Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoprothrombin II-A anticoagulant was isolated from bovine prothrombin. Purified prothrombin was applied to DEAE-cellulose chromatography after incubation with thrombin. Four protein peaks were obtained where the third peak corresponded to the anti-coagulant effect. The fractions under the third peak were pooled together and the anticoagulant effect was evaluated with different methods. From 25,470 +/- 2,800 U of prothrombin, 5,800 +/- 1,400 U of inhibitor were obtained. The inhibitor was found to be most effective at pH 7.2--7.8. In vitro, the inhibitor inhibited the thrombin time and the plasma clotting time highly significantly but had no effect on euglobulin lysis time and fibrin plates. In vivo, when injected into rabbits, the inhibitor effect was also significant on the same tests. The autoprothombin II-A anticoagulant had a protective effect on DIC formation with rabbit brain thromboplastin administration. This protective effect was found to be statistically significant.
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PMID:Some properties of autoprothrombin II-A anticoagulant. 61 78

Thrombogenicity of the factor IX concentrate and its clinical use for stoppage of the bleeding in the case of hemophilia A with inhibitor were reported. (1) Factor IX concentrate contained the coagulation factors as prothrombin complex (factors II, VII, IX and X); Thrombin and factor Xa. (2) Prothrombin in the factor IX concentrate could be converted to thrombin without any additional procoagulant such as thromboplastin or factor V, but in just 2.5M glycine solution by the effect of factor Xa. (3) The infusion of factor IX concentrate into a rabbit induced DIC promptly which was proved by autopsy and coagulation-fibrinolytic studies. (4) Factor IX concentrate showed a great efficacy in stopping the bleeding in the case of hemophilia A with inhibitor.
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PMID:Characteristics and thrombogenicity of factor IX concentrate. 61 88

We studied a coagulation abnormality present in 12 members of five kindreds who bruised easily and bled excessively after minor trauma. Their activated partial thromboplastin times were between 32 and 39 seconds (normal, 22.8 to 28.8 seconds). Prothrombin times, thrombin times, platelet-function tests and the levels of factors XII, XI, IX, VIII, prekallikrein and high-molecular-weight kininogen were normal. Within these kindreds inheritance of prolonged partial thromboplastin times followed an autosomal and probably dominant pattern. The prolonged thromboplastin times were corrected by normal plasma and by normal plasma adsorbed with celite, but there was no mutual correction between plasmas of the patients. These subjects shared a common defect in the intrinsic pathway of coagulation that we designate by the proband's surname, Passovoy.
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PMID:The Passovoy defect: further characterization of a hereditary hemorrhagic diathesis. 64 12

Acute consumptive coagulopathy may be initiated by diverse events. It is frequently necessary to establish the diagnosis with urgency. Rational therapy can only be approached with knowledge of the relative impact the primary consumption exerts upon hemostasis as well as the effects of secondary fibrinolysis. A constellation of interlocking tests within the capability of the small laboratory is presented. This includes the prothrombin time, the activated partial thromboplastin time, the serial thrombin time, the heat precipitation fibrinogen level, the platelet count, red cell morphology, the levels of fibrin (fibrinogen) degradation products and selected factor assays. This series can be completed within 45 minutes. Interpretation, with particular emphasis upon the stage in the natural history of the process when evaluation is instituted, and underlying diseases which modify typical patterns are discussed. The discriminant function of the serial thrombin time is stressed.
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PMID:The seial thrombin time in the diagnosis of consumptive coagulopathy. 65 8

By means of CM-Sephadex column chromatography, Trimeresurus mucrosquamatus venom was separated into 20 fractions. Fraction XX had the marked anticoagulant action. This fraction was refractionated three times on Sephadex G-75, and a single peak was obtained. The patterns of microzone and disc electrophoresis also showed a single band. A single, symmetrical boundary with a value of 1.61 S was obtained by ultracentrifugation. It was a single peptide chain with a molecular weight of 11 700. The isoelectric point was higher than pH 10. The anticoagulant principle possessed phospholipase A activity and was calcium ion dependent. It did not possess proteolytic, tosyl-L-arginine methyl ester esterase, phosphodiesterase and alkaline phosphomonoesterase activities of the crude venom. The phospholipase A activity was heat-labile at pH 7.4, but was heat-stable at pH 5.6. The anticoagulant activity was more resistant to heat treatment as compared with phospholipase A activity. The anitoagulant action of the purified principle was competitively inhibited by platelet phospholid, tissue thromboplastin and cephalin, and was neutralized by antiserum. The anticoagulant principle inhibited platelet aggregation induced by ADP. It did not destroy fibrinogen, Factor X, prothrombin and thrombin; nor did it induce fibrinolysis nor interfere with the interaction between thrombin and fibrinogen. It is concluded that the anticoagulant action of this phospholipase A was due to the inhibition of the activations of Factors X and II through the inactivation of the procoagulant activity of phospholipids mediated partly by phospholipid-binding activity of this venom enzyme and partly by its enzymatic hydrolysis of phospholipids.
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PMID:Purification and characterization of the anticoagulant principle of Trimeresurus mucrosquamatus venom. 66 29

A common topic of discussion for many years has been whether stress induces hypercoagulability and/or hyperfibrinolysis. Ten healthy volunteers were subjected to strenuous physical effort on a bicycle ergometer. Blood samples were collected 10 min before and immediately after exercise. The well-known activation of blood coagulation was demonstrated by significant shortening of the activated partial thromboplastin time, thrombin and reptilase times. However, no fibrinopeptide A (FPA) was generated, nor did the ethanol gelatin test turn positive. A significant shortening of the euglobulin lysis time was indicative of fibrinolysis but no fibrin(ogen) degradation products (FDP) could be detected. These results show that the so-called hypercoagulability is not accompanied by thrombin-mediated release of fibrinopeptide A, and suggest that the activation of coagulation does not involve fibrinogen to fibrin conversion.
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PMID:[Missing thrombinemia in the so-called hypercoagulability following physical exertion (proceedings)]. 69 96

A patient is reported who sustained bilaterial iliacus haematoma with femoral nerve palsy during treatment with constant intravenous infustion of heparin for deep venous thrombosis. She was promptly treated with operative decompression and recovered completely from the palsy. Daily examinations of the blood revealed that the plasma heparin concentration, activated partial thromboplastin time, APTT, and thrombin time all were above the therapeutic range at the time when the bleeding started, and before the initial symptoms occurred. Early operative decompression is considered to be the ideal treatment in patients who develop this complication during anticoagulant therapy.
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PMID:Bilateral iliacus haematoma with femoral nerve palsy complicating anticoagulant therapy. 69 56

The clinical and laboratory data on the 12 patients with an acquired inhibitor to factor V have been reviewed. The degree of clinical bleeding in these patients varied from none to severe, and in most patients the inhibitor was transient. The combination of a markedly prolonged partial thromboplastin time and Quick prothrombin time and failure of normal plasma to correct these tests, in the presence of a normal thrombin and prothrombin and proconvertin time, seems to be pathognomonic for a factor V inhibitor. The inhibitors have physicochemical properties of immunoglobulins and a few have been characterized as polyclonal IgG antibodies or a mixture of IgM and IgG antibodies. The etiology and pathophysiologic mechanism of their development is unknown, but there seems to be a close relationship to major surgery. When tested with inhibitor plasma, the plasmas from 9 patients with hereditary factor V deficiency from 7 unrelated families did not contain factor V antibody-neutralizing material.
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PMID:Acquired inhibitors of factor V. 70 95

This is an investigation into thromboplastin time, partial thromboplastin time, plasma thrombin time, fibrinogen, and platelets in 30 patients with severe brain injury over 7--14 days. Platelets showed a very marked initial decrease and a slow return to normal around the seventh day. Fibrinogen was initially lowered in most of the cases, and raised from the second day onward. Changes in the other laboratory values were less definite. Latent signs of consumption coagulopathy were not accompanied by bleeding disorders, or by disseminated intravascular coagulation at autopsy. The severity of laboratory value changes clearly correlated with the extent of brain damage, and was significantly higher when the patient did not survive the first week after injury.
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PMID:Disturbances of the coagulatory system in patients with severe cerebral trauma. I. 70 71

A lupus-type anticoagulant which causes strong inhibition of the partial thromboplastin time with kaolin (PTTK), the stypven time, and the thrombin generation tests has been investigated. All tests for platelet function were normal, as were all specific coagulation factor assays with the exception of a slightly reduced factor XI in this patient. A diethylaminoethyl-cellulose-immunoglobulin (DEAE-cellulose-IgG) fractionation of the patient's plasma produced two peaks containing inhibitory activity in the PTTK test. The first of these peaks had a cloudy appearance, suggesting the presence of immunoglobulin aggregates. Studies with IgG aggregates prepared from normal IgG and from the patient's IgG demonstrated that such aggregates were not the cause of inhibition. It was possible to neutralize the inhibitory activity of the purified IgG but not platelet-poor plasma (PPP) with a rabbit anti-IgG. The inhibition of the patient's PPP in the thrombin generation, the contact product, and the stypven time tests were corrected by the inclusion in the test system of platelets activated either by aggregation due to adenosine diphosphate (ADP) or formalin fixation and washing. These studies lend support to earlier findings that platelets interact at several sites in the coagulation cascade.
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PMID:Demonstration of a platelet bypass mechanism in the clotting system using an acquired anticoagulant. 73 36


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