profuse, intense diarrhea with a high risk of dehydration. As no life-threatening symptoms generally emerge from this, no fatalities from DSP have ever been recorded. ...
A trypsin inhibitor (TI) is a protein and a type of serine protease inhibitor (serpin) that reduces the biological activity of trypsin by controlling the activation and catalytic reactions of proteins.[1] Trypsin is an enzyme involved in the breakdown of many different proteins, primarily as part of digestion in humans and other animals such as monogastrics and young ruminants. When trypsin inhibitor is consumed it acts as an irreversible and competitive substrate.[2] It competes with proteins to bind to trypsin and therefore renders it unavailable to bind with proteins for the digestion process.[1] As a result, protease inhibitors that interfere with digestion activity have an antinutritional effect. Therefore, trypsin inhibitor is considered an anti-nutritional factor or ANF.[3] Additionally, trypsin inhibitor partially interferes with chymotrypsin function. Trypsinogen is an inactive form of trypsin, its inactive form ensures protein aspects of the body, such as the pancreas and muscles, are ...
Zinc has been used therapeutically at a dose of 150 mg/day for months and in some cases for years, and in one case at a dose of up to 2000 mg/day zinc for months.[7][8][9][10][11] A decrease in copper levels and hematological changes have been reported; however, those changes were completely reversed with the cessation of zinc intake.[9] However, zinc has been used as zinc gluconate and zinc acetate lozenges for treating the common cold[12] and therefore the safety of usage at about 100 mg/day level is a relevant question. Thus, given that doses of over 150 mg/day for months to years has caused no permanent harm in many cases, a one-week usage of about 100 mg/day of zinc in the form of lozenges would not be expected to cause serious or irreversible adverse health issues in most persons. Unlike iron, the elimination of zinc is concentration-dependent.[13] ...
As of 2012, rFVIIa is not supported by the evidence for treating most cases of major bleeding.[1] There is a significant risk of arterial thrombosis with its use and thus, other than in those with factor VII deficiency, it should only be given in clinical trials.[1] Recombinant human factor VII, while initially looking promising in intracerebral hemorrhage, failed to show benefit following further study and is no longer recommended.[2][3] In people with hemophilia type A and B who have a deficiency of factors VIII and IX, these two factors are administered for controlling bleeding or as prophylaxis medication before starting surgeries. However, in some cases they subsequently develop neutralizing antibodies, called inhibitors, against the drug. These inhibitors often increase over time and inhibit the action of coagulation in the body. rFVIIa, which is an activated form of factor VII, bypasses factors VIII and IX and causes coagulation without the need for factors VIII and IX. It can't be given ...