-
Journal of Clinical Pathology Sep 1972The great convenience of a method using a suspension of antibody-coated latex particles for the titration of fibrinogen-related antigens over the tanned red cell... (Comparative Study)
Comparative Study
The great convenience of a method using a suspension of antibody-coated latex particles for the titration of fibrinogen-related antigens over the tanned red cell haemaglutination immunoassay (TRCHII test) of Merskey, Lalezari, and Johnson (1969) has been demonstrated. The usefulness of Ca-Ancrod for the defibrination of heparinized plasma is presented here.
Topics: Animals; Anticoagulants; Antigens; Calcium; Erythrocytes; Fibrinogen; Hemagglutination Tests; Heparin; Humans; Immunoassay; Latex Fixation Tests; Methods; Rabbits; Thrombin; Venoms
PubMed: 4673612
DOI: 10.1136/jcp.25.9.757 -
British Journal of Cancer Jun 1977
Topics: Ancrod; Animals; Coumarins; Diet; Lung Neoplasms; Mice; Mice, Inbred C57BL; Neoplasm Metastasis; Neoplasm Transplantation; Neoplasms, Experimental; Transplantation, Isogeneic; Vitamin K Deficiency
PubMed: 871374
DOI: 10.1038/bjc.1977.135 -
The Journal of Biological Chemistry Aug 1989Heparin cofactor II (HCII) is a highly specific serine proteinase inhibitor, which complexes covalently with thrombin in a reaction catalyzed by heparin and other...
Heparin cofactor II (HCII) is a highly specific serine proteinase inhibitor, which complexes covalently with thrombin in a reaction catalyzed by heparin and other polyanions. The molecular basis for the thrombin specificity may be explained by the identification here of a segment of HCII including residues 54-75 that binds to thrombin. A synthetic peptide, HCII(54-75), based on this segment of HCII, Gly-Glu-Glu-Asp-Asp-Asp-Tyr-Leu-Asp-Leu-Glu- Lys-Ile-Phe-Ala-Glu-Asp-Asp-Asp-Tyr-Ile-Asp inhibited thrombin's cleavage of fibrinogen. Clotting activity of thrombin was inhibited 50% at a concentration of 28 microM. Polyacrylamide gel electrophoresis showed that HCII(54-75) inhibited thrombin's cleavage of both the A alpha and B beta polypeptides in fibrinogen. However, the peptide did not block thrombin's active site, as hydrolysis of chromogenic substrates was not inhibited. HCII(54-75) probably binds to the same site on thrombin as do carboxyl-terminal residues of hirudins, thrombin inhibitors of leeches. HCII(54-75) inhibited binding of thrombin to a synthetic peptide corresponding to residues 54-66 of hirudin PA, but the hirudin peptide was about 30-fold more potent in binding and clotting assays. Both synthetic peptides, as a result of their polyanionic character, might be expected to stimulate the reaction of HCII with thrombin. However, the hirudin-related peptide inhibited this reaction, suggesting that it blocked a site on thrombin required for interaction with HCII. HCII(54-75) had a net stimulatory effect on the thrombin-HCII reaction as a consequence of its lower affinity for thrombin and greater negative charge relative to the hirudin-related peptide. These studies suggest that residues 54-75 of HCII interact with a noncatalytic binding site on thrombin and that this interaction contributes to efficient inhibition of thrombin by HCII.
Topics: Amino Acid Sequence; Ancrod; Antithrombins; Binding Sites; Drug Interactions; Fibrinogen; Glycoproteins; Heparin Cofactor II; Hirudins; Molecular Sequence Data; Peptide Fragments; Thrombin; Thrombin Time
PubMed: 2760054
DOI: No ID Found -
British Journal of Cancer Apr 1974Experiments were undertaken to test a new hypothesis for the mechanism underlying the Révész effect. The hypothesis proposes that lethally irradiated (LI) tumour cells...
Experiments were undertaken to test a new hypothesis for the mechanism underlying the Révész effect. The hypothesis proposes that lethally irradiated (LI) tumour cells enhance the take probability of a small number of transplanted viable (V) tumour cells mixed with them by exerting a thromboplastic effect at the site of injection; local fibrin formation prevents emigration of V cells from the site or secures their survival there. The evidence presented to support this hypothesis is as follows: in the case of 3 isogeneically transplanted tumours, admixed particulate brain extract simulated the effect of LI cells in increasing the take probability of V cells; brain extract simulated the effect of LI cells in greatly delaying the disappearance of (125)IUdR-labelled viable carcinoma cells from the injection site; V cells acquired a raised take probability by their incorporation in fibrin clots; it was confirmed that admixed erythrocytes increased the take probability of V cells; using a newly devised microscopical test for detection of the thromboplastic activity of individual cells, it was found that cell death was almost always required for the display of such activity; lymphocytes and bone marrow cells, ineffective in enhancing the take of V cells, were almost totally devoid of thromboplastic activity. Possible explanations are given for failure of a fibrinogen depleting agent, ancrod (Arvin) to inhibit the Révész effect when administered to recipients. It is concluded that the evidence strongly supports the hypothesis presented whilst seriously weakening the long-standing theories that admixed LI cells act by provision of nutrients or by local quenching of postulated immune reactivity.
Topics: Animals; Brain; Cell Line; Cell Survival; Fibrin; Leukemia, Experimental; Mice; Mice, Inbred Strains; Neoplasm Metastasis; Neoplasm Transplantation; Neoplasms; Neoplasms, Experimental; Peptide Hydrolases; Radiation Effects; Thromboplastin; Tissue Extracts; Venoms
PubMed: 4854893
DOI: 10.1038/bjc.1974.68 -
Blood May 1992
Topics: Ancrod; Humans; Thrombosis
PubMed: 1571563
DOI: No ID Found -
The Journal of Thoracic and... Aug 2000
Topics: Ancrod; Anticoagulants; Aprotinin; Cardiopulmonary Bypass; Chondroitin Sulfates; Coronary Disease; Dermatan Sulfate; Drug Combinations; Heparin; Heparitin Sulfate; Humans; Serine Proteinase Inhibitors; Thrombocytopenia; Thrombosis; Treatment Failure
PubMed: 10917979
DOI: 10.1067/mtc.2000.108285 -
British Journal of Experimental... Apr 1979Injection of bacterial lipopolysaccharide into pregnant mice resulted in fibrinogen accumulation, thrombosis and haemorrhage in the placental tissue and foetal death....
Injection of bacterial lipopolysaccharide into pregnant mice resulted in fibrinogen accumulation, thrombosis and haemorrhage in the placental tissue and foetal death. Depletion of circulating fibrinogen by a thrombin-like enzyme from the venom of Malayan pit viper, Arvin, prevents foetal death. Foetal protection was also obtained by treating the mothers with a preparation of phospholipase C from Bacillus cereus known to inactivate tissue thromboplastin. It is suggested the lipopolysaccharide causes foetal death by inducing thrombosis as a consequence of activation of placental thromboplastin.
Topics: Ancrod; Animals; Female; Fetal Death; Fibrinogen; Lipopolysaccharides; Mice; Phospholipases; Placenta; Pregnancy; Thrombosis
PubMed: 444421
DOI: No ID Found -
Blood Jan 1980
Topics: Amino Acids; Ancrod; Animals; Fibrin Fibrinogen Degradation Products; Fibrinogen; Goats; Hematocrit; Male; Rabbits; Selenomethionine; Thrombin; Time Factors; Urokinase-Type Plasminogen Activator
PubMed: 7350940
DOI: No ID Found -
European Journal of Biochemistry Feb 1974
Topics: Amines; Arginine; Benzamides; Binding Sites; Chlorine; Esters; Ethanol; Hemostatics; Histidine; Hydrolysis; Isoflurophate; Ketones; Kinetics; Molecular Weight; Nitrobenzenes; Peptide Hydrolases; Phosphorus Radioisotopes; Protease Inhibitors; Serine; Venoms
PubMed: 4830197
DOI: 10.1111/j.1432-1033.1974.tb03317.x -
British Medical Journal Feb 1977
Topics: Ancrod; Drug Resistance; Endopeptidases; Humans; Thromboembolism
PubMed: 837184
DOI: 10.1136/bmj.1.6059.508-c