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)

Ontogeny of selected hemostatic system components was studied in 120 bovine fetuses which had been divided into eight monthly gestational age groups. Fetal blood was subjected to the following tests: platelet count, partial thromboplastin time, prothrombin time, thrombin time, fibrinogen quantitation, and assays for prothrombin and factors V and VIII. Platelet numbers corresponding to adult numbers were in fetal blood at least as early as gestation day 60, and their numbers varied only slightly thereafter. Bovine blood was incapable of in vitro coagulation at gestation day 90, with all samples coagulating by gestation day 150. Fetal coagulation screening test times (partial thromboplastin time, prothrombin time, and thrombin time) shortened during gestation and were near times of adults at birth. Of the four individual coagulation factors tested, only factor VIII reached adult values in the fetus in utero. Amounts of fibrinogen, prothrombin, and factors V and VIII in the neonate exceeded that of normal adult cattle.
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PMID:Ontogeny of bovine hemostasis. 52 61

Studies of 11 patients with haemorrhagic stroke revealed no significant change in kaolin cephalin clotting time, prothrombin time, thrombin time, PF 3 availability, platelet count and factor V and VIII during the first week. Plasma fibrinogen was significantly increased while factors VII + X were decreased (borderline significance). Prolongation of plasma recalcification time and decrease in heparin tolerance reached borderline significance. There was moderate, but significant, increase in serum antithrombin activity and plasma (euglobulin fraction) fibrinolytic activity.
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PMID:Blood coagulation and fibrinolysis in haemorrhagic stroke. 58 May 8

Factors II, V, X, VIII, thrombin time, platelet count and the thrombelastogram were estimated in 58 persons who had suffered cerebrocranial injuries of varying degree of severity. The aim of the investigation was to elucidate whether and to what extent the injury affected these parameters and whether the destruction of brain tissue could be regarded as the sole cause of the impairment of the clotting mechanism. First estimations in cases of cerebrocranial trauma uncomplicated by other injuries and in cases of cerebrocranial trauma complicated by moderately severe other injuries showed changes in factors II, V, X, VII as well as a pathological thrombelastogram, viz.: hypercoagulability. More pronounced changes were observed in cases where the cerebrocranial injuries were associated with severe complicating lesions: factors II, V, VII, X and the platelet count were reduced by 50-70 per cent of their normal values. Subsequent estimations carried out over a period of 15 days showed that the clotting mechanism had returned to nearly normal within 6-10 days. The use of heparin for normalizing disturbances of the clotting mechanism in cerebrocranial injuries is discussed.
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PMID:[Disturbances of the clotting mechanism in severe cerebro-cranial injuries (author's transl)]. 59 29

Recent observations suggest that plasma F VIII consists of a series of molecules with different molecular weights. The data described in this paper suggest that sup F VIII represents the molecules with relatively low molecular weights whereas the molecules with the highest molecular weights appear in cryo F VIII. Sup F VIII was associated with VIII:C and VIIIR:Ag, but ristocetin cofactor activity was lacking. Although the immunoprecipitation characteristics of sup F VIII with rabbit antifactor VIII were different from those of cryo F VIII, immunological identity was observed in immunodiffusion and crossed immunoelectrophoresis. In 0.8M NaCl sup F VIII dissociated into VIIIR:Ag of relatively high molecular weight and VIII:C of low molecular weight. No indications were obtained that the presence of sup F VIII was the result of proteolytic degradation of factor VIII. VIII:C of sup F VIII was more labile in vitro than VIII:C in plasma. It could be activated by traces of thrombin in a way similar to plasma F VIII. In patients with classic von Willebrand's disease relatively more VIII:C remained in the supernatant after cryoprecipitation of plasma.
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PMID:Heterogeneity of human factor VIII. I. Characterization of factor VIII present in the supernatant of cryoprecipitate. 61 89

The current experiments examine the reaction between purified human alpha-thrombin and purified human factor VIII and compare this with the reaction between alpha-thrombin and the low molecular weight factor VIII procoagulant activity obtained by high ionic strength dissociation. The reaction patterns of both procoagulants are similar, demonstrating in initial increase in factor VIII activity followed by a decay of procoagulant activity. The extent of activation which is observed in the initial phase decreases with lower temperatures and with lower thrombin concentrations. A pseudo-first order relationship is demonstrated for the activation phase. The labile factor VIII procoagulant activity produced by the initial action of thrombin appears to be intrinsically unstable, since the addition of hirudin or diisopropylfluorophosphate does not prevent the subsequent decay of the procoagulant activity. The similar activation and decay patterns of purified factor VIII and the dissociated low molecular weight factor VIII procoagulant support the concept that the low molecular weight procoagulant itself represents the functional coagulant moiety of the factor VIII complex.
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PMID:Thrombin activation of factor VIII. II. A comparison of purified factor VIII and the low molecular weight factor VIII procoagulant. 63 56

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

Factor V and VIII activity was measured by a one-stage assay on capillary blood issuing from a skin cut. This activity increases during bleeding. The phenomenon is suppressed by a previous injection of a low dose of heparin. These data give evidence of a very early local formation of thrombin during hemostasis. The study of this activation process in patients with congenital deficiency of blood clotting factor allows to investigate the mechanism of thrombin formation in vivo. This demonstrates the preeminence of the tissue factor pathway and the need of factor VIII for factor X activation in the extrinsic system.
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PMID:Factor V and VIII activation "in vivo" during bleeding. Evidence of thrombin formation at the early stage of hemostasis. 79 11

The role of thrombin in ADP-induced aggregation and release in vitro was critically examined. The addition of heparin or hirudin to citrated platelet rich plasma did not prevent aggregation or release. The addition of citrate to heparinized plasma restored secondary aggregation and release. Hirudin did not prevent irreversible aggregation. These results are incompatible with the hypothesis that thrombin is a primary and necessary mediator of platelet aggregation (Ardlie & Han, 1974; Han & Ardlie, 1974a, b, c). This hypothesis is based in part on the assumption that EDTA enhances the elution of clotting factors from platelets; we found no enhanced elution of factors II, V, X, VIII, IX or XI when platelets were washed in EDTA.
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PMID:The role of thrombin in ADP-induced platelet aggregation and release: a critical evaluation. 81 Dec 45

Possible increased activation of the coagulation pathway was measured in a group of patients with neoplastic diseases. In addition to standard tests, the thromboplastin generation test, thrombin generation test and immunologic and coagulant activities of both Factor VIII and antithrombin III were utilized in the evaluation. The correlation between immuno-Factor VIII (VIII-Ag) and its clotting activity (VIII-C1) was good (r = 0.83). In contrast, this was not the situation for antithrombin III-Ag and its clotting activity. Thromboplastin generation was accelerated in 60% and thrombin generation was accelerated in 40% of the patients. Fibrinogen was elevated in half the cases: in most of these patients, thrombin times were slightly prolonged. These results indicate that some patients who have cancer have abnormal clotting patterns and are often in a potentially hypercoagulable state that is reflected by the thromboplastin generation test, thrombin generation test, and high levels of Factor VIII (both VIII-Ag and VIII-C1).
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PMID:Antithrombin III and Factor VIII in patients with neoplasms. 87

Blood coagulation tests were performed in 93 newborn infants with different Apgar score at the 1st and 5th minutes of life. The laboratorial determinations were periodically performed at 0, 24 and 48 hours of life. The following tests were performed: bleeding time, whole blood clotting time, prothrombin time, kaolin-cephalin clotting time, thrombin time, dosage of factors I, V, VIII and X, clot retraction, platelet count, englobulin lysis time and the tourniquet test. Immediately after birth, the mean values of the blood coagulation factors were significantly different among the groups, with the exception of the whole blood clotting time and the platelet count. Those differences were due to the presence of the more depressed neonates. Although these results could indicate some degree of hepatic damage, it was apparent that an activation of the blood coagulation mechanisms took place, leading to a consumption coagulopathy. The infants who died (10) presented clinical and laboratorial data suggestive of disseminated intravascular coagulation (DIC). Necroscopic findings of microthrombosis in the liver and in the central nervous system were diagnosed in two infants.
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PMID:Apgar score and blood coagulation factors. 93 62


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