Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four haemophiliacs with antibodies to factor VIII were treated on 7 occasions with fraction FEIBA. Satisfactory clinical results were achieved in patients receiving large doses of the preparation (63-105 units/kg). The administration of fraction FEIBA produced shortening of the whole blood clotting time but there was only a slight correction in the activated partial thromboplastin time. Two patients received prothrombin complex concentrate without clinical improvement in 1 case a good haemostatic effect was achieved after the infusion of cryoprecipitate and in 1 postoperative bleeding ceased with the administration of porcine factor VIII Immunosuppressive therapy with cyclophosphamide in 3 patients failed to prevent the anamnestic rise in antibody titer.
Acta Haematol Pol
PMID:[Treatment of patients with hemophilia A having antibodies to factor VIII]. 47 44

Factor IX concentrate was obtained using DEAE-Sephadex A-50 as an adsorbent. The yield of factor IX in vitro averaged 81%. Each bottle of the concentrate contained 288-512 u. of factor II, 96--360 u. of factor VII, 440--660 u. of factor IX and 256--680 u. of factor X. The results of studies showed trace amounts of factor Xa in the final product, in the range of 0.01--0.04 u/ml. The concentrate was found to be free of thrombin. In the years 1976--1977 the new concentrate was administered 48 times to 10 patients with severe haemophilia B. The in vivo recovery of factor IX was 27--65%. Clinical results of treatment were satisfactory in all patients. No significant changes were observed in platelet count, fibrinogen level and the concentration of fibrinogen degradation products after infusion of the concentrate. The ethanol gelation test was negative in all cases.
Acta Haematol Pol
PMID:[Preparation and clinical use of a new factor IX concentrate]. 66 30

Our studies showed that the nifedipine in daily doses of 30 mg/kg given to rabbits treated with a diet containing 1% cholesterol for 6 months, decreased cholesterol content in aorta homogenates, urine excretion of desmosines and prolonged partial thromboplastin time, while it did not alter serum lipids. These results may have some value for understanding of the antiatherogenic mechanism of nifedipine.
Pol J Pharmacol Pharm
PMID:Influence of nifedipine on aortal cholesterol content, blood coagulation and elastin metabolism in cholesterol-fed rabbits. 129 10

Prothrombin isolated from duck sodium citrate plasma was activated in a system containing duck factor Xa and calcium ions. Polyacrylamide gel electrophoresis showed that intermediates and the final product, thrombin, of Mr in the range 21 500-52 000 were present in the incubation mixture Serine and isoleucine were found to be the N-terminal amino acids of the intermediate form 1 and thrombin, respectively.
Acta Biochim Pol 1985
PMID:Activation of duck prothrombin by factor Xa and thrombin. 383 1

Pigs received for 24 weeks a high-lipid diet containing cholesterol and coconut oil. Blood lipid fractions were assayed, electrophoretic separation of lipoproteids was carried out, and tests for blood coagulation parameters (fibrinogen content, partial thromboplastin time, paracoagulation test, blood platelets aggregation) were carried out. In the blood serum of experimental animals the content of triglycerides, cholesterol, free fatty acids, lipid phosphorous and beta-lipoproteids gradually increased. A hyperlipidemia corresponding to type IV of Fredrickson was obtained. No parallel changes in the results of studies on blood coagulation parameters were observed.
Pol J Pharmacol Pharm
PMID:A model of experimental atherosclerosis in pigs. Part I. Study on blood lipids and coagulation. 731 19

The aim of the study was to evaluate the efficacy of low molecular weight heparine (enoxaparin) in comparison to heparin during haemodialysis (HD) in prevention of blood clotting chestry extracorporeal circulation. Enoxaparin (Clexan, Rhone-Poulenc Rorer, in syringes, 20 mg) was evaluated in 42 patients with end stage renal failure treated with HD. In the first part of study heparine and in the second part enoxaparin given into arterial lines were evaluated during 6 following HD with the same type of dialysator. Clotting of extracorporeal circulation and bleeding time from the needle site after HD were evaluated. Activated partial thromboplastin time (APTT) before, after 1 hour of HD and after HD during heparine and enoxaparin were measured. There was advantage of enoxaparin in 23 patients when compared to heparine. It was depended on the reduction of number of injections of enoxaparin when compared to heparine (22 patients have received heparine in 2 or more doses when only 5 patients have received enoxaparin in 2 doses) on the reduction of clotting events in extracorporeal circulation (16 events during heparine treatment -6.3% of all HD and 5 events during enoxaparin treatment -2.0% of all HD), and on the shortening of the bleeding time from the needle site after HD (5.9 +/- 3.4 min. during heparin and 4.5 +/- 1.6 min. during enoxaparin treatment; p < 0.02). Increase of APTT after 1 hour of HD when compared to the value from before HD was significantly lower during enoxaparin than heparine therapy (1.73 +/- 0.4 and 2.55 +/- 0.91 respectively; p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Pol Arch Med Wewn 1994 Jun
PMID:[Antithrombotic activity of low molecular weight heparin (enoxaparin) during hemodialysis in patients with terminal kidney failure]. 797 64

106 women was screened for a lupus anticoagulant. Activated partial thromboplastin time, tissue thromboplastin inhibition test and euglobulin lysis time was performed. Ten of 61 women (16%) with spontaneous multiple abortions, foetal death, intrauterine growth retardation (IUGR) and gestosis had one or two pathological results of tests while no one of the 41 women which had no pregnancy complication. Significance of difference between this two groups was verified by Fischer exact test (P less than 0.05).
Ginekol Pol 1995 Feb
PMID:[Hemostatic disturbances in women with unexplained fetal loss]. 857 82

The contact activation of intrinsic pathway in the coagulation system accompanied by plasma kallikrein-induced kinin generation is thought to be involved in the pathogenesis of diabetic retinopathy. Plasma prekallikrein (PPK), a proenzyme of plasma kallikrein, is a single-chain glycoprotein synthesized mainly in the liver. The aim of our study was to evaluate plasma prekallikrein level in diabetic patients and to examine the relationship between PPK and the metabolic control of diabetes and development of retinopathy. In 53 diabetic patients and 33 healthy subjects as controls the following parameters have been assessed: plasma prekallikrein, serum fructosamine, glycated haemoglobin HbA1c, prothrombin time, partial thromboplastin time and antithrombin III (AT III). Compared to the control group, PPK level was significantly higher in diabetics, especially in patients with proliferative retinopathy. The significant positive correlations have been found between PPK and HbA1c in diabetic patients and between PPK and serum fructosamine concentration but only in diabetics without retinopathy. No differences in prothrombin time and AT III have been observed between diabetics and healthy subjects. A suggestion is presented on increase of plasma prekallikrein level in diabetics due to hyperglycaemia-stimulated glycoprotein over-synthesis in the liver, what would confirm the role of kallikrein-kinin system in the pathogenesis of microangiopathy.
Pol Arch Med Wewn 1995 Aug
PMID:[Elevated plasma prekallikrein level in patients with diabetes]. 859 45

Tissue factor pathway inhibitor (TFPI) is a protease inhibitor with three tandem Kunitz-type inhibitory domains (K1, K2 and K3), which inhibits coagulation factor Xa via K2 domain and factor VIIa-tissue factor complex via K1 domain. Thus TFPI blocks the initial steps of the extrinsic coagulation pathway. TFPI is present in human plasma in three forms, i.e., an LDL/VLDL-associated form, an HDL-associated form and a free form. But the majority of in vivo TFPI is associated with the vascular endothelial cells. The interaction of TFPI with heparin has been demonstrated. The heparin binding site of TFPI (HBS-1) locates in its C-terminal basic portion. We found another heparin-binding site in K3 domain of TFPI, using each of the three Kunitz domains prepared by the limited cleavage of TFPI and also synthetic peptides mimicking the amino acid sequence of a Kunitz domain. These heparin binding sites of TFPI will play an important role for the association with endothelial cells, interacting with heparin sulphate on the surface. We have established a method to measure TFPI activities of lipoprotein-associated forms and a free form of TFPI in plasma and a method to measure a free form of TFPI antigen. We, then, applied these methods for the analysis of hypercholesterolemic patients. Relationship between plasma TFPI levels and endothelial cells-associated TFPI level will be discussed.
Pol J Pharmacol
PMID:Tissue factor pathway inhibitor; its structure, function and clinical significance. 911 30

Heparin cofactor II (HC II) is a plasma glycoprotein which inhibits thrombin but not factor Xa and which requires heparin or other glycosaminoglycans for its activation. Although several pedigrees have been reported in which 50% decreases in plasma HC II were associated with venous or arterial thrombosis, the role of HC II deficiency in inherited thrombophilia remains unproved. The present study was performed to determine the prevalence of HC II deficiency among patients with a history of venous thrombosis. HC II antigen was measured by electroimmunoassay in 122 unrelated patients with first episode of deep vein thrombosis developed before the age of 45 and in 114 healthy volunteers. Of the controls, 1 had a low HC II concentration (37%), while in the remaining 113, levels ranged from 65 to 180% with the mean value of 98.6 +/- 20.6%. In thrombosis patients, the mean HC concentration was 99.9 +/- 28.0%: individual values ranged from 52 to 180%. Seven patients (5.7%) exhibited values beneath the lower limit of the normal range (65%). These results indicate that HC II deficiency is more prevalent among patients with venous thromboembolism than in healthy subjects.
Pol J Pharmacol
PMID:Prevalence of heparin cofactor II deficiency in patients with a history of venous thrombosis. 911 38


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