Venoms from snakes of the genus Naja (family Elapidae). They contain many specific proteins that have cytotoxic, hemolytic, neurotoxic, and other properties. Like other elapid venoms, they are rich in enzymes. They include cobramines and cobralysins.
Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator.
A family of extremely venomous snakes, comprising coral snakes, cobras, mambas, kraits, and sea snakes. They are widely distributed, being found in the southern United States, South America, Africa, southern Asia, Australia, and the Pacific Islands. The elapids include three subfamilies: Elapinae, Hydrophiinae, and Lauticaudinae. Like the viperids, they have venom fangs in the front part of the upper jaw. The mambas of Africa are the most dangerous of all snakes by virtue of their size, speed, and highly toxic venom. (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, p329-33)
Most abundant proteins in COBRA venom; basic polypeptides of 57 to 62 amino acids with four disulfide bonds and a molecular weight of less than 7000; causes skeletal and cardiac muscle contraction, interferes with neuromuscular and ganglionic transmission, depolarizes nerve, muscle and blood cell membranes, thus causing hemolysis.
Limbless REPTILES of the suborder Serpentes.
Venoms from snakes of the subfamily Crotalinae or pit vipers, found mostly in the Americas. They include the rattlesnake, cottonmouth, fer-de-lance, bushmaster, and American copperhead. Their venoms contain nontoxic proteins, cardio-, hemo-, cyto-, and neurotoxins, and many enzymes, especially phospholipases A. Many of the toxins have been characterized.
Venoms obtained from Apis mellifera (honey bee) and related species. They contain various enzymes, polypeptide toxins, and other substances, some of which are allergenic or immunogenic or both. These venoms were formerly used in rheumatism to stimulate the pituitary-adrenal system.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
Solutions or mixtures of toxic and nontoxic substances elaborated by snake (Ophidia) salivary glands for the purpose of killing prey or disabling predators and delivered by grooved or hollow fangs. They usually contain enzymes, toxins, and other factors.
Toxins, contained in cobra (Naja) venom that block cholinergic receptors; two specific proteins have been described, the small (short, Type I) and the large (long, Type II) which also exist in other Elapid venoms.
Venoms from SNAKES of the viperid family. They tend to be less toxic than elapid or hydrophid venoms and act mainly on the vascular system, interfering with coagulation and capillary membrane integrity and are highly cytotoxic. They contain large amounts of several enzymes, other factors, and some toxins.
Venoms produced by the wasp (Vespid) family of stinging insects, including hornets; the venoms contain enzymes, biogenic amines, histamine releasing factors, kinins, toxic polypeptides, etc., and are similar to bee venoms.
Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.
A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.
Venoms from snakes of the family Elapidae, including cobras, kraits, mambas, coral, tiger, and Australian snakes. The venoms contain polypeptide toxins of various kinds, cytolytic, hemolytic, and neurotoxic factors, but fewer enzymes than viper or crotalid venoms. Many of the toxins have been characterized.
Venoms of arthropods of the order Araneida of the ARACHNIDA. The venoms usually contain several protein fractions, including ENZYMES, hemolytic, neurolytic, and other TOXINS, BIOLOGICAL.
The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.
Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host.
Venoms from animals of the order Scorpionida of the class Arachnida. They contain neuro- and hemotoxins, enzymes, and various other factors that may release acetylcholine and catecholamines from nerve endings. Of the several protein toxins that have been characterized, most are immunogenic.
Venoms from animals of the phylum Arthropoda. Those most investigated are from scorpions and spiders of the class Arachnidae and from ant, bee, and wasp families of the Insecta order Hymenoptera. The venoms contain protein toxins, enzymes, and other bioactive substances and may be lethal to man.
C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX.
A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-.
A serum protein which is important in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. This enzyme cleaves the COMPLEMENT C3B-bound COMPLEMENT FACTOR B to form C3bBb which is ALTERNATIVE PATHWAY C3 CONVERTASE.
Antisera used to counteract poisoning by animal VENOMS, especially SNAKE VENOMS.
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
A genus of poisonous snakes of the VIPERIDAE family. About 50 species are known and all are found in tropical America and southern South America. Bothrops atrox is the fer-de-lance and B. jararaca is the jararaca. (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, p336)
Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.
Phospholipases that hydrolyze the acyl group attached to the 2-position of PHOSPHOGLYCERIDES.
A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb.
Venoms produced by FISHES, including SHARKS and sting rays, usually delivered by spines. They contain various substances, including very labile toxins that affect the HEART specifically and all MUSCLES generally.
Venoms from the superfamily Formicoidea, Ants. They may contain protein factors and toxins, histamine, enzymes, and alkaloids and are often allergenic or immunogenic.
Phospholipases that hydrolyze one of the acyl groups of phosphoglycerides or glycerophosphatidates.
Venoms from mollusks, including CONUS and OCTOPUS species. The venoms contain proteins, enzymes, choline derivatives, slow-reacting substances, and several characterized polypeptide toxins that affect the nervous system. Mollusk venoms include cephalotoxin, venerupin, maculotoxin, surugatoxin, conotoxins, and murexine.
Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections.
Bites by snakes. Bite by a venomous snake is characterized by stinging pain at the wound puncture. The venom injected at the site of the bite is capable of producing a deleterious effect on the blood or on the nervous system. (Webster's 3d ed; from Dorland, 27th ed, at snake, venomous)
A screening assay for circulating COMPLEMENT PROTEINS. Diluted SERUM samples are added to antibody-coated ERYTHROCYTES and the percentage of cell lysis is measured. The values are expressed by the so called CH50, in HEMOLYTIC COMPLEMENT units per milliliter, which is the dilution of serum required to lyse 50 percent of the erythrocytes in the assay.
A serine protease that is the complex of COMPLEMENT C3B and COMPLEMENT FACTOR BB. It cleaves multiple COMPLEMENT C3 into COMPLEMENT C3A (anaphylatoxin) and COMPLEMENT C3B in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY.
Arthropods of the order Scorpiones, of which 1500 to 2000 species have been described. The most common live in tropical or subtropical areas. They are nocturnal and feed principally on insects and other arthropods. They are large arachnids but do not attack man spontaneously. They have a venomous sting. Their medical significance varies considerably and is dependent on their habits and venom potency rather than on their size. At most, the sting is equivalent to that of a hornet but certain species possess a highly toxic venom potentially fatal to humans. (From Dorland, 27th ed; Smith, Insects and Other Arthropods of Medical Importance, 1973, p417; Barnes, Invertebrate Zoology, 5th ed, p503)
A dermal inflammatory reaction produced under conditions of antibody excess, when a second injection of antigen produces intravascular antigen-antibody complexes which bind complement, causing cell clumping, endothelial damage, and vascular necrosis.
A trypanosome found in the blood of adult rats and transmitted by the rat flea. It is generally non-pathogenic in adult rats but can cause lethal infection in suckling rats.
A genus of snakes of the family VIPERIDAE. About 30 species are currently recognized, found in southeast Asia and adjacent island chains. The Okinawa habu frequently enters dwellings in search of rats and mice; the Chinese habu is often found in suburban and agricultural areas. They are quite irritable. (Moore: Poisonous Snakes of the World, 1980, p136)
The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g.
A genus of venomous snakes of the subfamily Crotalinae. Twelve species of this genus are found in North and Central America and Asia. Agkistrodon contortrix is the copperhead, A. piscivorus, the cottonmouth. The former is named for its russet or orange-brown color, the latter for the white interior of its mouth. (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, p336; Moore, Poisonous Snakes of the World, 1980, p75)
A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. C5a is a 74-amino-acid glycopeptide with a carboxy-terminal ARGININE that is crucial for its spasmogenic activity. Of all the complement-derived anaphylatoxins, C5a is the most potent in mediating immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE), smooth MUSCLE CONTRACTION; HISTAMINE RELEASE; and migration of LEUKOCYTES to site of INFLAMMATION.
Venoms produced by frogs, toads, salamanders, etc. The venom glands are usually on the skin of the back and contain cardiotoxic glycosides, cholinolytics, and a number of other bioactive materials, many of which have been characterized. The venoms have been used as arrow poisons and include bufogenin, bufotoxin, bufagin, bufotalin, histrionicotoxins, and pumiliotoxin.

Endothelial targeting and enhanced antiinflammatory effects of complement inhibitors possessing sialyl Lewisx moieties. (1/439)

The complement inhibitor soluble complement receptor type 1 (sCR1) and a truncated form of sCR1, sCR1[desLHR-A], have been generated with expression of the selectin-reactive oligosaccharide moiety, sialyl Lewisx (sLex), as N-linked oligosaccharide adducts. These modified proteins, sCR1sLex and sCR1[desLHR-A]sLex, were assessed in the L-selectin- and P-selectin-dependent rat model of lung injury following systemic activation of complement by cobra venom factor and in the L-selectin-, P-selectin-, and E-selectin-dependent model of lung injury following intrapulmonary deposition of IgG immune complexes. In the cobra venom factor model, sCR1sLex and sCR1[desLHR-A]sLex caused substantially greater reductions in neutrophil accumulation and in albumin extravasation in lung when compared with the non-sLex-decorated forms. In this model, increased lung vascular binding of sCR1sLex and sCR1[desLHR-A]sLex occurred in a P-selectin-dependent manner, in contrast to the absence of any increased binding of sCR1 or sCR1[desLHR-A]. In the IgG immune complex model, sCR1[desLHR-A]sLex possessed greater protective effects relative to sCR1[desLHR-A], based on albumin extravasation and neutrophil accumulation. Enhanced protective effects correlated with greater lung vascular binding of sCR1[desLHR-A]sLex as compared with the non-sLex-decorated form. In TNF-alpha-activated HUVEC, substantial in vitro binding occurred with sCR1[desLHR-A]sLex (but not with sCR1[desLHR-A]). This endothelial cell binding was blocked by anti-E-selectin but not by anti-P-selectin. These data suggest that sLex-decorated complement inhibitors have enhanced antiinflammatory effects and appear to have enhanced ability to localize to the activated vascular endothelium.  (+info)

Inhibition of a membrane complement regulatory protein by a monoclonal antibody induces acute lethal shock in rats primed with lipopolysaccharide. (2/439)

Rats pretreated with traces of LPS developed acute fatal shock syndrome after i.v. administration of a mAb that inhibits the function of a membrane complement regulatory molecule. Such a shock was not observed after the administration of large amounts of LPS instead of the mAb following LPS pretreatment. The lethal response did not occur in rats depleted of either leukocytes or complement, and a C5a receptor antagonist was found to inhibit the reaction. Furthermore, LPS-treated rats did not suffer fatal shock following the injection of cobra venom factor, which activates complement in the fluid phase so extensively as to exhaust complement capacity. Therefore, complement activation on cell membranes is a requirement for this type of acute reaction.  (+info)

Mechanisms of enhanced lung injury during sepsis. (3/439)

A major complication in sepsis is progressively impaired lung function and susceptibility to intrapulmonary infection. Why sepsis predisposes the lung to injury is not clear. In the current studies, rats were rendered septic by cecal ligation/puncture and evaluated for increased susceptibility to injury after a direct pulmonary insult (deposition of IgG immune complexes or airway instillation of lipopolysaccharide). By itself, cecal ligation/puncture did not produce evidence of lung injury. However, after a direct pulmonary insult, lung injury in septic animals was significantly enhanced. Enhanced lung injury was associated with increased accumulation of neutrophils in lung, enhanced production of CXC chemokines (but not tumor necrosis factor-alpha) in bronchoalveolar lavage fluids, and increased expression of lung vascular intercellular adhesion molecule-1 (ICAM-1). Complement depletion or treatment with anti-C5a abolished all evidence of enhanced lung injury in septic animals. When stimulated in vitro, bronchoalveolar lavage macrophages from septic animals had greatly enhanced CXC chemokine responses as compared with macrophages from sham-operated animals or from septic animals that had been complement depleted. These data indicate that the septic state causes priming of lung macrophages and suggest that enhanced lung injury in the septic state is complement dependent and related to increased production of CXC chemokines.  (+info)

Role of group II secretory phospholipase A2 in atherosclerosis: 2. Potential involvement of biologically active oxidized phospholipids. (4/439)

Secretory nonpancreatic phospholipase A2 (group II sPLA2) is induced in inflammation and present in atherosclerotic lesions. In an accompanying publication we demonstrate that transgenic mice expressing group II sPLA2 developed severe atherosclerosis. The current study was undertaken to determine whether 1 mechanism by which group II sPLA2 might contribute to the progression of inflammation and atherosclerosis is by increasing the formation of biologically active oxidized phospholipids. In vivo measurements of bioactive lipids were performed, and in vitro studies tested the hypothesis that sPLA2 can increase the accumulation of bioactive phospholipids. We have shown previously that 3 oxidized phospholipids derived from the oxidation of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (PAPC) stimulated endothelial cells to bind monocytes, a process that is known to be an important step in atherogenesis. We now show that these 3 biologically active phospholipids are significantly increased in livers of sPLA2 transgenic mice fed a high-fat diet as compared with nontransgenic littermates. We present in vitro evidence for several mechanisms by which these phospholipids may be increased in sPLA2 transgenics. These studies demonstrated that polyunsaturated free fatty acids, which are liberated by sPLA2, increased the formation of bioactive phospholipids in LDL, resulting in increased ability to stimulate monocyte-endothelial interactions. Moreover, sPLA2-treated LDL was oxidized by cocultures of human aortic endothelial cells and smooth muscle cells more efficiently than untreated LDL. Analysis by electrospray ionization-mass spectrometry revealed that the bioactive phospholipids, compared with unoxidized PAPC, were less susceptible to hydrolysis by human recombinant group II sPLA2. In addition, HDL from the transgenic mice and human HDL treated with recombinant sPLA2 in vitro failed, in the coculture system, to protect against the formation of biologically active phospholipids in LDL. This lack of protection may in part relate to the decreased levels of paraoxonase seen in the HDL isolated from the transgenic animals. Taken together, these studies show that levels of biologically active oxidized phospholipids are increased in sPLA2 transgenic mice; they also suggest that this increase may be mediated by effects of sPLA2 on both LDL and HDL.  (+info)

A nonhuman primate model for the selective elimination of CD8+ lymphocytes using a mouse-human chimeric monoclonal antibody. (5/439)

Nonhuman primates provide valuable animal models for human diseases. However, studies assessing the role of cell-mediated immune responses have been difficult to perform in nonhuman primates. We have shown that CD8+ lymphocyte-mediated immunity in rhesus monkeys can be selectively eliminated using the mouse-human chimeric anti-CD8 monoclonal antibody cM-T807. In vitro, this antibody completely blocked antigen-specific expansion of cytotoxic T cells and decreased major histocompatibility complex class I-restricted, antigen-specific lysis of target cells but did not mediate complement-dependent cell lysis. In vivo administration of cM-T807 in rhesus monkeys resulted in near total depletion of CD8+ T cells from the blood and lymph nodes for up to 6 weeks. This depletion was not solely complement-dependent and persisted longer in adults than in juveniles. Preservation of B cell and CD4+ T cell function in monkeys depleted of CD8+ lymphocytes was demonstrated by their ability to develop humoral immune responses to the administered chimeric monoclonal antibody. Furthermore, during CD8+ lymphocyte depletion, monkeys developed delayed-type hypersensitivity reactions comprised only of CD4+ T cells but not CD8+ T cells. This CD8+ lymphocyte depletion model should prove useful in defining the role of cell-mediated immune responses in controlling infectious diseases in nonhuman primates.  (+info)

Binding of nucleotide triphosphates to cardiotoxin analogue II from the Taiwan cobra venom (Naja naja atra). Elucidation of the structural interactions in the dATP-cardiotoxin analogue ii complex. (6/439)

Snake venom cardiotoxins have been recently shown to block the enzymatic activity of phospholipid protein kinase and Na+,K+-ATPase. To understand the molecular basis for the inhibitory effects of cardiotoxin on the action of these enzymes, the nucleotide triphosphate binding ability of cardiotoxin analogue II (CTX II) from the Taiwan cobra (Naja naja atra) venom is investigated using a variety of spectroscopic techniques such as fluorescence, circular dichroism, and two-dimensional NMR. CTX II is found to bind to all the four nucleotide triphosphates (ATP, UTP, GTP, and CTP) with similar affinity. Detailed studies of the binding of dATP to CTX II indicated that the toxin molecule is significantly stabilized in the presence of the nucleotide. Molecular modeling, based on the NOEs observed for the dATP.CTX II complex, reveals that dATP binds to the CTX II molecule at the groove enclosed between the N- and C-terminal ends of the toxin molecule. Based on the results obtained in the present study, a molecular mechanism to account for the inhibition of the enzymatic activity of the phospholipid-sensitive protein kinase and Na+,K+-ATPase is also proposed.  (+info)

Effect of ranitidine bismuth citrate on the phospholipase A2 activity of Naja naja venom and Helicobacter pylori: a biochemical analysis. (7/439)

BACKGROUND: Helicobacter pylori has become recognized as a fundamental pathogen in the development of gastritis and peptic ulcer disease. Bismuth compounds in combination with antibiotics are widely used to treat H. pylori associated peptic ulcer disease. METHODS: In this study we measured and analysed the inhibitory effect of ranitidine bismuth citrate (RBC, Pylorid, Tritec) on the activity and kinetics of phospholipase A2 (PLA2) (E.C.3.1.1.4) of commercial cobra (Naja naja) venom and H. pylori (French press lysates) using L-alpha-dipalmitoyl-(2[1-14C]palmitoyl)-phosphatidylcholine as substrate. RESULTS: Our data suggest that RBC might exert a dose-dependent uncompetitive inhibition on PLA2 activity of both H. pylori and Naja naja venom. the inhibitory effect of RBC on the PLA2 activity cannot be abolished by the optimal concentration of calcium (10 mM), indicating its mechanism to be unrelated to the displacement of calcium from the activation site of the enzyme. CONCLUSION: Our results suggest that one of the mechanisms by which bismuth compounds are therapeutically effective in the treatment of H. pylori associated gastritis is by inhibiting the activity of the degradative PLA2 enzyme secreted by H. pylori. As a consequence of the inhibitory action of RBC on PLA2 of the bacteria, the extracellular and/or intracellular phospholipid components of the gastric mucosal barrier are preserved.  (+info)

Heparin binding to cobra basic phospholipase A2 depends on heparin chain length and amino acid specificity. (8/439)

Heparin is shown to bind specifically to the carboxy-terminal region of toxic type I phospholipase A2 from Naja nigricollis (N-PLA2) by competition assay using synthetic polypeptides and heparin affinity chromatography. The binding strength is seen to depend on heparin chain length and the presence of N-sulfate groups of heparin. It is observed that both electrostatic and non-electrostatic interactions are involved in the specific binding of heparin to the carboxy-terminus. When heparin's size is at least a decasaccharide, about two molecules of N-PLA2 bind to one molecule of heparin, as evidenced by the chemical estimate of protein to carbohydrate ratio in such N-PLA2/heparin complexes. Based on such a stoichiometric measurement and computer modeling of the N-PLA2/heparin complex, it is suggested that the binding sites of the two N-PLA2 molecules on one heparin molecule lie on the opposite sides of the heparin chain.  (+info)

Cobra venoms are a type of snake venom that is produced by cobras, which are members of the genus Naja in the family Elapidae. These venoms are complex mixtures of proteins and other molecules that have evolved to help the snake immobilize and digest its prey.

Cobra venoms typically contain a variety of toxic components, including neurotoxins, hemotoxins, and cytotoxins. Neurotoxins target the nervous system and can cause paralysis and respiratory failure. Hemotoxins damage blood vessels and tissues, leading to internal bleeding and organ damage. Cytotoxins destroy cells and can cause tissue necrosis.

The specific composition of cobra venoms can vary widely between different species of cobras, as well as between individual snakes of the same species. Some cobras have venoms that are primarily neurotoxic, while others have venoms that are more hemotoxic or cytotoxic. The potency and effects of cobra venoms can also be influenced by factors such as the age and size of the snake, as well as the temperature and pH of the environment.

Cobra bites can be extremely dangerous and even fatal to humans, depending on the species of cobra, the amount of venom injected, and the location of the bite. Immediate medical attention is required in the event of a cobra bite, including the administration of antivenom therapy to neutralize the effects of the venom.

Venom is a complex mixture of toxic compounds produced by certain animals, such as snakes, spiders, scorpions, and marine creatures like cone snails and stonefish. These toxic substances are specifically designed to cause damage to the tissues or interfere with the normal physiological processes of other organisms, which can lead to harmful or even lethal effects.

Venoms typically contain a variety of components, including enzymes, peptides, proteins, and small molecules, each with specific functions that contribute to the overall toxicity of the mixture. Some of these components may cause localized damage, such as tissue necrosis or inflammation, while others can have systemic effects, impacting various organs and bodily functions.

The study of venoms, known as toxinology, has important implications for understanding the evolution of animal behavior, developing new therapeutics, and advancing medical treatments for envenomation (the process of being poisoned by venom). Additionally, venoms have been used in traditional medicine for centuries, and ongoing research continues to uncover novel compounds with potential applications in modern pharmacology.

Elapidae is a family of venomous snakes, also known as elapids. This family includes many well-known species such as cobras, mambas, death adders, and sea snakes. Elapids are characterized by their fixed fangs, which are located at the front of the upper jaw and deliver venom through a hollow canal. The venom of these snakes is typically neurotoxic, causing paralysis and respiratory failure in prey or attackers.

Elapids are found throughout the world, with the greatest diversity occurring in tropical regions. They vary widely in size, from small species like the death adders that measure only a few inches long, to large species like the king cobra, which can reach lengths of up to 18 feet (5.5 meters).

Elapids are generally shy and avoid confrontations with humans whenever possible. However, they will defend themselves aggressively if threatened or cornered. Bites from elapid snakes can be medically significant and may require antivenom treatment.

Cobra cardiotoxin proteins are a type of toxin found in the venom of some cobra snakes. These toxins belong to a larger group of proteins known as three-finger toxins, due to their distinctive three-dimensional shape. Cardiotoxins are so named because they specifically target and disrupt the function of heart muscle cells, leading to serious cardiovascular symptoms such as abnormal heart rhythms, low blood pressure, and even heart failure in severe cases.

Cardiotoxins work by binding to and inserting themselves into the membrane of heart muscle cells, where they form pores that disrupt the electrical activity of the cells. This can lead to arrhythmias, or abnormal heart rhythms, which can be life-threatening in severe cases. Cardiotoxins can also cause direct damage to heart muscle cells, leading to decreased contractility and reduced pumping efficiency of the heart.

Cobra cardiotoxin proteins are being studied for their potential therapeutic uses, particularly in the development of new drugs for the treatment of heart disease. However, they are also a significant medical concern in areas where cobra snakes are common, as their venom can cause serious and potentially fatal symptoms in humans and animals.

I'm sorry for any confusion, but "snakes" is not a medical term. It refers to a group of legless reptiles that can be found on every continent except Antarctica. If you have any questions about snakes in a different context, please provide more information and I'll do my best to help!

Crotalid venoms are the toxic secretions produced by the members of the Crotalinae subfamily, also known as pit vipers. This group includes rattlesnakes, cottonmouths (or water moccasins), and copperheads, which are native to the Americas, as well as Old World vipers found in Asia and Europe, such as gaboon vipers and saw-scaled vipers.

Crotalid venoms are complex mixtures of various bioactive molecules, including enzymes, proteins, peptides, and other low molecular weight components. They typically contain a variety of pharmacologically active components, such as hemotoxic and neurotoxic agents, which can cause extensive local tissue damage, coagulopathy, cardiovascular dysfunction, and neuromuscular disorders in the victim.

The composition of crotalid venoms can vary significantly between different species and even among individual specimens within the same species. This variability is influenced by factors such as geographic location, age, sex, diet, and environmental conditions. As a result, the clinical manifestations of crotalid envenomation can be highly variable, ranging from mild local reactions to severe systemic effects that may require intensive medical treatment and supportive care.

Crotalid venoms have been the subject of extensive research in recent years due to their potential therapeutic applications. For example, certain components of crotalid venoms have shown promise as drugs for treating various medical conditions, such as cardiovascular diseases, pain, and inflammation. However, further studies are needed to fully understand the mechanisms of action of these venom components and to develop safe and effective therapies based on them.

Bee venom is a poisonous substance that a honeybee (Apis mellifera) injects into the skin of a person or animal when it stings. It's produced in the venom gland and stored in the venom sac of the bee. Bee venom is a complex mixture of proteins, peptides, and other compounds. The main active components of bee venom include melittin, apamin, and phospholipase A2.

Melittin is a toxic peptide that causes pain, redness, and swelling at the site of the sting. It also has hemolytic (red blood cell-destroying) properties. Apamin is a neurotoxin that can affect the nervous system and cause neurological symptoms in severe cases. Phospholipase A2 is an enzyme that can damage cell membranes and contribute to the inflammatory response.

Bee venom has been used in traditional medicine for centuries, particularly in China and other parts of Asia. It's believed to have anti-inflammatory, analgesic (pain-relieving), and immunomodulatory effects. Some studies suggest that bee venom may have therapeutic potential for a variety of medical conditions, including rheumatoid arthritis, multiple sclerosis, and chronic pain. However, more research is needed to confirm these findings and to determine the safety and efficacy of bee venom therapy.

It's important to note that bee stings can cause severe allergic reactions (anaphylaxis) in some people, which can be life-threatening. If you experience symptoms such as difficulty breathing, rapid heartbeat, or hives after being stung by a bee, seek medical attention immediately.

The complement system is a group of proteins found in the blood and on the surface of cells that when activated, work together to help eliminate pathogens such as bacteria, viruses, and fungi from the body. The proteins are normally inactive in the bloodstream. When they encounter an invading microorganism or foreign substance, a series of reactions take place leading to the activation of the complement system. Activation results in the production of effector molecules that can punch holes in the cell membranes of pathogens, recruit and activate immune cells, and help remove debris and dead cells from the body.

There are three main pathways that can lead to complement activation: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteins that work together in a cascade-like manner to amplify the response and generate effector molecules. The three main effector molecules produced by the complement system are C3b, C4b, and C5b. These molecules can bind to the surface of pathogens, marking them for destruction by other immune cells.

Complement proteins also play a role in the regulation of the immune response. They help to prevent excessive activation of the complement system, which could damage host tissues. Dysregulation of the complement system has been implicated in a number of diseases, including autoimmune disorders and inflammatory conditions.

In summary, Complement System Proteins are a group of proteins that play a crucial role in the immune response by helping to eliminate pathogens and regulate the immune response. They can be activated through three different pathways, leading to the production of effector molecules that mark pathogens for destruction. Dysregulation of the complement system has been linked to various diseases.

Snake venoms are complex mixtures of bioactive compounds produced by specialized glands in snakes. They primarily consist of proteins and peptides, including enzymes, neurotoxins, hemotoxins, cytotoxins, and cardiotoxins. These toxins can cause a variety of pharmacological effects on the victim's body, such as disruption of the nervous system, blood coagulation, muscle function, and cell membrane integrity, ultimately leading to tissue damage and potentially death. The composition of snake venoms varies widely among different species, making each species' venom unique in its toxicity profile.

Cobra neurotoxin proteins refer to a group of toxic proteins found in the venom of cobra snakes. These toxins primarily affect the nervous system and cause paralysis, which can lead to respiratory failure and death in prey or envenomed individuals. Cobra neurotoxins are classified as phospholipases A2 (PLA2) enzymes, which are capable of hydrolyzing membrane phospholipids and inducing various biological effects.

The two main types of cobra neurotoxin proteins are:

1. Short-chain neurotoxins: These toxins consist of 60-74 amino acid residues, with four disulfide bridges that stabilize their structure. They primarily interact with the nicotinic acetylcholine receptors (nAChRs) at the neuromuscular junction, causing muscle paralysis by preventing the binding of acetylcholine to its receptors.
2. Long-chain neurotoxins: These toxins contain 110-120 amino acid residues and have five disulfide bridges. They can be further divided into two subcategories:

a. Cardiotoxins: Although they primarily affect the heart, causing cardiac arrhythmias and decreased contractility, these toxins can also interact with nAChRs and contribute to neuromuscular paralysis.

b. Cytotoxins: These toxins mainly cause damage to various cell types by forming pores in the cell membrane, leading to cell lysis and death. They have minimal effects on the nervous system.

Understanding cobra neurotoxin proteins is essential for developing effective antivenoms and treatments for cobra envenomation.

"Viper venoms" refer to the toxic secretions produced by members of the Viperidae family of snakes, which include pit vipers (such as rattlesnakes, copperheads, and cottonmouths) and true vipers (like adders, vipers, and gaboon vipers). These venoms are complex mixtures of proteins, enzymes, and other bioactive molecules that can cause a wide range of symptoms in prey or predators, including local tissue damage, pain, swelling, bleeding, and potentially life-threatening systemic effects such as coagulopathy, cardiovascular shock, and respiratory failure.

The composition of viper venoms varies widely between different species and even among individuals within the same species. However, many viper venoms contain a variety of enzymes (such as phospholipases A2, metalloproteinases, and serine proteases) that can cause tissue damage and disrupt vital physiological processes in the victim. Additionally, some viper venoms contain neurotoxins that can affect the nervous system and cause paralysis or other neurological symptoms.

Understanding the composition and mechanisms of action of viper venoms is important for developing effective treatments for venomous snakebites, as well as for gaining insights into the evolution and ecology of these fascinating and diverse creatures.

Wasp venoms are complex mixtures of bioactive molecules produced by wasps (Hymenoptera: Vespidae) to defend themselves and paralyze prey. The main components include:

1. Phospholipases A2 (PLA2): Enzymes that can cause pain, inflammation, and damage to cell membranes.
2. Hyaluronidase: An enzyme that helps spread the venom by breaking down connective tissues.
3. Proteases: Enzymes that break down proteins and contribute to tissue damage and inflammation.
4. Antigen 5: A major allergen that can cause severe allergic reactions (anaphylaxis) in sensitive individuals.
5. Mastoparan: A peptide that induces histamine release, leading to localized inflammation and pain.
6. Neurotoxins: Some wasp venoms contain neurotoxins that can cause paralysis or neurological symptoms.

The composition of wasp venoms may vary among species, and individual sensitivity to the components can result in different reactions ranging from localized pain, swelling, and redness to systemic allergic responses.

Complement inactivator proteins are a group of regulatory proteins that help to control and limit the activation of the complement system, which is a part of the immune system. The complement system is a complex series of biochemical reactions that help to eliminate pathogens and damaged cells from the body. However, if not properly regulated, the complement system can also cause damage to healthy tissues and contribute to the development of various diseases.

Complement inactivator proteins work by inhibiting specific components of the complement system, preventing them from activating and causing an immune response. Some examples of complement inactivator proteins include:

1. C1 inhibitor (C1INH): This protein regulates the activation of the classical pathway of the complement system by inhibiting the C1 complex, which is a group of proteins that initiate this pathway.
2. Decay-accelerating factor (DAF or CD55): This protein regulates the activation of both the classical and alternative pathways of the complement system by accelerating the decay of the C3/C5 convertases, which are enzymes that activate the complement components C3 and C5.
3. Membrane cofactor protein (MCP or CD46): This protein regulates the activation of the alternative pathway of the complement system by serving as a cofactor for the cleavage and inactivation of C3b, a component of the C3 convertase.
4. Factor H: This protein also regulates the activation of the alternative pathway of the complement system by acting as a cofactor for the cleavage and inactivation of C3b, and by preventing the formation of the C3 convertase.

Deficiencies or dysfunction of complement inactivator proteins can lead to various diseases, including hereditary angioedema (C1INH deficiency), atypical hemolytic uremic syndrome (factor H deficiency or dysfunction), and age-related macular degeneration (complement component overactivation).

Complement C3 is a protein that plays a central role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C3 can be activated through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Once activated, it breaks down into two fragments, C3a and C3b.

C3a is an anaphylatoxin that helps to recruit immune cells to the site of infection or injury, while C3b plays a role in opsonization, which is the process of coating pathogens or damaged cells with proteins to make them more recognizable to the immune system. Additionally, C3b can also activate the membrane attack complex (MAC), which forms a pore in the membrane of target cells leading to their lysis or destruction.

In summary, Complement C3 is an important protein in the complement system that helps to identify and eliminate pathogens and damaged cells from the body through various mechanisms.

Elapid venoms are the toxic secretions produced by elapid snakes, a family of venomous snakes that includes cobras, mambas, kraits, and coral snakes. These venoms are primarily composed of neurotoxins, which can cause paralysis and respiratory failure in prey or predators.

Elapid venoms work by targeting the nervous system, disrupting communication between the brain and muscles. This results in muscle weakness, paralysis, and eventually respiratory failure if left untreated. Some elapid venoms also contain hemotoxins, which can cause tissue damage, bleeding, and other systemic effects.

The severity of envenomation by an elapid snake depends on several factors, including the species of snake, the amount of venom injected, the location of the bite, and the size and health of the victim. Prompt medical treatment is essential in cases of elapid envenomation, as the effects of the venom can progress rapidly and lead to serious complications or death if left untreated.

Spider venoms are complex mixtures of bioactive compounds produced by the specialized glands of spiders. These venoms are primarily used for prey immobilization and defense. They contain a variety of molecules such as neurotoxins, proteases, peptides, and other biologically active substances. Different spider species have unique venom compositions, which can cause different reactions when they bite or come into contact with humans or other animals. Some spider venoms can cause mild symptoms like pain and swelling, while others can lead to more severe reactions such as tissue necrosis or even death in extreme cases.

Complement activation is the process by which the complement system, a part of the immune system, is activated to help eliminate pathogens and damaged cells from the body. The complement system consists of a group of proteins that work together to recognize and destroy foreign substances.

Activation of the complement system can occur through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteolytic reactions that ultimately result in the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, leading to its lysis and removal.

The classical pathway is typically activated by the binding of antibodies to antigens on the surface of a pathogen or damaged cell. The lectin pathway is activated by the recognition of specific carbohydrate structures on the surface of microorganisms. The alternative pathway can be spontaneously activated and serves as an amplification loop for both the classical and lectin pathways.

Complement activation plays a crucial role in the immune response, but uncontrolled or excessive activation can also lead to tissue damage and inflammation. Dysregulation of complement activation has been implicated in various diseases, including autoimmune disorders, inflammatory conditions, and neurodegenerative diseases.

Complement inactivating agents are substances or drugs that inhibit the complement system, which is a part of the immune system responsible for the recognition and elimination of foreign substances and microorganisms. The complement system consists of a group of proteins that work together to help eliminate pathogens from the body.

Complement inactivating agents are used in medical settings to prevent or treat various conditions associated with excessive or unwanted activation of the complement system, such as inflammation, autoimmune diseases, and transplant rejection. These agents can inhibit different components of the complement pathway, including C1 esterase inhibitors, C3 convertase inhibitors, and C5a receptor antagonists.

Examples of complement inactivating agents include eculizumab, ravulizumab, and Alexion's Ultomiris, which are monoclonal antibodies that target C5, a protein involved in the final steps of the complement pathway. These drugs have been approved for the treatment of paroxysmal nocturnal hemoglobinuria (PNH), atypical hemolytic uremic syndrome (aHUS), and other complement-mediated diseases.

Other complement inactivating agents include C1 esterase inhibitors, such as Berinert and Ruconest, which are used to treat hereditary angioedema (HAE). These drugs work by inhibiting the activation of the classical pathway of the complement system, thereby preventing the release of inflammatory mediators that can cause swelling and pain.

Overall, complement inactivating agents play an important role in the treatment of various complement-mediated diseases, helping to reduce inflammation, prevent tissue damage, and improve patient outcomes.

Scorpion venoms are complex mixtures of neurotoxins, enzymes, and other bioactive molecules that are produced by the venom glands of scorpions. These venoms are primarily used for prey immobilization and defense. The neurotoxins found in scorpion venoms can cause a variety of symptoms in humans, including pain, swelling, numbness, and in severe cases, respiratory failure and death.

Scorpion venoms are being studied for their potential medical applications, such as in the development of new pain medications and insecticides. Additionally, some components of scorpion venom have been found to have antimicrobial properties and may be useful in the development of new antibiotics.

Arthropod venoms are toxic secretions produced by the venom glands of various arthropods, such as spiders, scorpions, insects, and marine invertebrates. These venoms typically contain a complex mixture of bioactive molecules, including peptides, proteins, enzymes, and small molecules, which can cause a range of symptoms and effects in humans and other animals.

The specific composition of arthropod venoms varies widely depending on the species and can be tailored to serve various functions, such as prey immobilization, defense, or predation. Some arthropod venoms contain neurotoxins that can disrupt nerve function and cause paralysis, while others may contain cytotoxins that damage tissues or hemotoxins that affect the blood and cardiovascular system.

Arthropod venoms have been studied for their potential therapeutic applications, as some of their bioactive components have shown promise in treating various medical conditions, including pain, inflammation, and neurological disorders. However, it is important to note that arthropod venoms can also cause severe allergic reactions and other adverse effects in susceptible individuals, making it essential to exercise caution when handling or coming into contact with venomous arthropods.

Complement C5 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. The complement system is a complex series of biochemical reactions that help to identify and destroy foreign substances, such as bacteria and viruses.

Complement C5 is one of several proteins in the complement system that are activated in a cascading manner in response to an activating event, such as the binding of an antibody to a pathogen. Once activated, Complement C5 can be cleaved into two smaller proteins, C5a and C5b.

C5a is a powerful anaphylatoxin, which means it can cause the release of histamine from mast cells and basophils, leading to inflammation and increased vascular permeability. It also acts as a chemoattractant, drawing immune cells to the site of infection or injury.

C5b, on the other hand, plays a role in the formation of the membrane attack complex (MAC), which is a protein structure that can punch holes in the membranes of pathogens, leading to their lysis and destruction.

Overall, Complement C5 is an important component of the immune system's response to infection and injury, helping to eliminate pathogens and damaged cells from the body.

Phospholipases are a group of enzymes that catalyze the hydrolysis of phospholipids, which are major components of cell membranes. Phospholipases cleave specific ester bonds in phospholipids, releasing free fatty acids and other lipophilic molecules. Based on the site of action, phospholipases are classified into four types:

1. Phospholipase A1 (PLA1): This enzyme hydrolyzes the ester bond at the sn-1 position of a glycerophospholipid, releasing a free fatty acid and a lysophospholipid.
2. Phospholipase A2 (PLA2): PLA2 cleaves the ester bond at the sn-2 position of a glycerophospholipid, releasing a free fatty acid (often arachidonic acid) and a lysophospholipid. Arachidonic acid is a precursor for eicosanoids, which are signaling molecules involved in inflammation and other physiological processes.
3. Phospholipase C (PLC): PLC hydrolyzes the phosphodiester bond in the headgroup of a glycerophospholipid, releasing diacylglycerol (DAG) and a soluble head group, such as inositol trisphosphate (IP3). DAG acts as a secondary messenger in intracellular signaling pathways, while IP3 mediates the release of calcium ions from intracellular stores.
4. Phospholipase D (PLD): PLD cleaves the phosphoester bond between the headgroup and the glycerol moiety of a glycerophospholipid, releasing phosphatidic acid (PA) and a free head group. PA is an important signaling molecule involved in various cellular processes, including membrane trafficking, cytoskeletal reorganization, and cell survival.

Phospholipases have diverse roles in normal physiology and pathophysiological conditions, such as inflammation, immunity, and neurotransmission. Dysregulation of phospholipase activity can contribute to the development of various diseases, including cancer, cardiovascular disease, and neurological disorders.

Complement Factor D is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Specifically, Factor D is a serine protease that is involved in the alternative pathway of the complement system.

In this pathway, Factor D helps to cleave another protein called Factor B, which then activates a complex called the C3 convertase. The C3 convertase cleaves complement component 3 (C3) into C3a and C3b, leading to the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, causing its lysis and removal from the body.

Deficiencies or mutations in Complement Factor D can lead to an impaired alternative pathway and increased susceptibility to certain infections, particularly those caused by Neisseria bacteria. Additionally, abnormal regulation of the complement system has been implicated in a variety of diseases, including autoimmune disorders, inflammatory conditions, and neurodegenerative diseases.

Antivenins, also known as antivenoms, are medications created specifically to counteract venomous bites or stings from various creatures such as snakes, spiders, scorpions, and marine animals. They contain antibodies that bind to and neutralize the toxic proteins present in venom. Antivenins are usually made by immunizing large animals (like horses) with small amounts of venom over time, which prompts the animal's immune system to produce antibodies against the venom. The antibody-rich serum is then collected from the immunized animal and purified for use as an antivenin.

When administered to a victim who has been envenomated, antivenins work by binding to the venom molecules, preventing them from causing further damage to the body's tissues and organs. This helps minimize the severity of symptoms and can save lives in life-threatening situations. It is essential to seek immediate medical attention if bitten or stung by a venomous creature, as antivenins should be administered as soon as possible for optimal effectiveness.

Hemolysis is the destruction or breakdown of red blood cells, resulting in the release of hemoglobin into the surrounding fluid (plasma). This process can occur due to various reasons such as chemical agents, infections, autoimmune disorders, mechanical trauma, or genetic abnormalities. Hemolysis may lead to anemia and jaundice, among other complications. It is essential to monitor hemolysis levels in patients undergoing medical treatments that might cause this condition.

"Bothrops" is a genus of venomous snakes commonly known as lancehead vipers, found primarily in Central and South America. The name "Bothrops" comes from the Greek words "bothros," meaning pit, and "ops," meaning face, referring to the deep pits on the sides of their heads that help them detect heat and locate prey. These snakes are known for their aggressive behavior and potent venom, which can cause severe pain, swelling, tissue damage, and potentially life-threatening systemic effects if left untreated.

The genus "Bothrops" includes over 30 species of pit vipers, many of which are considered medically important due to their ability to inflict serious envenomations in humans. Some notable examples include Bothrops asper (the terciopelo or fer-de-lance), Bothrops atrox (the common lancehead), and Bothrops jararaca (the jararaca).

If you encounter a snake of this genus, it is essential to seek medical attention immediately if bitten, as the venom can cause significant harm if not treated promptly.

Complement C3-C5 convertases are proteins that play a crucial role in the activation of the complement system, which is a part of the immune system. The complement system helps to eliminate pathogens and damaged cells from the body by marking them for destruction and attracting immune cells to the site of infection or injury.

The C3-C5 convertases are formed during the activation of the complement component 3 (C3) protein, which is a central player in the complement system. The formation of the C3-C5 convertase involves two main steps:

1. C3 convertase formation: In this step, a complex of proteins called the C3 convertase is formed by the cleavage of C3 into C3a and C3b fragments. This complex can then cleave additional C3 molecules into C3a and C3b fragments, amplifying the complement response.
2. C5 convertase formation: In this step, the C3b fragment from the C3 convertase binds to another protein called C4b2a, forming a new complex called the C5 convertase. The C5 convertase can then cleave the C5 protein into C5a and C5b fragments.

The C5b fragment goes on to form the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, leading to its lysis or destruction. The C3a and C5a fragments are small proteins called anaphylatoxins that can cause inflammation and attract immune cells to the site of infection or injury.

Overall, the formation of Complement C3-C5 convertases is a critical step in the activation of the complement system and plays a key role in the body's defense against pathogens and damaged cells.

Phospholipase A2 (PLA2) is a type of enzyme that catalyzes the hydrolysis of the sn-2 ester bond in glycerophospholipids, releasing free fatty acids, such as arachidonic acid, and lysophospholipids. These products are important precursors for the biosynthesis of various signaling molecules, including eicosanoids, platelet-activating factor (PAF), and lipoxins, which play crucial roles in inflammation, immunity, and other cellular processes.

Phospholipases A2 are classified into several groups based on their structure, mechanism of action, and cellular localization. The secreted PLA2s (sPLA2s) are found in extracellular fluids and are characterized by a low molecular weight, while the calcium-dependent cytosolic PLA2s (cPLA2s) are larger proteins that reside within cells.

Abnormal regulation or activity of Phospholipase A2 has been implicated in various pathological conditions, such as inflammation, neurodegenerative diseases, and cancer. Therefore, understanding the biology and function of these enzymes is essential for developing novel therapeutic strategies to target these disorders.

Complement Factor B is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. Specifically, Factor B is a component of the alternative pathway of the complement system, which provides a rapid and amplified response to microbial surfaces.

Factor B is cleaved by another protease called Factor D into two fragments, Ba and Bb. The formation of the C3 convertase (C3bBb) is essential for the activation of the alternative pathway. This complex can cleave and activate more C3 molecules, leading to a cascade of reactions that result in the formation of the membrane attack complex (MAC), which forms pores in the membranes of target cells, causing their lysis and elimination.

Deficiencies or mutations in Complement Factor B can lead to various complement-mediated diseases, such as atypical hemolytic uremic syndrome (aHUS) and age-related macular degeneration (AMD).

Fish venoms are toxic substances produced by some species of fish, primarily found in their spines, fins, or skin. These venoms are used for defense against predators and can cause painful injuries to humans who come into contact with them. The venomous fishes belong to various taxonomic groups, including catfishes (order Siluriformes), stingrays (superorder Batoidea), scorpionfishes (family Scorpaenidae), weevers (family Trachinidae), and stonefishes (family Synanceiidae).

The composition of fish venoms varies among species, but they typically contain a mixture of proteins, enzymes, and small molecules that can induce local and systemic effects. Local reactions usually involve pain, swelling, and redness at the site of the injury, while systemic symptoms may include nausea, vomiting, difficulty breathing, paralysis, or even death in severe cases.

Immediate medical attention is required for fish venom injuries to manage pain, prevent infection, and treat potential systemic effects. Treatment usually involves removing any remaining venomous spines or fragments, immersing the wound in hot water (>45°C/113°F) to denature the proteins in the venom, and administering appropriate analgesics, antibiotics, and supportive care as needed.

Ant venoms are toxic secretions produced by various species of ants as a defense mechanism against predators and to incapacitate their prey. The composition of ant venoms varies among different species, but they typically contain a mixture of alkaloids, peptides, and proteins that can cause a range of symptoms in humans, from mild irritation and pain to severe allergic reactions.

The venom of some ant species, such as the fire ants (Solenopsis spp.), contains alkaloids that can cause painful pustules and itching, while the venom of other species, like the bulldog ants (Myrmecia spp.), contains proteins that can induce severe allergic reactions and even anaphylactic shock in sensitive individuals.

Understanding the composition and effects of ant venoms is important for developing effective treatments for ant stings and for studying their potential therapeutic applications, such as using ant venom components in pain management or as leads for new drug development.

Phospholipases A are a group of enzymes that hydrolyze phospholipids into fatty acids and lysophospholipids by cleaving the ester bond at the sn-1 or sn-2 position of the glycerol backbone. There are three main types of Phospholipases A:

* Phospholipase A1 (PLA1): This enzyme specifically hydrolyzes the ester bond at the sn-1 position, releasing a free fatty acid and a lysophospholipid.
* Phospholipase A2 (PLA2): This enzyme specifically hydrolyzes the ester bond at the sn-2 position, releasing a free fatty acid (often arachidonic acid, which is a precursor for eicosanoids) and a lysophospholipid.
* Phospholipase A/B (PLA/B): This enzyme has both PLA1 and PLA2 activity and can hydrolyze the ester bond at either the sn-1 or sn-2 position.

Phospholipases A play important roles in various biological processes, including cell signaling, membrane remodeling, and host defense. They are also involved in several diseases, such as atherosclerosis, neurodegenerative disorders, and cancer.

Mollusk venoms are toxic substances produced by certain species of mollusks, a group of marine animals that includes snails, slugs, clams, octopuses, and squids. These venoms are primarily used for defense against predators or for hunting prey. They can contain a variety of bioactive molecules, such as proteins, peptides, and neurotoxins, which can cause a range of effects on the victim's body, from mild irritation to paralysis and death.

One well-known example of a mollusk venom is that of the cone snail, which uses its venom to capture prey. The venom of some cone snails contains compounds called conotoxins, which are highly selective for specific ion channels in the nervous system and can cause paralysis or death in their victims. These conotoxins have been studied for their potential therapeutic applications, such as pain relief and treatment for neurological disorders.

It's important to note that while some mollusk venoms can be dangerous or even deadly to humans, most species of mollusks are not harmful to people. However, it's always a good idea to exercise caution when handling any marine animals, as even non-venomous species can cause injury with their sharp shells or other structures.

The alternative complement pathway is one of the three initiating pathways of the complement system, which is a part of the innate immune system that helps to clear pathogens and damaged cells from the body. The other two pathways are the classical and lectin pathways.

The alternative pathway is continuously activated at a low level, even in the absence of infection or injury, through the spontaneous cleavage of complement component C3 into C3a and C3b by the protease factor D in the presence of magnesium ions. The generated C3b can then bind covalently to nearby surfaces, including pathogens and host cells.

On self-surfaces, regulatory proteins like decay-accelerating factor (DAF) or complement receptor 1 (CR1) help to prevent the formation of the alternative pathway convertase and thus further activation of the complement system. However, on foreign surfaces, the C3b can recruit more complement components, forming a complex called the alternative pathway convertase (C3bBb), which cleaves additional C3 molecules into C3a and C3b.

The generated C3b can then bind to the surface and participate in the formation of the membrane attack complex (MAC), leading to the lysis of the target cell. The alternative pathway plays a crucial role in the defense against gram-negative bacteria, fungi, and parasites, as well as in the clearance of immune complexes and apoptotic cells. Dysregulation of the alternative complement pathway has been implicated in several diseases, including autoimmune disorders and atypical hemolytic uremic syndrome (aHUS).

Properdin is defined as a positive regulatory protein in the complement system, which is a part of the immune system. It plays a crucial role in the alternative pathway of complement activation. Properdin stabilizes the C3 convertase (C3bBb), preventing its decay and increasing the efficiency of the alternative pathway. This results in the production of the membrane attack complex, which leads to the lysis of foreign cells or pathogens. Deficiencies in properdin can lead to an increased susceptibility to bacterial infections.

A snake bite is a traumatic injury resulting from the puncture or laceration of skin by the fangs of a snake, often accompanied by envenomation. Envenomation occurs when the snake injects venom into the victim's body through its fangs. The severity and type of symptoms depend on various factors such as the species of snake, the amount of venom injected, the location of the bite, and the individual's sensitivity to the venom. Symptoms can range from localized pain, swelling, and redness to systemic effects like coagulopathy, neurotoxicity, or cardiotoxicity, which may lead to severe complications or even death if not treated promptly and appropriately.

A Complement Hemolytic Activity Assay is a laboratory test used to measure the functionality and activity level of the complement system, which is a part of the immune system. The complement system is a group of proteins that work together to help eliminate pathogens from the body.

The assay measures the ability of the complement system to lyse (break open) red blood cells. This is done by mixing the patient's serum (the liquid portion of the blood) with antibody-coated red blood cells and incubating them together. The complement proteins in the serum will then bind to the antibodies on the red blood cells and cause them to lyse.

The degree of hemolysis (red blood cell lysis) is directly proportional to the activity level of the complement system. By measuring the amount of hemolysis, the assay can determine whether the complement system is functioning properly and at what level of activity.

This test is often used to diagnose or monitor complement-mediated diseases such as autoimmune disorders, infections, and some types of cancer. It may also be used to evaluate the effectiveness of treatments that target the complement system.

Complement C3 Convertase, Alternative Pathway is a complex enzyme composed of the proteins C3b and Bb. It plays a crucial role in the alternative pathway of the complement system, which is a part of the innate immune system that helps to defend the body against invading pathogens.

The alternative pathway is continuously activated at a low level, and C3 Convertase is responsible for amplifying this activation. It does so by cleaving the complement component C3 into C3a and C3b. The C3b then binds to the surface of the pathogen and can form additional C3 Convertases, leading to a positive feedback loop that results in the rapid accumulation of complement components on the surface of the pathogen.

This accumulation of complement components helps to mark the pathogen for destruction by other immune cells, such as neutrophils and macrophages. Additionally, the cleavage products C3a and C5a generated during this process can act as anaphylatoxins, inducing inflammation and attracting more immune cells to the site of infection.

Regulation of Complement C3 Convertase is critical to prevent damage to host tissues. Several regulatory proteins, such as factor H and decay-accelerating factor (DAF), help to limit the formation and activity of C3 Convertase on host cells and tissues. Dysregulation of the complement system, including the alternative pathway and Complement C3 Convertase, has been implicated in a variety of diseases, including autoimmune disorders, inflammatory diseases, and infectious diseases.

I believe there may be some confusion in your question as "scorpions" are not a medical term, but instead refer to a type of arachnid. If you're asking about a medical condition that might involve scorpions, then perhaps you're referring to "scorpion stings."

Scorpion stings occur when a scorpion uses its venomous stinger to inject venom into another animal or human. The effects of a scorpion sting can vary greatly depending on the species of scorpion and the amount of venom injected, but generally, they can cause localized pain, swelling, and redness at the site of the sting. In more severe cases, symptoms such as numbness, difficulty breathing, muscle twitching, or convulsions may occur. Some species of scorpions have venom that can be life-threatening to humans, especially in children, the elderly, and those with compromised immune systems.

If you are looking for information on a specific medical condition or term, please provide more details so I can give you a more accurate answer.

The Arthus reaction is a type of localized immune complex-mediated hypersensitivity reaction (type III hypersensitivity). It is named after the French scientist Nicolas Maurice Arthus who first described it in 1903. The reaction occurs when an antigen is injected into the skin or tissues of a sensitized individual, leading to the formation of immune complexes composed of antigens and antibodies (usually IgG). These immune complexes deposit in the small blood vessels, causing complement activation, recruitment of inflammatory cells, and release of mediators that result in tissue damage.

Clinically, an Arthus reaction is characterized by localized signs of inflammation, such as redness, swelling, pain, and warmth at the site of antigen injection. In severe cases, it can lead to necrosis and sloughing of the skin. The Arthus reaction typically occurs within 2-8 hours after antigen exposure and is distinct from immediate hypersensitivity reactions (type I), which occur within minutes of antigen exposure.

The Arthus reaction is often seen in laboratory animals used for antibody production, where repeated injections of antigens can lead to sensitization and subsequent Arthus reactions. In humans, it can occur as a complication of immunizations or diagnostic tests that involve the injection of foreign proteins or drugs. To prevent Arthus reactions, healthcare providers may perform skin testing before administering certain medications or vaccines to assess for preexisting sensitization.

Trypanosoma lewisi is a species of protozoan parasites belonging to the family Trypanosomatidae. It is primarily found in rats and is transmitted through the bite of fleas. This parasite typically infects the erythrocytes (red blood cells) of rats, causing a benign infection known as "rat trypanosomiasis" or "lewisi disease."

In a medical context, Trypanosoma lewisi is not considered a significant pathogen for humans. However, rare cases of human infections have been reported, usually due to accidental laboratory exposure or through the consumption of contaminated water or food. In these instances, the infection typically resolves on its own without causing severe symptoms or complications.

It's worth noting that Trypanosoma lewisi is often used as a model organism in scientific research related to trypanosomatid biology and parasitology due to its relatively simple life cycle and ease of cultivation in the laboratory.

"Trimeresurus" is a genus of venomous pit vipers found primarily in Asia. Commonly known as "Asian pit vipers" or " temple pit vipers," these snakes are characterized by the presence of a heat-sensing pit organ between the eye and the nostril, which they use to detect the body heat of their prey. They are responsible for causing serious bites and occasionally fatal accidents in human beings.

It's important to note that "Trimeresurus" is a taxonomic term used in the field of biology, specifically in systematics and classification of organisms. It does not have a direct medical definition, but it refers to a group of snakes with medical significance due to their venomous nature.

Complement C3b is a protein fragment that plays a crucial role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. C3b is generated during the activation of the complement system, particularly via the classical, lectin, and alternative pathways.

Once formed, C3b can bind covalently to the surface of microbes or other target particles, marking them for destruction by other components of the immune system. Additionally, C3b can interact with other proteins in the complement system to generate the membrane attack complex (MAC), which forms pores in the membranes of targeted cells, leading to their lysis and removal.

In summary, Complement C3b is a vital protein fragment involved in the recognition, tagging, and elimination of pathogens and damaged cells during the immune response.

'Agkistrodon' is a genus of venomous snakes commonly known as pit vipers, found predominantly in North America and parts of Asia. This genus includes several species, among them the copperhead (A. contortrix), cottonmouth or water moccasin (A. piscivorus), and the cantil (A. bilineatus). These snakes are characterized by their triangular heads, heat-sensing pits between the eyes and nostrils, and elliptical pupils. They deliver venom through hollow fangs and can cause significant harm to humans if they bite.

It is important to note that 'Agkistrodon' species are often misidentified due to their similarities with other pit vipers. Accurate identification of a snakebite victim is crucial for proper medical treatment, so seeking professional help from herpetologists or medical professionals is highly recommended in such situations.

The Complement Membrane Attack Complex (MAC), also known as the Terminal Complement Complex (TCC), is a protein structure that forms in the final stages of the complement system's immune response. The complement system is a part of the innate immune system that helps to eliminate pathogens and damaged cells from the body.

The MAC is composed of several proteins, including C5b, C6, C7, C8, and multiple subunits of C9, which assemble on the surface of target cells. The formation of the MAC creates a pore-like structure in the cell membrane, leading to disruption of the membrane's integrity and ultimately causing cell lysis or damage.

The MAC plays an important role in the immune response by helping to eliminate pathogens that have evaded other immune defenses. However, uncontrolled activation of the complement system and formation of the MAC can also contribute to tissue damage and inflammation in various diseases, such as autoimmune disorders, age-related macular degeneration, and ischemia-reperfusion injury.

An antigen-antibody complex is a type of immune complex that forms when an antibody binds to a specific antigen. An antigen is any substance that triggers an immune response, while an antibody is a protein produced by the immune system to neutralize or destroy foreign substances like antigens.

When an antibody binds to an antigen, it forms a complex that can be either soluble or insoluble. Soluble complexes are formed when the antigen is small and can move freely through the bloodstream. Insoluble complexes, on the other hand, are formed when the antigen is too large to move freely, such as when it is part of a bacterium or virus.

The formation of antigen-antibody complexes plays an important role in the immune response. Once formed, these complexes can be recognized and cleared by other components of the immune system, such as phagocytes, which help to prevent further damage to the body. However, in some cases, the formation of large numbers of antigen-antibody complexes can lead to inflammation and tissue damage, contributing to the development of certain autoimmune diseases.

Complement C5a is a protein fragment that is generated during the activation of the complement system, which is a part of the immune system. The complement system helps to eliminate pathogens and damaged cells from the body by tagging them for destruction and attracting immune cells to the site of infection or injury.

C5a is formed when the fifth component of the complement system (C5) is cleaved into two smaller fragments, C5a and C5b, during the complement activation cascade. C5a is a potent pro-inflammatory mediator that can attract and activate various immune cells, such as neutrophils, monocytes, and eosinophils, to the site of infection or injury. It can also increase vascular permeability, promote the release of histamine, and induce the production of reactive oxygen species, all of which contribute to the inflammatory response.

However, excessive or uncontrolled activation of the complement system and generation of C5a can lead to tissue damage and inflammation, contributing to the pathogenesis of various diseases, such as sepsis, acute respiratory distress syndrome (ARDS), and autoimmune disorders. Therefore, targeting C5a or its receptors has been explored as a potential therapeutic strategy for these conditions.

Amphibian venoms are toxic secretions produced by certain species of amphibians, such as frogs, toads, and salamanders. These secretions are often produced by specialized glands in the skin and can contain a variety of bioactive compounds, including alkaloids, steroids, peptides, and proteins. Some amphibian venoms can cause painful burns or irritation upon contact with the skin, while others can be deadly if ingested or introduced into the bloodstream through wounds or mucous membranes.

The study of amphibian venoms has gained increasing attention in recent years due to their potential as sources of novel bioactive compounds with therapeutic applications. For example, some peptides found in amphibian venoms have been shown to have potent analgesic, anti-inflammatory, and antimicrobial properties, making them promising candidates for the development of new drugs.

It is important to note that not all amphibians produce venom, and even those that do may use their toxic secretions primarily for defense against predators rather than for hunting prey. Additionally, while some amphibian venoms can be dangerous or even lethal to humans, most cases of envenomation occur in the context of intentional handling or accidental contact with these animals in their natural habitats.

"The Crown - Cobra Speed Venom". Discogs. Retrieved 24 March 2021. "The Crown announces new album, 'Cobra Speed Venom'". Metal ... Cobra Speed Venom". Anti Hero Magazine. Ray Van Horn Jr. "The Crown "Cobra Speed Venom"". Blabbermouth.net. Retrieved 24 March ... Cobra Speed Venom' - Album Review". Rock 'N' Load. "Review: The Crown - Cobra Speed Venom". Toilet ov Hell. 16 March 2018. ... Cobra Speed Venom". Brave Words. Retrieved 24 March 2021. Morin, Max (14 March 2018). "The Crown - Cobra Speed Venom". Exclaim ...
"Wounded cobra's venom". The Times. 21 October 2002. Mamrud, Roberto (12 March 2020). "Darko Pančev - International Appearances ... The Italian press got down on the striker too, derisively modifying his Red Star moniker Il Cobra to Il Ramarro (green lizard ... "Bidoni calcio: Darko Pancev, da cobra a ramarro dell'Inter" (in German). Ecco dello Sport. 11 May 2010. Archived from the ... "Cobra" in patria, "Ramarro" in Italia: Bagnoli insegna (in Italian) (CS1 Macedonian-language sources (mk), CS1 Italian-language ...
"The Crown - Cobra Speed Venom". Discogs. 16 March 2018. Retrieved 16 March 2018. "THE CROWN Set March Release For Royal ... Cobra Speed Venom (2018) Royal Destroyer (2021) Forever Heaven Gone (1993) Forget the Light (1994) The Crown Invades Karlsruhe ... from their then-upcoming tenth studio album Cobra Speed Venom, on 12 January 2018. On that album, The Crown used a string ...
Venom makes an appearance of sorts. Venom's image appears and persists on the screen of the Brainwave Scanner as Billy, Cobra ... Venom had taken over. They sneak back into Cobra's base and place Billy in the scanner, confronting Venom in Billy's mind. ... When the Joes thwart the scheme, Venom pilots a HISS Tank that takes himself, Cobra Commander, and Destro to safety. Venom ... However, Venom had earlier used the plane's radio to transmit a message to Cobra in morse so he had a lawyer waiting for him at ...
Gaucher recommended treatment with cobra venom. Boinet, in 1913, tried increasing doses of bee stings (up to 4000). Scorpions ...
"Sullivan to put venom in Cobras". The Sun News-Pictorial. Melbourne, VIC. p. 73. The Age, "Losing with style", 6 May 2009, Paul ...
Unlike some other African cobras (for example, the red spitting cobra), this species does not spit venom. The Egyptian cobra ... The venom of the Egyptian cobra consists mainly of neurotoxins and cytotoxins. The average venom yield is 175 to 300 mg in a ... and because Egyptian cobra venom is slow-acting and does not always cause death. The Egyptian cobra garnered increased ... Venom potency ranged from 0.08 mg/kg to 1.7 mg/kg via intravenous injections on mice. The study also found that Egyptian cobra ...
Amanda Buivids (6 April 1989). "Sullivan to put venom in Cobras". The Sun News-Pictorial. Melbourne, VIC. p. 73. Caulfield ...
"Amino acid sequences of nerve growth factors derived from cobra venoms". FEBS Letters. 279 (1): 38-40. doi:10.1016/0014-5793(91 ... It has also been found in several snake venoms. In the peripheral and central neurons, neurotrophins are important regulators ... "Purification and amino-acid sequence of a nerve growth factor from the venom of Vipera russelli russelli". Biochimica et ...
Stanley Ho (24 March 2001). "Jaguars hope Bennett will cut out Cobras' venom". Today. p. 38. Stanley Ho (9 February 2002). " ...
COBRA fields six rugby teams: COBRA Blacks (1st XV) COBRA Stings (2nd XV) COBRA Development (Under 19s) COBRA Venom (Ladies) ... The COBRA Blacks, Stings & Development teams train every Tuesday and Friday. The COBRA Venom team trains every Wednesday & ... COBRA is the first rugby club in Malaysia with its OWN Clubhouse. COBRA is the home of 10-a-side rugby or better known as rugby ... Over the years COBRA has produced many outstanding rugby players at the national and state level. Members of COBRA are also ...
from the University of Edinburgh in 1904 with a thesis on the pharmacology of cobra venom. He was Hunterian Professor at the ... Elliot, Robert Henry (1904). "A contribution to the pharmacology of cobra venom". {{cite journal}}: Cite journal requires , ... On snakes, Professor Elliot declared that the cobra is timid and inoffensive, will not strike unless alarmed by a sudden ... Researches into the Nature and Action of Snake Venom, British Medical Journal, 1900, 1, 309 and 1146; 2, 217 Sclero-Corneal ...
Macht, D.I, Experimental and Clinical Study of Cobra Venom as an Analgesic Proc Natl Acad Sci U S A. 1936 January; 22(1): 61-71 ... Research into the pharmacological applications of cobra venom.[2] The term "psychopharmacology" (the branch of science ... In 1930, he reported it could be used to demonstrate the presence of snake venom and menotoxin (a toxin thought to be present ...
"Official Website of the Carolina Cobras: Venom Hunnies". "Arena football set to return to Greensboro Coliseum with Carolina ... The NAL Cobras use a logo similar in style to the defunct AFL Cobras' logo, but otherwise has no direct connection to the AFL ... The Cobras inaugural season finished with a regular season record of 10-5, taking second place in the league. The Cobras then ... Based in Greensboro, North Carolina, the Cobras play their home games at the Greensboro Coliseum Complex. The Cobras is the ...
King Cobra' Tate spitting venom over title clash". Luton on Sunday. May 6, 2012. Retrieved October 2, 2022. "La NUIT DES ... "Andrew Tate ("King Cobra") , MMA Fighter Page". Tapology. Archived from the original on October 3, 2022. Retrieved January 7, ... "Andrew Tate ("King Cobra") , MMA Fighter Page". Tapology. Archived from the original on October 3, 2022. Retrieved October 3, ... "Andrew 'King Cobra' Tate". Sherdog. Archived from the original on July 30, 2022. Retrieved July 11, 2022. "Andrew Tate : ...
The Cobra's Venom). Gebal Al Mout (جبال الموت) (The Mountains of Death). Zeaab Wa Demaa (ذئاب و دماء) (Wolves and Blood). ... The Empire of Venom). Al Khedaa Al Akheera (الخدعة الأخيرة) (The Last Ruse). Entiqam Al Akraab (انتقام العقرب) (The Revenge of ...
The Cobra robot shoots venom and laser beams. In two-player cooperative mode control of the G.I. Joe training game is split ... "Soft Spot: G.I. Joe Cobra Strike". Video Games. 1 (11): 68. August 1983. G.I. Joe: Cobra Strike at Atari Mania G.I. Joe: Cobra ... before changing his name to Cobra Commander and creating the Cobra Organization later in the series. In a 1983 review, Video ... G.I. Joe: Cobra Strike is a video game written by John Emerson for the Atari 2600 in 1983. The game was developed and published ...
JOHNSON M, KAYE MA, HEMS R, KREBS HA (1953). "Enzymic hydrolysis of adenosine phosphates by cobra venom". Biochem. J. 54 (4): ...
Berthé, R. A., De Pury, S., Bleckmann, H., & Westhoff, G. (2009). "Spitting cobras adjust their venom distribution to target ... Toxungen deployment offers a key evolutionary advantage compared to poisons and venoms. Poisons and venoms require direct ... Some Spitting cobras have modified their secretion so that the cardiotoxins are more injurious to eye membranes. Nelsen, D. R ... Ismail,M., Al-Bekairi, A.M., El-Bedaiwy, A.M. & Abd-El Salam,M. A. (1993). "The ocular effect of spitting cobras: II. Evidence ...
Spitting cobras accurately squirt venom from their fangs at the eyes of potential predators, striking their target eight times ... Mayell, Hillary (February 10, 2005). "Cobras Spit Venom at Eyes With Nearly Perfect Aim". National Geographic. O. Wilson, ... The functional morphology of venom spitting in cobras". Journal of Experimental Biology. 207 (20): 3483-3494. doi:10.1242/jeb. ...
... the King Cobra (Ophiophagus hannah). Ophanin is produced in the venom glands of the King Cobra (O. Hannah). Although the venom ... Ophanin is a toxin found in the venom of the King Cobra (Ophiophagus hannah), which lives throughout South East Asia. This ... Pung YF (2005). A novel protein from King Cobra (Ophiophagus hannah) venom (Ph.D. Thesis). Singapore: National University of ... Osipov AV, Levashov MY; Tsetlin VI (2005). "Cobra venom contains a pool of cysteine-rich secretory proteins". Biochemical and ...
... the Philippine cobra is considered to possess one of the more toxic venoms among the Naja (cobra) species. According to Tan et ... The Philippine cobra (Naja philippinensis) also called Philippine spitting cobra or northern Philippine cobra, is a stocky, ... gave an overall average venom yield per cobra per extraction of 0.33 ml (wet) or 70.1 mg (dried). The venom of the Philippine ... Salafranca, ES (1972). "Venom yields of the Philippine cobra, Naja naja philippinensis" (PDF). Zoologica. 57 (3): 127-134. ...
Osipov AV, Levashov MY, Tsetlin VI, Utkin YN (March 2005). "Cobra venom contains a pool of cysteine-rich secretory proteins". ... Among the four CRISPs isolated from the Monocled Cobra (Naja kaouthia) and the three from the Egyptian Cobra (Naja haje), ion ... These venoms are toxic due to their blocking of calcium channels and also because they reduce potassium-induced smooth muscle ... One of the N. haje CRISPs was the first example of an acidic CRISP in reptilian venom. The selective ion channel activity of ...
α-Cobratoxin is a substance of the venom of certain Naja cobras. It is a nicotinic acetylcholine receptor (nAChR) antagonist ... including the Thailand cobra, the Indo-Chinese spitting cobra (Naja siamensis) and the Chinese cobra (Naja atra). The cobras ... It appears to be that cobra venoms such as cobratoxin have an 'antiviral, immunomodulatory and a neuromodulatory activity'. ... The venom, produced by these snakes, is a mixture of proteins, carbohydrates, and other substances. The venom is only used when ...
Vogel CW, Müller-Eberhard HJ (1982). "The Cobra Venom Factor-dependentC 3 Convertase of Human Complement". J Biol Chem. 257 (14 ... Two fluid phase C5 convertases have been described: the classical pathway enzyme, C4b2boxy3b and the cobra venom factor- ...
"THE CROWN To Release 'Cobra Speed Venom' Album In March; 'Iron Crown' Video Available". Blabbermouth.net. January 8, 2018. ... "VENOM Reveal Cover Artwork And Track Listing For New Studio Album 'Storm The Gates'". Metal Forces. November 1, 2018. Retrieved ...
Cobra venom also contains hemotoxins which clot or solidify blood. Most members are venomous to varying extents, and some are ... The venom of spitting cobras is more cytotoxic rather than neurotoxic. It damages local cells, especially those in eyes, which ... Cobras, mambas, and taipans are mid- to large sized snakes which can reach 2 m (6 ft 7 in) or above. The king cobra is the ... Large species, mambas and cobras included, are dangerous for their capability of injecting high quantities of venom upon single ...
... (RNase V1) is a ribonuclease enzyme found in the venom of the Caspian cobra (Naja oxiana). It cleaves double- ... Lowman HB, Draper DE (April 1986). "On the recognition of helical RNA by cobra venom V1 nuclease". The Journal of Biological ... "Mapping tRNA structure in solution using double-strand-specific ribonuclease V1 from cobra venom". Nucleic Acids Research. 9 ( ... aminoacyl-tRNA synthetase complexes with cobra venom ribonuclease". Biochemistry. 20 (4): 1006-11. doi:10.1021/bi00507a055. ...
The venom also consists of cardiotoxins and cytotoxins. Although the venom of the Equatorial spitting cobra (N. sumatrana) ... golden spitting cobra, Sumatran spitting cobra, or Palawan spitting cobra, is a species of spitting cobra found in Southeast ... protein composition of the Equatorial spitting cobra venom is distinct from venoms of the other two sympatric spitting cobras, ... The Equatorial spitting cobra (Naja sumatrana) also called the black spitting cobra, Malayan spitting cobra, ...
Teshima K, Ikeda K, Hamaguchi K, Hayashi K (July 1983). "Bindings of cobra venom phospholipases A2 to micelles of n- ... particularly in terms of their binding affinity with cobra venom. In 1987 the phospholipids were found to be potent toxins on ...
"The Crown - Cobra Speed Venom". Discogs. Retrieved 24 March 2021. "The Crown announces new album, Cobra Speed Venom". Metal ... Cobra Speed Venom". Anti Hero Magazine. Ray Van Horn Jr. "The Crown "Cobra Speed Venom"". Blabbermouth.net. Retrieved 24 March ... Cobra Speed Venom - Album Review". Rock N Load. "Review: The Crown - Cobra Speed Venom". Toilet ov Hell. 16 March 2018. ... Cobra Speed Venom". Brave Words. Retrieved 24 March 2021. Morin, Max (14 March 2018). "The Crown - Cobra Speed Venom". Exclaim ...
When taunted, the cobras Santra and Wüster filmed all spat more downward than forward, with the venom exiting the fangs at a ... Spitting cobras stand out from many of their relatives in the family Elapidae because they possess venoms that are highly ... Spit Take: Surprise! Indian Monocled Cobras Can Spit Venom. Science SushiBy Christie WilcoxJun 29, 2017 10:13 AM ... Some spitting cobras can launch their venoms more than six feet, and aim for sensitive areas like eyeballs. ...
ICD-10 code T63.041S for Toxic effect of cobra venom, accidental (unintentional), sequela is a medical classification as listed ... Toxic effect of cobra venom, accidental (unintentional), sequela T63. Includes: bite or touch of venomous animal. pricked or ... ICD-10-CM Code for Toxic effect of cobra venom, accidental (unintentional), sequela T63.041S ICD-10 code T63.041S for Toxic ... effect of cobra venom, accidental (unintentional), sequela is a medical classification as listed by WHO under the range - ...
Cobra, Cobra N+, Cobra Tuning & Lifestyle, GT-R, High resolution, images, Nissan GT-R, R35, wallpapers ... The rear is upgraded with a new COBRA N+ rear apron with integrated diffuser, and a larger COBRA N+ rear airfoil. The COBRA N+ ... For customizing the interior COBRA N+ offers two different options. Nissan GT-R owners can choose from a luxurious COBRA N+ ... The development of an extensive tuning program at COBRA N+, the division of Cobra Technology & Lifestyle (Alleestrasse 15-19, D ...
... he spits venom like the cobras on Noahs Ark and farts brimstone. ...
Check out the Cobra Venom community on Discord - hang out with 94 other members and enjoy free voice and text chat. ...
"We tested how venom components affected pain-sensing nerves and showed thatspitting cobra venoms are more effective at causing ... made the discovery by studying the composition of spitting cobra venoms fromthree groups of snakes - Asian spitting cobras, ... Venom from spitting cobras has evolved to cause predators extreme pain as aform of self-defence, rather than for capturing prey ... "The fangs of these snakes are adapted to spray venom as far as 2.5 metres -the venom is aimed directly at the face, ...
This Cobra like many others in South Africa is a replica and has its base with the Company called Venom cars. Much like KKC ... Cobra running a Jag suspension with its major difference in the Chassis of the vehicle and then the red colour of this car ... looking to be a boy racer out of The Fast and Furious or just a guy with a very cool car that turns heads then this Red Cobra ...
Includes the unmatched Venom flight case and accessories. Shop the replacement lenses here INCLUDES: COBRA PRO Sunglasses Venom ... Hard Case Includes polish cloth and accessories Fast and free shipping from sunny Arizona, USA Venom Limited Lifetime Wa ... The Venom Cobra sunglasses. Built tough to last a lifetime, guaranteed. ... The Venom Cobra sunglasses. Built tough to last a lifetime, guaranteed. Includes the unmatched Venom flight case and ...
stratfordvolleyballclub.com powered by MBSportsWeb
Handmade Motiv Venom Cobra Bowling Jersey. Free worldwide shipping and one of the fastest turnaround in the business. ... Motiv Venom Cobra Bowling Jersey by Motiv Bowling. This is a limited version of the oversea bowling ball from Motiv Bowling. ... Be the first to review "Motiv Venom Cobra Bowling Jersey". Your email address will not be published. Required fields are marked ...
Updated with the new Cobra Core, its now even better. More support means better roll speed, more even wear, and super crisp ... The 72mm Cannibal made Venom wheels a household name with its winning combination of durability, grip, and smooth controllable ... Cobra Core Features:. -Fiberglass Reinforced. -12x Stiffer. -39mm Tall 43mm Wide. -No Flex Zone (Patent Pending) ... Updated with the new Cobra Core, its now even better. More support means better roll speed, more even wear, and super crisp ...
Жалобы и Venom by Cobra Trading отзывы клиентов о разводе и махинациях в торговых операциях. ... "Что не так с Venom by Cobra Trading? ... Venom by Cobra Trading Venom by Cobra Trading: Отзывы Трейдеров ... Venom by Cobra Trading рассчитан на новичков, которые проверять информацию не будут. Брокер выманивает все денежные средства у ... Компания Venom by Cobra Trading приглашает к сотрудничеству, акцентируя внимание на нескольких важных достоинствах:. *Команда ...
venom of cobras within him.. 15 "He swallows riches,. But will vomit them up;. God will expel them from his belly.. ... his food will turn rancid in his stomach it will become a cobras poison inside him. ... his food is turned sour in his stomach; it becomes the venom of serpents within him. ... in his bowels his food is turned, [the] venom of horned vipers [is] {within him}. ...
Home / Products tagged "Where to buy king cobra venom ...
The Harlot HITP wheels by Venom are meant for slashing and sliding around, but are suitable for low speed freeriding, carving ...
Decrease quantity for ZCMU0017 - CX50 CLUTCH COVER GASKET - VENOM Increase quantity for ZCMU0017 - CX50 CLUTCH COVER GASKET - ...
Where to buy king cobra venom Online. Home / Products tagged "Where to buy king cobra venom Online" ...
Venom-injecting fangs evolved independently in vipers and cobras. Kings College London biologists shed new light on the ... Venom-injecting fangs evolved independently in vipers and cobras. Kings College London biologists shed new light on the ...
Venom Cobra 43919 with Automatic movement. - Shop the biggest Invicta collection in Europe! - Fast Shipping! ... Invicta Reserve - Venom Cobra 43919 Mens Automatic Watch - 54mm. In stock Order before 15.00 CET, Shipped today ...
These brand new Venom wheels are built to last! Measuring 76mm in diameter and 78a in hardness, they pack a super smooth ride. ... Venom Cobra Core Cannibal White / Red Skateboard Wheels - 76mm 78a (Set of 4) Love to cruise? ... Venom Cobra Core Cannibal White / Red Skateboard Wheels - 78a are sold in (1) set of four (4) wheels. ... Venom Cobra Core Cannibal White / Red Skateboard Wheels - 76mm 78a (Set of 4) ...
Home 1 › KING COBRA GLOSSY POSTER PICTURE PHOTO snakes venom dangerous plane india 2 746 @media screen and (min-width: 750px ... KING COBRA GLOSSY POSTER PICTURE PHOTO snakes venom dangerous plane india. Regular price $11.99 ...
While king cobras are highly venomous, mongoose has evolved to be resistant to their venom, making them a formidable opponent. ... 5 Time King Cobra Pays With His Life When Spits Venom On Mongoose. ... The quick reflexes and agility of the mongoose, combined with their immunity to the snakes venom, make them a natural predator ... Its fascinating to see the interplay between different species in the animal kingdom, and the encounter between a king cobra ...
Did you know that some algae can be more deadly than cobra venom?. Posted at 13:42h in Cyanobacteria by Ipanema2020 ... Did you know that some algae can be more deadly than cobra venom?. 25 February, 2020 ... we will tell you that some cyanotoxins produced by these algae are known to be more toxic than the deadly cobra poison! ...
... artículo original ... The monocled cobra (Naja kaouthia) is among the most feared snakes in Southeast Asia due to its toxicity, which is ... This study is the first to demonstrate neutralization of whole snake venom by a single recombinant monoclonal antibody, thus ... The optimized antibody prevented lethality when incubated with N. kaouthia whole venom prior to intravenous injection. ...
Purification and characterization of a myotoxic phospholipase-a2 from indian cobra (Naja-Naja-Naja) venom ... Purification and characterization of a myotoxic phospholipase A2 from Indian cobra (Naja naja naja) venom. Toxicon27, 861-873, ... The ld50 value (i.p.) of NN-XIII-PLA2 is 2.4 mg/kg body weight (whole venoms ld50 is 2.8 mg/kg body weight). It induces ... Bhat, M. K. and Gowda, T. V. (1989) Purification and characterization of a myotoxic phospholipase-a2 from indian cobra (Naja- ...
This study describes the structural characterization of a totally new family of peptides from the venom of the snake green ... The glycosylated cytotoxin, discovered in the venom of the Tai cobra Naja kaouthia, weighs around 9-10 kDa instead of 7 kDa due ... Soares, S.G., Oliveira, L.L.: Venom-Sweet-Venom: N-Linked Glycosylation in Snake Venom Toxins. Protein Pept. Lett. 16(8), 913- ... Cytotoxin from the Naja kaouthia Cobra Venom. Eur. J. Biochem. 271(10), 2018-2027 (2004) ...
Cobra Speed Venom. *. *. *. *. *. *. 2. Year:. 2018. Tracks:. 13. Bitrate:. 320 kbps. $1.82Buy ...
Cobra Sport brings four decades of innovative design and unparalleled manufacturing expertise to their range of performance ... Cobra Cat Back System (Venom Range - Note Very Loud) VW Scirocco R 2.0 TSI 09-18 quantity. ... Home / Exhausts / Exhaust Systems / Cobra Cat Back System (Venom Range - Note Very Loud) VW Scirocco R 2.0 TSI 09-18. ... Cobra Cat Back System (Venom Range - Note Very Loud) VW Scirocco R 2.0 TSI 09-18. ...
... from cobra venom. Home / Uncategorized / We showed recently that nerve development element (NGF) from cobra venom ... We showed recently that nerve development element (NGF) from cobra venom. June 27, 2019. mycareerpeer0 comments ... We showed recently that nerve development element (NGF) from cobra venom inhibited the development of Ehrlich ascites carcinoma ...
  • There are fourteen species of spitting cobras in the genus Naja -seven from Africa, and seven from Asia. (discovermagazine.com)
  • A major phospholipase A2 (NN-XIII-PLA2) which constitutes 20% of the whole Naja naja naja venom was purified to homogeneity on CM-Sephadex C-25 column chromatography. (uni-mysore.ac.in)
  • The monocled cobra (Naja kaouthia) is among the most feared snakes in Southeast Asia due to its toxicity, which is predominantly derived from long-chain α-neurotoxins. (ucr.ac.cr)
  • Spitting cobras stand out from many of their relatives in the family Elapidae because they possess venoms that are highly cytotoxic-which destroy tissues-rather than the paralysis-inducing neurotoxic venoms found in other elapids. (discovermagazine.com)
  • Treatment for a snake bite is defined according to whether the venom is cytotoxic, haemotoxic or neurotoxic and the wrong treatment will not only be of little or no help but could even be dangerous. (rentokil.co.uk)
  • Immobilise the limb but do NOT restrict blood flow unless you are certain the bite was from a snake that delivers neurotoxic venom. (rentokil.co.uk)
  • The neurotoxic effects of cobra venom are reversible, though motor recovery may take up to 7 days - and as many as 10 weeks. (medscape.com)
  • Venom of these snakes contains primarily neurotoxic components, which cause a presynaptic neuromuscular blockade, potentially causing respiratory paralysis. (msdmanuals.com)
  • Santra and his colleague, Wolfgang Wüster from Bangor University, not only tell the story of this initial spitting individual, they also document other known cases and the mechanics of monocled cobra spitting. (discovermagazine.com)
  • The pair and their colleagues have witnessed spitting in approximately 120 to 130 adult monocled cobras from the Hooghly, Burdwan, and Nadia districts-the overwhelming majority of the monocled cobras they've caught there-as well as in animals from the Bishnupur and Imphal West districts in Manipur State and the State of Arunachal Pradesh in northeastern India. (discovermagazine.com)
  • When taunted, the cobras Santra and Wüster filmed all spat more downward than forward, with the venom exiting the fangs at a more acute angle than seen in African spitting species. (discovermagazine.com)
  • Venom from spitting cobras has evolved to cause predators extreme pain as aform of self-defence, rather than for capturing prey, according to newresearch. (gemepet.com)
  • An international team including scientists from The University of Queensland,made the discovery by studying the composition of spitting cobra venoms fromthree groups of snakes - Asian spitting cobras, African spitting cobras andrinkhals. (gemepet.com)
  • We tested how venom components affected pain-sensing nerves and showed thatspitting cobra venoms are more effective at causing pain than their non-spitting counterparts," she said. (gemepet.com)
  • The three different groups of venom-spitting snakes had increased productionof an enzyme toxin, phospholipase-A2, which works cooperatively with othervenom toxins to maximise pain. (gemepet.com)
  • Lead author Professor Nick Casewell from the Liverpool School of TropicalMedicine said venom spitting was ideally suited to deterring attacks fromhumans. (gemepet.com)
  • Coagulopathy is not an expected feature of bites by most cobras, though prolonged bleeding and failure of clot retraction have been reported following bites by African spitting cobras and anticoagulant proteins have been identified in the venom of the African ringhals ( Hemachatus haemachatus ). (medscape.com)
  • Spitting cobras don't really spit venom. (sott.net)
  • Scientists have long known that spitting cobras don't actually spit. (sott.net)
  • It is the venom of vipers within him. (knowing-jesus.com)
  • Pit Vipers, such as rattlesnakes, copperheads, and water moccasins have slit-like pupils, triangular heads (due to venom pouches), and a pit located between the eyes and nostrils). (cdc.gov)
  • The complex venom of most North American pit vipers has local effects as well as systemic effects such as coagulopathy. (msdmanuals.com)
  • The venom of most North American pit vipers causes very minor changes in neuromuscular conduction, except for Mojave and eastern diamondback rattlesnake venom, which may cause serious neurologic deficits. (msdmanuals.com)
  • As a general rule-of-thumb, elapidae venom causes neuromuscular deficits - mainly flaccid paralysis - while viperidae venom focuses on local effects, including tissue necrosis, rhabdomyolysis, coagulopathy, and bleeding. (medscape.com)
  • Monocled cobras, which can reach lengths of about 5 feet, are highly venomous animals, so Santra knew to avoid a quick strike. (discovermagazine.com)
  • While king cobras are highly venomous, mongoose has evolved to be resistant to their venom, making them a formidable opponent. (newstoday17.com)
  • If no symptoms have occurred within half an hour of the bite then indications would be that it was not a venomous snake, it failed to inject any venom or the snake was very old and had little or no venom left. (rentokil.co.uk)
  • All the venomous species have a venom gland that synthesizes, stores and secretes a complex mixture of biological molecules including proteins. (nature.com)
  • The signs and symptoms that develop from venomous snakebites may vary in severity based on the type and amount of venom injected. (cdc.gov)
  • The fangs of these snakes are adapted to spray venom as far as 2.5 metres -the venom is aimed directly at the face, specifically the eyes, causingintense pain and can lead to the loss of eyesight," Dr Robinson said. (gemepet.com)
  • Professor Vetter said the snakes had independently evolved the ability to spittheir venoms at enemies. (gemepet.com)
  • Recounting his near-death experience after being bitten by one of these majestic yet deadly snakes, conservationist and TED Fellow Gowri Shankar shares the epiphany he had when the antivenom failed: there's more than one unique species of king cobra. (ted.com)
  • This documentary on NatGeo Wild and Smithsonian channels showcases the life and breeding biology of king cobras, along with the reverence for these snakes by the people of Malnad (Agumbe, Karnatka, India). (ted.com)
  • SVEVs isolated from lyophilized venoms collected from four different species of snakes ( Agkistrodon contortrix contortrix , Crotalus atrox , Crotalus viridis and Crotalus cerberus oreganus ) were analyzed by mass spectrometry-based proteomic, which allowed the identification of proteins belonging to eight main functional protein classes such as SVMPs, serine proteinases, PLA 2 , LAAO, 5′nucleotidase, C-type lectin, CRISP and Disintegrin. (nature.com)
  • Proteins constitute almost 95% of snake venom's dry weight and are produced and released by venom glands in a solubilized form during a snake bite. (nature.com)
  • This study shows that proteins can be secreted and confined in snake venom extracellular vesicles (SVEVs) presenting a size distribution between 50 nm and 500 nm. (nature.com)
  • In addition, the molecular function of some of the described proteins suggests a central role for SVEVs in the cytotoxicity of the snake venom and sheds new light in the envenomation process. (nature.com)
  • Snake venoms are complex substances, chiefly proteins, with enzymatic activity. (msdmanuals.com)
  • Rather, muscle contractions squeeze the cobra's venom gland, forcing venom to stream out of the snake's fangs, explains Bruce Young, a researcher at the University of Massachusetts. (sott.net)
  • But feats like that require special adaptations to the fangs and head, which monocled cobras do not possess. (discovermagazine.com)
  • But the animal didn't lunge-instead, from over a foot away, the serpent spat at Santra's face, getting a small amount of venom into his eye. (discovermagazine.com)
  • Toxins with hemorrhagic and myonecrotic activity are generally found in the venoms of the Viperidae family due to synergic action of proteolytic enzymes, such as metalloproteinases and serine proteinases 4 . (nature.com)
  • The muscles can produce enough pressure to spray venom up to six feet (nearly 2 meters). (sott.net)
  • This enzyme has low enzymatic activity but is more toxic to mice than the whole venom. (uni-mysore.ac.in)
  • The optimized antibody prevented lethality when incubated with N. kaouthia whole venom prior to intravenous injection. (ucr.ac.cr)
  • Regarding only snake venoms, several high mass enzymes have been found to be glycosylated. (springer.com)
  • Although enzymes play an important role, the lethal properties of venom are caused by certain smaller polypeptides. (msdmanuals.com)
  • To help you to understand this problem, we will tell you that some cyanotoxins produced by these algae are known to be more toxic than the deadly cobra poison! (ipanema2020.com)
  • Most venom components appear to bind to multiple physiologic receptors, and attempts to classify venom as toxic to a specific system (eg, neurotoxin, hemotoxin, cardiotoxin, myotoxin) are misleading and can lead to errors in clinical judgment. (msdmanuals.com)
  • Pain-causing toxins from animal venoms can be useful tools to help usunderstand pain signalling at a molecular level, and are helping us toidentify new targets for future painkillers," Dr Robinson said. (gemepet.com)
  • Animal venoms represent a very large group of bioactive peptide toxins. (springer.com)
  • The quick reflexes and agility of the mongoose, combined with their immunity to the snake's venom, make them a natural predator of the king cobra. (newstoday17.com)
  • The definitive therapy for cobra envenomation is antivenom administration. (medscape.com)
  • 2. The manufacturer of the product must submit the specified number of antivenom product samples from at least two (2) batch lots of the product to WHO, along with the specified quantities of each of the immunizing venoms used to manufacture the antivenom. (who.int)
  • In vitro discovery of a human monoclonal antibody that neutralizes lethality of cobra snake venom. (ucr.ac.cr)
  • The lethality of the venom itself varies significantly - depending on the species, age of the individual snake, suspected seasonal variation in venom composition, route of enoculation (intravenous, intradermal, subcutaneous, etc), and many more factors. (medscape.com)
  • Cobra Speed Venom is the tenth studio album by Swedish melodic death metal band The Crown. (wikipedia.org)
  • On March 16th Metal Blade will release Cobra Speed Venom , the tenth album by Swedish stalwarts The Crown . (nocleansinging.com)
  • It's fascinating to see the interplay between different species in the animal kingdom, and the encounter between a king cobra and a mongoose is a classic example. (newstoday17.com)
  • Gowri Shankar educates Indians on the importance of the king cobra, a feared, maligned and now threatened reptile species. (ted.com)
  • This paper announces the discovery of four species of king cobras - against the one species, as believed for the last 185 years. (ted.com)
  • Intriguingly, while Santra and Wüster have shown that monocled cobras from eastern India readily spit when threatened, populations in places like Thailand do not seem to. (discovermagazine.com)
  • This documentary on National Geographic showcases the first-ever radio telemetry study done on a king cobra in India. (ted.com)
  • This paper talks about the deleterious effects of long-distance translocation of king cobras and highlight the scale of snake translocation problem in India. (ted.com)
  • This paper investigates people's perceptions toward king cobras in the tropical rainforests of the Western Ghats eco-region of southern India. (ted.com)
  • The Crown announced that their album Cobra Speed Venom would be released in January 2018. (wikipedia.org)
  • Nissan GT-R owners can choose from a luxurious COBRA N+ interior with specially sewn upholstery for seats and doors, made from a high-quality combination of leather and Alcantara, and a COBRA N+ racing cockpit with ultra-light carbon-fiber racing seats, six-point seatbelts and roll cage. (ausmotive.com)
  • Single intraperitoneal administration of high doses of cobra poison (50-150 microng/kg) decreased the incorporation of 14C-thimidine into DNA 1.2-1.9-fold. (msk.ru)
  • Microdoses of cobra poison caused a distinct increase in weight of experimental mice. (msk.ru)
  • If Venom is spat in to a person's eyes use any liquid available, preferably a neutral one such as water or milk - but anything at all will do, to flush out the eye. (rentokil.co.uk)
  • Cobra envenomation is an extremely variable process. (medscape.com)
  • Austriancharts.at - The Crown - Cobra Speed Venom" (in German). (wikipedia.org)
  • Cut the bite or attempt to suck the venom out. (rentokil.co.uk)
  • Reports of death within 1 hour of cobra bite exist, but a timeframe of 2-6 hours is more typical of fatal cases. (medscape.com)
  • A king cobra has enough venom to kill 10 people in a single bite. (ted.com)
  • Three-piece, extremely lightweight 21-inch COBRA N+ light-alloy wheels are slated to fill out the space beneath the wheel arches perfectly. (ausmotive.com)
  • When C5a was generated in vivo by infusion of purified cobra venom factor (CVF), thymocyte apoptosis was significantly increased. (jci.org)
  • The 72mm Cannibal made Venom wheels a household name with its winning combination of durability, grip, and smooth controllable slides. (thisskateshop.com)
  • COBRA N+ also adds further sporty character to suspension, wheels and brakes of the new top-of-the-line model from the Japanese carmaker. (ausmotive.com)
  • The Harlot HITP wheels by Venom are meant for slashing and sliding around, but are suitable for low speed freeriding, carving and cruising as well. (skatepro.ee)
  • These brand new Venom wheels are built to last! (bethesdaboards.com)
  • lys) when in complex with C3b or with cobra venom factor (CVF). (lu.se)
  • Did you know that some algae can be more deadly than cobra venom? (ipanema2020.com)
  • A COBRA N+ coil-over suspension gives the sports car even better handling. (ausmotive.com)
  • Much like KKC Cobra running a Jag suspension with its major difference in the Chassis of the vehicle and then the red colour of this car isn't paintwork but a pigment in the Gelcoat of the Fibreglass, and then there is the large roll over hope that it is different to other cars and an added safety feature. (creativerides.co.za)
  • Chronic medical conditions, medications, and age may increase sensitivity to the effects of venom and worsen outcomes [Spyres et al. (cdc.gov)
  • Also under development is a free-flow COBRA N+ stainless-steel high-performance exhaust system with metal catalysts. (ausmotive.com)
  • Despite this high burden, snake antivenoms are often unavailable to those in need, hampering effective treatment, and when they are, they may have been prepared from poor quality snake venoms that are not regionally representative, or have been poorly designed and manufactured and have limited efficacy. (who.int)
  • This study describes the structural characterization of a totally new family of peptides from the venom of the snake green mamba ( Dendroaspis angusticeps) . (springer.com)
  • movement will increase blood flow and transport the venom to the heart much faster. (rentokil.co.uk)
  • Plans exist for a COBRA N+ RACE PERFORMANCE engine version with 620 hp / 456.3 kW and a peak torque of approximately 800 Nm. (ausmotive.com)
  • Among the first of its kind, this book offers insights into the natural history of king cobras. (ted.com)
  • The COBRA N+ tuning program for the Nissan GT-R will be available for the car's European market launch in the spring of 2009. (ausmotive.com)
  • This paper investigates the capture and relocation of 106 king cobras ( Ophiophagus hannah ) from human settlements. (ted.com)
  • U.S. Marine Corps UH-1Y Venoms and AH-1Z Cobras conduct Aerial Gunnery Range. (military.com)