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)

Antithrombin III, purified to homogeneity according to polyacrylamide gel disc electrophoresis and immunoelectrophoresis, inhibited the activity of purified factor IXa and Xa, whereas factor VII was not inhibited either in the active or in the native form. Antithrombin III is the single most important inhibitor of factor Xa in plasma. Factor Xa does not, however, reduce the activity of antithrombin III against thrombin.
 ...
PMID:The effect of antithrombin III on the activity of the coagulation factors VII, IX and X. 6 31

A follow-up study of blood clotting and platelet aggregation was performed on 21 women who had received long-term hormone replacement treatment with conjugated equine oestrogens. The prothrombin time and factor VII and X values were significantly accelerated after three months, but there was no further increase with continual administration for 18 months. After 12 to 18 months' treatment, however, thrombin-induced platelet aggregation (Chandler's tube) was also significantly accelerated, which suggested a widening spectrum of effect. No overall acceleration of "intrinsic" clotting (partial thromboplastin time and thromboelastography) was found during the study, but the relatively small numbers may have been responsible. Further efforts are therefore required to find formulations and doses of oestrogens which, while relieving menopausal symptoms, cause less acceleration of blood clotting and platelet aggregation.
 ...
PMID:Conjugated equine oestrogens and blood clotting: a follow-up report. 19 5

Detailed coagulation studies were performed in a group of 19 patients with primary hepatocellular cancer (PHC) and the results were compared statistically with the findings in 19 control subjects. Various funcitonal and immunochemical methods were employed in determining the possible presence of functional or structural coagulant protein abnormalities. The patient group was characterized by prolonged prothrombin times, partial thromboplastin times, and Reptilase times, increased levels of fibrinogen, factor VIII, and factor VIII-related antigen, moderately devreased levels of factor V, factor IX, factor X, antithrombin III, and plasminogen, and reduced levels of factor II and factor VII. Functional, immunochemical, and biochemical analysis failed to detect the presence of acquired protein abnormalities. These findings indicate that hemostatic changes in primary hepatocellular cancer are nonspecific in character. Severe alterations in the plasma levels of one or more of these hemostatic factors may occur.
 ...
PMID:Hemostatic factors in primary hepatocellular cancer. 19 99

Cancer procoagulant A (CPA) was originally described in extracts of tumor tissue, but whether this represented a quantitative and/or a qualitative difference from procoagulant activity in normal tissue extracts was not clear. Procoagulant activity was quantitated in extracts of 12 matched normal and malignant human tissue samples from the large intestine, breast, lung, and kidney. The specific activity of procoagulants in the tumor extracts was not greater than that in the extracts of normal tissue. Two enzymatic characteristics of CPA that distinguish it from tissue thromboplastin are its inhibition by diisopropylfluorophosphate (DFP) and its lack of dependence on factor VII. These specific tests were used to evaluate qualitative differences between procoagulants from normal and malignant intestinal tissues. In the paired normal and malignant tissue extracts, all tumor samples were inhibited by DFP and were active in factor VII-depleted bovine plasma (F7D-BP). In contrast, the extracts of normal tissue were insensitive to DFP and, except for one extract, were inactive in F7D-BP. Four of 9 other tumor extracts (44%) were positive for both of these tests for CPA, whereas the other 5 extracts were positive for only one of the two tests. The results suggest that extracts of normal and malignant tissues contained similar levels of procoagulant. However, malignant tissue contained a procoagulant enzymatically different from normal tissue thromboplastin. Furthermore, most of the malignant tissue extracts seemed to contain little or no thromboplastin.
 ...
PMID:Comparison of procoagulant activities in extracts of normal and malignant human tissue. 28 92

The activated parial thromboplastin time is susceptible to changing concentrations of factor VII even in the presence of heparin. Heparin delays, but does not abolisn, thrombin generation, and this delay is obviated by factor VIII. It is not known if activated parial thromboplastin time shortened by increased factor VIII demands an increase in heparin administration.
 ...
PMID:Heparin monitoring and thrombosis. 44 97

A new factor VII abnormality is presented. The propositus was a 9-yr-old child who presented a mild bleeding tendency characterized by epistaxis and easy bruising. The parents were not consanguineous, but they came from the same area. The laboratory features were mild prolongation of prothrombin time and P.P. test and normal partial thromboplastin and Stypven cephalin clotting times. The Thrombotest was moderately prolonged. Factor VII was 40%-50% of normal using rabbit or human brain thromboplastin, but only 13%-24% using ox brain thromboplastin. Factor VII cross-reacting material (CRM) was about 50% of normal. The father, a paternal aunt, and a paternal cousin showed similar clinical and laboratory findings. The brother of the propositus, the mother, and other members of her family showed about 50% factor VII activity and CRM and were considered to be heterozygotes for true factor VII deficiency. Similar findings were also present in the father and in the brother of the affected cousin. The defect in the propositus seems to consist of a double heterozygosity between abnormal factor VII and heterozygous factor VII true deficiency. The factor VII abnormality appears to consist of abnormal reactivity toward ox brain tissue thromboplastins and appears to be different from previously described factor VII abnormalities. The name factor VII Paudua2 is proposed for this condition.
 ...
PMID:Factor VII Padua 2: another factor VII abnormality with defective ox brain thromboplastin activation and a complex hereditary pattern. 44 74

An animal model for the production of stasis thrombi was employed to obtain the data reported in this study. Rabbits treated with warfarin (1.5 mg/kg/day) exhibited a maximal increase in prothrombin time and decreases in factor VII, factor X, and prothrombin within 48 hr with no additional changes occurring after 10 days of drug administration. In contrast, Xa inhibitory activity was unchanged after 48 hr of warfarin treatment but was significantly increased by the tenth day. When thrombosis was induced by infusions of 60 micrograms of tissue thromboplastin, the warfarin regimen produced an antithrombotic effect by the sixth hour, which increased to significance by day 2 and was further significantly increased by day 10. These three stages correspond to the initial depletion of the vitamin K-dependent clotting factors, the maximal depletion of these proteins, and the maximal increase in Xa inhibitory activity, respectively. Thus these experiments separate the antithrombotic potential of warfarin into two components: an early effect related to the decrease in factor VII and a delayed augmentation of Xa inhibitory acticity. Intravenous heparin alone (5 U/kg) did not protect against infusions of 60 micrograms of tissue thromboplastin but did provide an antithrombotic effect against 45 micrograms of the same infusate. Higher doses of heparin, however, did protect against infusion of 60 micrograms of tissue thromboplastin. After 48 hr of warfarin treatment, 5 U/kg heparin increased protection against 60 micrograms of tissue thromboplastin to a degree equivalent to that provided after 10 days of warfarin therapy alone.
 ...
PMID:The antithrombotic effects of warfarin and heparin following infusions of tissue thromboplastin in rabbits: clinical implications. 46 82

Evidence of developmental evolution of coagulation can be seen when the studies of 10 thriving extremely premature (EPT) infants are compared to normal full-term (FT) infants. The prothrombin time, partial thromboplastin time, and thrombin time all became shorter with increasing gestational age. Fibrinogen levels and platelet counts appear to be comparable to term infant and adult levels. Fibrin degradation products (FDP) of 10 micrograms/ml or less were found in the thriving EPT infants. When compared to healthy full-term infants, there is a definite gestational dependency of anti-thrombin III levels. Factors II and VII appear to be related to intrauterine maturation after the age of viability (24 wk), but factor VII-X complex does not. The contact factors XI, XII, high molecular weight kininogen (Fitzgerald factor), and prekallikrein (Fletcher factor) are all markedly decreased in thriving EPT infants. The mean factor V level is lower than that found in FT infants. This study confirms a gestational age dependency of factor VIII activity. The ratio of factor VIII antigen to factor VIII clotting activity is increased (2.8 vs 1.01 in FT and adults). Thriving small for gestational age (SGA) infants had coagulation studies which were not statistically different from those of thriving EPT infants. The coagulation changes which occurred in severely ill EPT were mainly in the factors which decrease during intravascular coagulation (factors I, V, and VIII). The present study suggests that because of the high antigen to activity ratio seen in thriving EPT infants, a dysfunctional or fetal factor VIII may have been produced. However, the further elevation of this ratio in the severely ill EPT infants is in keeping with a pathologic proteolysis or increased endothelial release of factor VIII antigen.
 ...
PMID:Coagulation studies in extremely premature infants. 52 93

The one-stage prothrombin time test for tissue thromboplastin activity was evaluated using the correction method. A strong influence of the intrinsic system was seen depending on the clotting time and the type of tubes. This test was unsuitable for quantitative comparison of thromboplastin activity of different preparations. Subsequently a two-stage assay for human thromboplastin is described using purified human factor VII, artifically prepared factor VII reagent, and a phospholipid suspension. The correction method, applicated to this two-stage assay, resulted in a rectilinear dose-response curve when the clotting times of a thromboplastin dilution series were plotted against the reciprocal of the concentrations. Using this test system it could be shown that thromboplastin from porcine tissue can activate human factor VII quite well, while that from bovine tissue cannot.
 ...
PMID:Determination of tissue thromboplastin activity. 55 36

During the early events of coagulation of human blood by the intrinsic pathway, factor XII is activated to a form which can activate factor XI, and is proteolytically fragmented to smaller species (30,000 daltons and 70,000 daltons) which have lost most of the ability to activate factor XI but which can activate prekallikrein rapidly. The effect of these fragments on factor VII was studied. It was found that these Hageman factor fragments promoted rapid proteolysis of one-chain factor VII to a more active two-chain form. The amino-terminal sequences of the chains of activated factor VII were found to be Ala-Asx-Gly- and Ile-Val-Gly-, the same as were earlier observed after activation of factor VII by activated factor X. This finding indicates that initiation of coagulation by the intrinsic pathway also primes the extrinsic pathway.
 ...
PMID:Activation of bovine factor VII by hageman factor fragments. 56 32


1 2 3 4 5 6 7 8 9 10 Next >>