Cobra Venoms
Venoms
Elapidae
Cobra Cardiotoxin Proteins
Crotalid Venoms
Bee Venoms
Complement System Proteins
Snake Venoms
Cobra Neurotoxin Proteins
Viper Venoms
Wasp Venoms
Complement Inactivator Proteins
Complement C3
Elapid Venoms
Spider Venoms
Complement Activation
Complement Inactivating Agents
Scorpion Venoms
Arthropod Venoms
Complement C5
Phospholipases
Complement Factor D
Hemolysis
Bothrops
Complement C3-C5 Convertases
Phospholipases A2
Complement Factor B
Fish Venoms
Ant Venoms
Phospholipases A
Mollusk Venoms
Complement Pathway, Alternative
Properdin
Snake Bites
Complement Hemolytic Activity Assay
Complement C3 Convertase, Alternative Pathway
Scorpions
Arthus Reaction
Trypanosoma lewisi
Trimeresurus
Complement C3b
Agkistrodon
Complement Membrane Attack Complex
Antigen-Antibody Complex
Complement C5a
Amphibian Venoms
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)There are two main types of hemolysis:
1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.
Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.
Some common causes of hemolysis include:
1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.
Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.
The venom from snake bites contains a variety of toxins that can affect different parts of the body, including the cardiovascular, nervous, and muscular systems. Some common symptoms of snake bites include:
* Pain and swelling at the bite site
* Blurred vision or difficulty seeing
* Slurred speech or difficulty speaking
* Weakness, numbness, or tingling in the face, arms, or legs
* Seizures or convulsions
* Difficulty breathing or swallowing
* Rapid heartbeat or slow heart rate
* Low blood pressure or high blood pressure
* Nausea and vomiting
In severe cases, snake bites can cause respiratory failure, cardiac arrest, and other life-threatening complications.
The diagnosis of a snake bite is typically made based on the symptoms and medical history of the patient. In some cases, imaging tests like X-rays or CT scans may be ordered to confirm the presence of venom in the body.
Treatment for snake bites usually involves administering antivenin (also known as antivenom) to neutralize the venom and manage symptoms. Antivenin is a type of medicine that contains antibodies specifically designed to counteract the effects of snake venom. In severe cases, patients may require hospitalization and intensive care to monitor and treat any complications.
Prevention is key in avoiding snake bites, and this includes avoiding areas where snakes are known to live, wearing protective clothing and footwear when in these areas, and using repellents or other deterrents to discourage snakes from approaching. Education and awareness about snake behavior and safety measures can also help reduce the risk of snake bites.
The Arthus reaction is named after French physician Louis-Jean-Baptiste Arthus, who first described the phenomenon in 1890. It is commonly seen in conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and other autoimmune disorders.
The reaction occurs when antibodies bind to antigens, such as proteins or cells, on the surface of tissues. The binding of antibodies to antigens can activate complement proteins, which are a group of proteins that work together to destroy pathogens. In the case of the Arthus reaction, the activation of complement proteins leads to the formation of a membrane attack complex (MAC), which is composed of various proteins and can cause damage to tissues.
The Arthus reaction can cause a range of symptoms, including joint pain, swelling, and warmth, as well as fever and fatigue. In severe cases, it can lead to permanent joint damage and disability. Treatment options for the Arthus reaction include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive medications.
In summary, the Arthus reaction is an allergic response that occurs when antibodies bind to antigens and form immune complexes, leading to inflammation and tissue damage. It is commonly seen in autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis, and can cause a range of symptoms including joint pain and swelling, fever, and fatigue. Treatment options include NSAIDs, corticosteroids, and immunosuppressive medications.
Cobra Speed Venom
The Crown (band)
Darko Pančev
COBRA Rugby Club of Malaysia
Carolina Cobras (NAL)
G.I. Joe: Cobra Strike
Robert Elliot (surgeon)
David Macht
Ragol Al Mostaheel
ATP diphosphatase
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History of leprosy
Egyptian cobra
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Caulfield Football Club
C5-convertase
2018 in heavy metal music
Mad Cobra
Miltefosine
Neurotrophin
Paederinae
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Cult of the Cobra
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Kaa
Toxungen
Anti-predator adaptation
LNTX-1
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Toxin
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Kamakura (G.I. Joe)
Momordica foetida
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Five Deadly Venoms
Borikenophis portoricensis
B.A.T. (G.I. Joe)
Samar cobra
M2 Browning
Ophanin
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Ace (G.I. Joe)
Cobra (G.I. Joe)
Marine Aircraft Group 39
Rediocides A and G as potential antitoxins against cobra venom - PubMed
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In vitro discovery of a human monoclonal antibody that neutralizes lethality of cobra snake venom.
Ocular toxicity associated with indirect exposure to African spitting cobra venom. | Read by QxMD
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Cobra Envenomation Treatment & Management: Prehospital Care, Emergency Department Care, Inpatient Care
Snake19
- Snake venom injected into a horse causes the animal to create antibodies. (nofakenews.net)
- The antibodies are collected and used as an antidote for snake venom in humans. (nofakenews.net)
- Dr. Ardis believes the drug Remdesivir is snake venom and was purposely used to mitigate the disease so that even more people would perish. (nofakenews.net)
- Ardis also believes that the mRNA bioweapons create the protein structures of the synthetic snake venom and that these proteins cause a cytokine storm in humans that leads to complications and deaths. (nofakenews.net)
- The fact-checking police are full force calling Ardis a quack and the snake venom theory nonsense. (nofakenews.net)
- Suramin not only inhibits thrombin itself ( 71 ), but also the thrombin-like proteases of snake venom ( 72 ) and was therefore proposed as an antidote for snakebite. (nofakenews.net)
- Again, suramin inhibits mammalian phospholipase A2 ( 73 ), as well as the orthologues from snake venom ( 74 , - 76 ) and bee venom ( 77 ), suggesting that it can act as an antidote. (nofakenews.net)
- In vitro discovery of a human monoclonal antibody that neutralizes lethality of cobra snake venom. (ucr.ac.cr)
- Natural News ) Dr. Bryan Ardis has been making waves this week with allegations that the covid-19 virus, covid "vaccines" and at least one covid treatment all originated from snake venom molecules (the King Cobra, to be specific). (jerrywdavis.com)
- In the video, Bryan Ardis expresses concern that snake venom-related molecules (peptides or proteins) could have been dripped into the water supply (or released via other methods such as aerosolization) in order to create a covid-19 "outbreak" fear scenario that ultimately drove people into covid vaccines, lockdowns, mask mandates and other forms of mass medical hysteria. (jerrywdavis.com)
- In a largely unedited interview, Dr. Ardis shared with us his extensive research linking snake venom to antibodies, vaccine production, and eerily similar side effects observed from mRNA vaccines and covid treatments. (jerrywdavis.com)
- To anybody who doesn't yet realize that snake venom is routinely used to develop pharmaceuticals and medical interventions, check out today's announcement from a company actually called, "VenomTech. (jerrywdavis.com)
- Dr. Ardis believes that cobra venom was used as the starting point for gain-of-function augmentation of SARS-CoV-2, effectively transforming the virus into a venom-like payload delivery system that poisons the body much like a snake bite. (jerrywdavis.com)
- Watch As Snake Handler Does Venom Extraction On A King Cobra. (greatamericanoutdoors.com)
- Fairly accurate ELISA tests for identification of snake venoms in wound aspirate, serum, urine, and other body fluids have been developed but are not generally available in regions where cobras live. (medscape.com)
- A completely occlusive tourniquet might be considered when a victim has been bitten by a highly toxic snake, such as a cobra, and travel time to medical care is short. (medscape.com)
- Venom of the king cobra snake ( OPHIOPHAGUS HANNAH ) that consists primarily of neurotoxins. (nih.gov)
- So, take these proteins, look at their structures and make changes that would make them more stable, more broadly reactive (across various snake species) and more potent in their interaction, so they would out-compete the venom binding in your body. (nih.gov)
- Restrict movement, and keep the affected area at heart level if bitten by a pit viper (rattlesnake, copperhead, cottonmouth) in North America, or below heart level if bitten by a coral snake, cobra, or exotic snake, to reduce the flow of venom. (medlineplus.gov)
Snakes8
- Ardis believes the King Cobra and Krait snakes were the venoms used because of the 19 neurotoxins they contain. (nofakenews.net)
- 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)
- Snakes-the Chinese krait and the Chinese cobra-may be the original source of the newly discovered coronavirus that has triggered an outbreak of a deadly infectious respiratory illness in China this winter. (jerrywdavis.com)
- In the Center's Serpentarium, dozens of the world's most dangerous and exotic snakes are on display, including a thirteen-foot king cobra and a fourteen-foot burmese python. (greatamericanoutdoors.com)
- Venoms of sea snakes ( HYDROPHIIDAE ) found around Pacific islands. (nih.gov)
- The venoms contain fewer enzymes and more neuro- or myotoxins than land snakes. (nih.gov)
- Venoms from snakes of the genus NAJA . (nih.gov)
- Then the neurotoxic snakes, like cobras and mambas, can shoot venom into your eyes, where it goes straight to the nervous system, slowing down breathing and heart rate. (nih.gov)
Ophiophagus3
- The king cobra (Ophiophagus hannah) is widely distributed throughout many parts of Asia. (nih.gov)
- This study aims to investigate the complexity of Malaysian Ophiophagus hannah (MOh) venom for a better understanding of king cobra venom variation and its envenoming pathophysiology. (nih.gov)
- A 2021 study also connected the Chinese Krait and King Cobra to the Covid-19 spike protein, explaining, "the discovery of a superantigen-like motif in the S1 Spike protein, as well as two other neurotoxin-like motifs that have peptide similarities to neurotoxins from Ophiophagus (cobra) and Bungarus genera. (jerrywdavis.com)
Naja naja1
- The effects of cobra (Naja naja) venom on blood coagulation , fibrinolysis and red blood cells were studied in vitro. (who.int)
Krait1
- Bungarus fasciatus ( Banded Krait) This venom produces a condition like an acute polioencephalitis and myelitis, both symptomatically and histologically. (abchomeopathy.com)
Cytotoxic1
- [ 18 , 17 ] Defer this technique for venomous bites known to cause local necrosis (such as with African spitting cobras) with cytotoxic and hemotoxic effects, as local tissue damage may be increased with its use. (medscape.com)
Antivenom1
- If available antivenom is polyspecific, covering all cobras in the region, precise species identification becomes much less important. (medscape.com)
Neurotoxic1
- The venoms contain polypeptide toxins of various kinds, cytolytic, hemolytic, and neurotoxic factors, but fewer enzymes than viper or crotalid venoms. (nih.gov)
Vitro2
- Rediocides A and G, the principle components of Trigonostemon reidioides (Kurz) Craib, which is known as Lotthanong in Thai, were investigated for a detoxification mechanism against Naja kaouthia venom by in silico, in vitro, and in vivo methods. (nih.gov)
- The in vitro SDS-PAGE and the in vivo results support the in silico detoxification mechanism of rediocides against cobra venom at a molecular level. (nih.gov)
Prey1
- Of the nearly 4,000 species known to science, about 600 are venomous, and the vast majority of these use venom to immobilize and digest their prey. (wordpress.com)
Proteins1
- A second approach is based on structural biology methodologies: Identify proteins that resemble the targets of venom (such as blood clotting cascades) and then enhance them through engineering. (nih.gov)
Viper1
- Later during the interview, Dr. Ardis touched on the fact that hydroxychloroquine, defamed by the media, has been known to block nicotine receptors in the brainstem from being injured by cobra and viper venom. (jerrywdavis.com)
Factor3
- Cobra Venom Factor (CVF) 1mg - 1 vial is backordered and will ship as soon as it is back in stock. (dnamethsoc.com)
- A similar outcome was observed in wild-type mice cotreated with the TLR ligands and cobra venom factor, a potent complement activator. (nih.gov)
- Unimmunized animals pretreated with cobra venom factor in a manner known to achieve complement depletion failed to respond with altered arterial oxygen tensions following similar aerosol challenge. (cdc.gov)
Primarily1
- Similar techniques has been shown to be helpful in delaying systemic absorption of venoms primarily by reducing lymphatic spread of venom (main mechniasm of spread), although high quality studies are lacking to substantiating efficacy. (medscape.com)
Exposure3
- Ocular toxicity associated with indirect exposure to African spitting cobra venom. (qxmd.com)
- Direct ocular inoculation with African spitting cobra (Naja nigricollis) venom in the United States is uncommon, especially in an urban setting, but can lead to serious acute and chronic ocular injury depending on the extent of exposure. (qxmd.com)
- As Dr. Ardis explains in the video (below), every single side effect attributed to covid-19 is also a known effect from toxic venom exposure. (jerrywdavis.com)
Venomous1
- The signs and symptoms that develop from venomous snakebites may vary in severity based on the type and amount of venom injected. (cdc.gov)
CROWN2
- Swedish death metal veterans THE CROWN will releae their new album, "Cobra Speed Venom" , on March 16 through Metal Blade Records . (eradioweb.com)
- Swedish death metal legends The Crown have announced their new album , Cobra Speed Venom , for a March 16th release through Metal Blade Records. (rockbrary.com)
Dose1
- Cobra venom had dose dependent inhibition effect on both intrinsic and extrinsic coagulation pathways. (who.int)
Believes1
- Ardis believes that in the initial stages of the plandemic, and even in the present, Cobra venom was placed in many public water supplies. (nofakenews.net)
Bites1
- This technique has been shown to be helpful in delaying systemic absorption of elapid venoms, but its use in cobra bites remains controversial. (medscape.com)
Video1
- A week or so ago I posited that the Covid "virus" was made from cobra venom after watching a video that implied that the covid "virus" was actually a poison put into public drinking water. (jerrywdavis.com)
Bitten1
- A private collector who presents after being bitten by his or her captive "Thai cobra" may have been envenomed by any 1 of at least 3 different species, each with different clinical consequences. (medscape.com)
Effects2
Blood3
- People injected with these types of venoms develop upper respiratory distress and problems with properly clotting their blood. (nofakenews.net)
- An appropriate approach to studyiung efficacy requires measurement of blood venom levels before and after removal of wrap to suggest the intervention limited systemic spread of venom. (medscape.com)
- other venoms can spur a blood clot leading to a heart attack or an embolism. (nih.gov)
High1
- However, cobra venom had neither fibrinolytic nor fibrinogenolytic effect even at high venom concentration (10 mg/ ml). (who.int)
African1
- We report 2 cases of indirect ocular inoculation with venom from an African spitting cobra, manifesting as periocular soft tissue swelling, extensive conjunctivitis, and corneal epithelial erosion. (qxmd.com)
Album1
- They eventually entered the classic Studio Fredman with Fredrik Nordstrom to record what would become their new album, Cobra Speed Venom . (rockbrary.com)
DRUG2
- Venomtech has been at the forefront of venom research for drug discovery for more than a decade. (jerrywdavis.com)
- Through this relationship with Charles River Laboratories - a global leader for drug discovery contract research - we can now showcase our innovative technology, introducing the wider industry to the potential of venoms for the successful delivery of more leads, more quickly, for a broad range of targets. (jerrywdavis.com)
Common2
- Other common constituents of metazoan venoms are phospholipases A2, which convert phospholipids into lysophospholipids. (nofakenews.net)
- What do lethal cobra venom, quantum dots and cancer diagnosis have in common? (lifeboat.com)
Effect1
- Furthemore, cobra venom had direct haemolytic effect shown by increased red cell fragility and raised plasma haemoglobin level. (who.int)
Eyes1
- 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)