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:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 19 patients with chronic subdural hematoma, coagulation and fibrinolysis in venous blood taken at the time of surgery and in the hematoma contents aspirated from chronic subdural hematoma were studied. Compared with coagulation results for venous blood, the hematoma contents demonstrated marked prolongation of the recalcification time, prothrombin time, and activated partial thromboplastin time, and marked reduction of clotting factor V, the hepaplastin test, prothrombin, and fibrinogen. Antithrombin III was also decreased, and fibrinopeptide A was increased in the hematomas. Fibrinolytic results demonstrated that both plasminogen and alpha 2-plasmin inhibitor were decreased, and both fibrinopeptide B beta 15-42 and fibrin and fibrinogen degradation products were increased in the hematomas. These findings indicate excessive activation of the clotting system, thrombin generation, and increased fibrinolytic activity occurring in the hematomas. From these results, excessive activation of both the clotting and fibrinolytic systems is emphasized to be the possible etiological factor for the origin and development of chronic subdural hematoma.
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PMID:Coagulation and fibrinolysis in chronic subdural hematoma. 275 76

Hemostatic changes were evaluated in ten patients with acute lymphoblastic leukemia and lymphoma who received chemotherapy with L-asparaginase, vincristine, and prednisolone for 1 week. Following treatment, prothrombin time and activated partial thromboplastin time were significantly prolonged, while a marked decrease in fibrinogen levels was observed. The values for cross-linked fibrin degradation products, however, remained within normal limits during treatment, which excluded the possibility of disseminated intravascular coagulation. The concentrations of coagulation inhibitors (antithrombin III, protein C, and protein S), plasminogen, and alpha 2 antiplasmin also significantly decreased; however, levels of both tissue-type plasminogen activator and plasminogen activator inhibitor, which are synthesized in endothelial cells, increased during the treatment. Although a decrease was observed in concentrations of many coagulation factors, including subunits A and B of factor XIII, the activity and antigenicity of factor VII significantly increased following the treatment. From this study, we concluded that these hemostatic abnormalities caused by the administration of L-asparaginase produced a labile condition that easily inclines to bleeding or thrombosis.
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PMID:Changes in hemostatic and fibrinolytic proteins in patients receiving L-asparaginase therapy. 275

This article describes the results of a dietary intervention study performed in three different centers. In the study the effect of a diet enriched with fish on the coagulation tendency of blood was investigated. Two groups of 40 volunteers were given a dietary supplement consisting of 135 g of canned mackerel or meat paste (control) for a 6 weeks period. Compliance, monitored by measuring the urinary excretion of lithium, added to the supplements, was about 80%. Before, during and at the end of the experimental period a number of hemostatic parameters, reflecting the coagulation tendency of blood and the procoagulant activity of monocytes, were measured. The fish supplement did not cause a significant effect on the prothrombin time and on the levels of factor VII, activated factor VII, antithrombin III, von Willebrand factor, fibrinogen, plasminogen and alpha 2-antiplasmin. A slight but transient prolongation in the activated partial thromboplastin time was observed as well as a significant increase in the factor X level, which became more pronounced with prolongation of the experimental period; no activated factor X was found. A tendency towards a stimulation of monocyte procoagulant activity was noticed.
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PMID:Effect of a moderate fish intake on haemostatic parameters in healthy males. 279 60

The effects on the fibrinolytic system after a single s.c. bolus injection (at 9 a.m.) of either 5000 IU conventional heparin or 5000 anti-Xa U of a fractionated low molecular weight heparin (Fragmin, KabiVitrum, Sweden) were investigated in 9 healthy volunteers. The effects were compared to those of an injection of normal saline in 6 volunteers. Samples for biochemical analyses were taken regularily during 6 hours after drug or placebo administration. In the coagulation system the following parameters were measured: Activated partial thromboplastin time (APTT), anti-Xa activity, thrombin time and fibrinogen. The fibrinolytic system was monitored by analysing: plasminogen, alpha 2-antiplasmin, fibrin(ogen) degradation products (FDP), euglobulin clot lysis time (ECLT), tissue plasminogen activator (t-PA) activity, t-PA antigen and plasminogen activator inhibitor (PAI) activity. Injection of the 2 drugs was followed by elevations in APTT and anti-Xa activity, and were more pronounced for Fragmin than heparin. The fibrinolytic system exhibited a diurnal variation with decreasing PAI activity and increasing t-PA activity during the day. Volunteers receiving normal saline (placebo) showed a similar pattern. The results were unrelated to heparin. It is concluded from this study that neither heparin nor Fragmin had any significant effect on the fibrinolytic parameters when measured after a single s.c. bolus injection since the observed variations were within the diurnal range.
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PMID:Heparin and fibrinolysis--comparison of subcutaneous administration of unfractionated and low molecular weight heparin. 283 26

Protein C--vitamin K-dependent protein of the blood coagulation system possessing anticoagulant and fibrinolytic activities was under investigation. Activated partial thromboplastin time was shown to prolong to 214 +/- 8.9% from the first minute after intravenous administration of 0.51 mg per rat bovine protein Ca. After 5 minutes the activity of plasminogen activators increased to 339 +/- 52.8%. Both effects gradually diminished and came back to the starting level within 60-90 minutes. The factor V activity reduced two-fold and didn't return to basal level. We propose that protein Ca reveals its enzymatic activity within first minutes after administration and is blocked then with its inhibitor.
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PMID:[Generation of blood anticoagulant and fibrinolytic activity after intravenous administration of protein C-a in rats]. 291 69

Incubation of HTC rat hepatoma cells with the synthetic glucocorticoid dexamethasone rapidly inhibits plasminogen activator (PA) activity secondary to the induction of a specific acid-stable inhibitor of plasminogen activation (Cwikel, B. J., Barouski-Miller, P.A., Coleman, P.L., and Gelehrter, T.D. (1984) J. Biol. Chem. 259, 6847-6851). We have further characterized this inhibitor with respect to its interaction with both urokinase and tissue plasminogen activator, and its protease specificity. The HTC PA inhibitor rapidly inhibits urokinase and tissue plasminogen activator with an apparent second-order rate constant of 3-5 x 10(7) M-1 X s-1. The inhibitor forms stable covalent complexes with both urokinase and tissue plasminogen activator, with which plasmin, trypsin, and factor Xa apparently do not compete. Complex formation is saturable and requires the active site of the PA. The mass of the inhibitor-PA complex is 50,000 daltons greater than that of PA alone, consistent with an Mr for the PA inhibitor of 50,000 as demonstrated directly by reverse fibrin autography. The HTC PA inhibitor does not inhibit thrombin and differs in its kinetic and biochemical properties from protease nexin.
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PMID:Characterization of the dexamethasone-induced inhibitor of plasminogen activator in HTC hepatoma cells. 293 42

A study of the absorption of 300 micrograms of 1-deamino-8-D-arginine vasopressin (DDAVP) given intranasally to normal blood donors was carried out to determine (a) the correlation between plasma levels of DDAVP and the percent rise of factor VIII procoagulant activity (VIII:C) and (b) the efficacy, specificity and safety of this treatment in increasing the recovery of factor VIII:C in donated blood. The maximum drug concentration was highly correlated to the maximum percent rise of VIII:C (r = 0.858, p less than 0.01). A differentiated effect of DDAVP on increases of VIII:C, VIII:Ag, vWF:Ag and vWF multimers was observed. A transient rise of fibrinopeptide A from 5 to 16 ng/ml, 30 min post-DDAVP, was not accompanied by changes in fibrinogen levels or generation of detectable factor Xa or thrombin. DDAVP had no effect on the factor XII-dependent pathway of plasminogen activation, or on the donor's vital signs and hematological parameters. Side effects were minor and of short duration. Intranasal DDAVP treatment of blood donors is considered to be a practical means of improving the recovery of VIII:C from normal donors.
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PMID:Effectiveness, specificity and safety of intranasal 1-deamino-8-D-arginine vasopressin treatment of normal blood donors. 297 94

BRL 26921 (Eminase registered trade mark in Belgium, Germany and The Netherlands) is the p-anisoyl derivative of the primary (human) lys plasminogen-streptokinase activator complex (APSAC). The acyl-enzyme has the theoretical advantage of causing fibrinolysis in situ in the presence of fibrin clotbound plasminogen. It was administered to 34 patients with severe pulmonary embolism (PE) in an open multicentre study. PE was suspected on clinical, blood gas, ECG, and radiographic data. Pulmonary angiograms performed pre- and post-treatment confirmed the diagnosis and were assessed using the Miller Index (MI). Fibrinogen, plasminogen, alpha-2-antiplasmin, fibrinogen degradation products (FDP), activated partial thromboplastin time (APTT), partial thromboplastin time (PTT) were closely monitored before and after each administration of APSAC. Median angiographic improvement was 50% (range 0-94%). The following adverse events were reported: bleeding at puncture sites (n = 12), haematuria (n = 1), epistaxis (n = 3), fever (n = 2). A blood transfusion was given in one patient with an inguinal haematoma. Systemic fibrinogenolysis occurred in 20/28 patients.
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PMID:Thrombolytic treatment of pulmonary embolism with APSAC. 306 87

Mice infected with Plasmodium berghei, during the ten days of infection, showed significant pulmonary oedema, delayed activated partial thromboplastin time, augmented plasma fibrinolytic activity, oscillations in fibrinogen and unchanged plasminogen levels. These alterations can be expected to cause the release of inflammatory peptides, leading to increased vascular permeability and the generation and/or maintenance of the pronounced pulmonary oedema affecting these animals.
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PMID:Plasmodium berghei: pulmonary oedema and changes in clotting and fibrinolysis during infection in mice. 307 22

Twenty-one patients, 14 with haemophilia A and seven with haemophilia B, completed a double-blind crossover study to evaluate the effects of danazol on factor VIII and factor IX levels. Clotting and immunoradiometric assays were used to measure factor levels at baseline, 2 weeks and 8 weeks on both danazol and placebo. Fibrinogen, plasminogen and activated partial thromboplastin time were measured on all patients during placebo and danazol treatment. Although plasminogen levels rose significantly (P less than 0.01) and fibrinogen decreased (P less than 0.01), factor VIII and IX levels did not change. While on danazol, three patients had increased bleeding and shortened euglobulin lysis times compared to their baseline levels. We conclude that danazol does not raise factor VIII or IX levels and increases bleeding in some patients.
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PMID:Danazol fails to increase factor VIII or IX levels in a double-blind crossover study of patients with haemophilia A and B. 309 73


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