Disease relevance of Russell's Viper

• Aortic medial necrosis with or without thrombosis in rabbits treated with Russell's viper venom and angiotensin II [1].
• Lupus anticoagulant [LAC, Russell viper venom time (RVVT) assay] and anticardiolipin (aCL, polyclonal assay) status of each subject was determined on a quarterly basis [2].
• Vascular changes included arteritis of the interlobular artery with C3 deposition in the arterial walls in Russell's viper cases and thrombophlebitis in both green-pit viper's and Russell's viper's victims [3].
• Preoperatively, to identify patients at high risk of pulmonary embolism, plasminogen activator inhibitor activity, dilute Russell's viper venom time, prothrombin time, and cholesterol levels were most predictive [4].
• Heparin therapy in Russell's viper bite victims with disseminated intravascular coagulation: a controlled trial [5].

High impact information on Russell's Viper

• In the absence of heparin, SAP (5-125 micrograms/ml) had no effect on clot times generated by Activated Thrombofax Reagent, brain thromboplastin, Russell's Viper Venom or thrombin when assessed in normal citrated plasma [6].
• Anti-beta2GPI mAbs directed against the third domain (Cof-20 and Cof-22) and fourth domain (Cof-21, EY1C8, and EY2C9) of beta2GPI inhibited the thrombin generation induced by Russell's viper venom in diluted plasma and that induced by the prothrombinase complex reconstituted with purified clotting factors [7].
• In the present study we have prepared activated Factor IX by incubating human Factor IX with calcium and Russell's viper venom covalently bound to agarose [8].
• Membrane phospholipid organization was determined by using bee venom phospholipase-A2 and indirectly by measuring clotting time on recalcification of normal human platelet-poor plasma in the presence of Russell's viper venom [9].
• Russell's viper venom, a control Factor X-activating serine protease, was not inhibited by either 0.1 mM HgCl2 or 1 mM iodoacetamide [10].

Chemical compound and disease context of Russell's Viper

• The "PCP test" is based on a phospholipid-rich Russells viper venom reagent, insensitive to heparin and lupus anticoagulants [11].
• The lupus anticoagulant (dilute Russell's Viper Venom time, dRVVT) and coagulation Factor XII were determined with routine tests (Dade Behring) [12].
• 2. Then we compared TTI at a 1:26 dilution with dilute Russell's Viper Venom Time (dRVVT) in 50 consecutive patients with suspected lupus anticoagulant not treated with warfarin or heparin [13].

Biological context of Russell's Viper

• We determined the complete amino acid sequence of RVV-X, the blood coagulation factor X activating enzyme, isolated from Russell's viper venom and studied structure-function relationships [14].
• STUDY DESIGN AND METHODS: Patients undergoing cardiac surgery were studied for the presence of the FV Leiden defect by the use of a Russell's viper venom clot-based assay and polymerase chain reaction [15].
• The dilute Russell's viper venom time detected the LA significantly more often than either the activated partial thromboplastin time or the kaolin clotting time (P < 0.001) [16].
• Renal hemodynamics and autoregulation of blood flow were investigated following intravenous injection of Russell's viper venom (0.1 mg/kg) in dogs anesthetized with sodium pentobarbital [17].
• Two commercially available procedures (protein C impedance [PCI] test and protein C pathway [PCP] test), using modified Russell's viper venom time (RVVT) assays, showed less overlap between normals and heterozygotes than did the APTT-based method [18].

Anatomical context of Russell's Viper

• Four other phospholipases A2--from venoms of Russell viper, Crotalus adamanteus, and bee, and from pig pancreas--are unaffected by 50 micrometer indomethacin, which inhibits leukocyte phospholipase A2 by 70% [19].
• When thrombin, tissue thromboplastin or Russell's viper venom was added to a suspension of either lymphocytes or neutrophils containing normal plasma, aggregation of these cells ensued [20].
• The influence of some variables on coagulation times of mouse and human plasmas were examined in activated partial thromboplastin time, one-stage prothrombin time, and Russell's viper venom time assays [21].

Associations of Russell's Viper with chemical compounds

• Factor IX is also converted to Factor IXaalpha by a protease from Russell's viper venom [22].
• Triggering was attempted by injection of Russell's viper venom (RVV), which is a proteolytic procoagulant, and histamine [23].
• The activation peptide cleaved near the amino terminus by a protease from Russell's viper venom differs in both size and sequence from those of other serine proteases [24].
• Factor X-activating glycoprotein of Russell's viper venom. Polypeptide composition and characterization of the carbohydrate moieties [25].
• Both factor Va, activated by thrombin or by the factor V activator from Russell's viper venom, and the isolated fragments, D (Mr = 105,000), C1 (Mr = 150,000), and F1F2 (Mr = 72,000), were studied [26].

Gene context of Russell's Viper

• The Factor V (Leiden) test: evaluation of an assay based on dilute Russell Viper Venom Time for the detection of the Factor V Leiden mutation [27].
• A functional assay for protein S is not readily available for clinical use; however, we have developed a functional protein S assay based on the prolongation of Russell viper venom (RVV) plasma clotting time by protein C activated by PROTAC [28].
• EMPs were measured using positivity for monoclonal antibodies (mAbs) CD31 and CD51, and their procoagulant activity was assessed using a Russell viper venom assay [29].
• The sequence of TSV-PA exhibits a high degree of sequence identity with other snake venom proteases: 66% with the protein C activator from Agkistrodon contortrix contortrix venom, 63% with batroxobin, and 60% with the factor V activator from Russell's viper venom [30].
• Following purification to homogeneity and activation by the factor X activator from Russell viper venom, the mutants were characterized with respect to their ability to assemble into the prothrombinase complex to activate prothrombin and interact with target plasma fXa inhibitors, tissue factor pathway inhibitor (TFPI) and antithrombin [31].

Analytical, diagnostic and therapeutic context of Russell's Viper

• We examined not only the levels of antibodies to prothrombin and anti-beta2-GP I (both IgG and IgM isotypes) using an ELISA system, but also LA activity detected using both diluted Russell's viper venom time (dRVVT) and STACLOT LA test in 124 patients with SLE [32].
• Recombinant mouse factor X was expressed in human embryonic kidney cells and secreted into cell culture supernatant as zymogen, which could be converted to catalytically active factor Xa by Russell's viper venom [33].

References