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)

The diagnosis of von Willebrand's disease can be made by a selected series of easily performed clotting tests. A STudy of 36 patients with the disease (all but one with a mild form) revealed a significantly increased reaction time in the thrombelastogram from 210 plus or minus 33 percent to 270 plus or minus 69 percent (P less than 0.001), and of the partial thromboplastin time from 43 plus or minus 3s to 54 plus or minus 9s (P less than 0.001 than 0.001). Factor VIII activity was corresponding significantly reduced from normal (127 plus or minus 51 percent) to 51 plus or minus 12 percent (P less than 0.001). Other plasma factors and platelet counts were within normal limits. A platelet defect was indicated by an abnormal change in the speed of clot formation (k-time) from 162 plus or minus 39 percent to 341 plus or minus 121 percent (P less than 0.001), maximal thrombelasticity from 121 plus or minus 16 percent to 75 plus or minus 22 percent (P less than 0.001), and marked reduction in platelet-factor 3 liberation from 122 plus or minus 59 percent to 23 plus or minus 16 percent (P less than 0.001). An increase in bleeding time, from 162 plus or minus 41s to 204 plus or minus 128s (P less than 0.05), was not always present. Recently introduced immunological methods for determining factor VIII and factor VIII-associated protein, as well as special platelet-function tests, give further information on the pathogenesis of the bleeding disease, but their complexity restricts them to special laboratories.
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PMID:[Coagulation tests in von Willebrand's disease(author's transl)]. 109 30

A case report of a Factor VIII deficient hemophiliac, who underwent surgery for a glioblastoma, is presented. Emphasis is placed on diagnosing the hemostatic deficiency by the use of four hematological tests: bleeding time, platelet count, partial thromboplastin time, and prothrombin time. With close cooperation of a hematologist during the intraoperative and postoperative period, there should be a low mortality associated with intracranial surgery in a hemophiliac patient.
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PMID:Removal of an intracranial glioblastoma in a hemophiliac. 118 86

The effects of a contraceptive with a low estrogen content (Neogynon), the estrogen component (50 mcg ethinyl estradiol) and consecutively the gestagen component (250 mcg D-Norgestrel) of the contraceptive on blood coagulation and fibrinolysis were studied in 8 women. Each treatment cycle was followed by a control cylce. At various times of the control and therapy cycles coagulation and fibrinolytic parameters were investigated. Statistical analyses were performed using multivariate 2-factorial analysis of variance. Plasminogen exhibited a statistically significant increase during the treatment with ethinyl estradiol and the combination of this steroid with D-norgestrel. No significant changes were found for all other parameters, including partial thromboplastin time, fibrinogen, Factors X, IX, VIII, Factor VIII-related antigen, antithrombin III, and fibrin(ogen)degradation products.
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PMID:[Blood coagulation and fibrinolysis in women receiving estrogen, gestagen and estrogen-gestagen-contraceptives (author's transl)]. 127 96

A patient with combined factor V and factor VIII deficiency is presented. The bleeding manifestations were: easy bruising, post-traumatic bleeding, bleeding after tooth extractions. The main laboratory feature was a prolonged partial thromboplastin time which was corrected by the addition of adsorbed normal plasma but not by the addition of normal serum, hemophilia A plasma of another patient with combined factor V and factor VIII deficiency. The thromboplastin generation test was clearly abnormal and was corrected by the addition of adsorbed normal plasma but not by addition of normal serum. Prothrombin consumption was also defective. Prothrombin time was slightly prolonged too, Thrombin time, platelet and vascular tests were within normal limits and there was no hyperfibrinolysis. Factor VIII was 8% of normal, whereas factor V was 14% of normal. Factor VIII associated antigen was normal. All other clotting factors were within normal limits. The parents of the propositus were consanguineous (first cousins) but had normal factor V and factor VIII activity and normal factor VIII antigen. The same was true for other family members. The hereditary transmission of the condition appears autosomal recessive.
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PMID:Combined deficiency of factor V and factor VIII. A report of another case. 127 81

Platelet count, prothrombin time, and activated partial thromboplastin time provide a baseline to evaluate patients with known coagulopathy, as well as present an opportunity to diagnose disease in previously symptom free patients. Current hematologic management of patients with Von Willebrand's disease uses heated Factor VIII that allows patients to undergo orthognathic surgery without significant risk of disease transmission from banked blood products.
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PMID:Preoperative laboratory assessment of hemostasis for orthognathic surgery. 140 16

A 2-year-old Japanese girl with easy bruising and arthropathy was demonstrated to have severe hemophilia A (Factor VIII activity: less than 0.01 U/ml). She had normal 46XX karyotype. Her brother also had hemophilia A, and her mother and grandmother seem to be hemophiliac carriers. Additionally, activated partial thromboplastin time (APTT) of the patient was disproportionately prolonged and there were reduced levels of coagulation factor XII in the patients and members of the maternal trait which are compatible with heterozygous factor XII deficiency. Her father had both normal factor VIII and factor XII levels. Southern blotting analysis of genomic DNA from the propositus and family members with factor VIII and factor XII DNA probes revealed no gross alterations. This patient represents a female hemophilia A combined with heterozygous factor XII deficiency. Nonrandom inactivation of a normal X-chromosome (extreme lyonization) may be the basis for the expression of hemophilia A in this female patient.
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PMID:A female hemophilia A combined with hereditary coagulation factor XII deficiency: a case report. 155 Jan 5

Various haemostatic analytes were systematically evaluated for four months pre-partum and five months post partum in 14 healthy mares. The plasma fibrinogen concentration and both Factor VIII:C and von Willebrand factor activity showed gradual increases from mid-gestation and reached maximal, or near maximal activity at parturition. These increases were paralleled by an increase in plasma fibronectin concentration, the appearance of fibrinogen degradation products, and a modest rise in antithrombin III concentration. In contrast, the activity of Factor VII and Factor IX, and the one-stage prothrombin (PT) time and the activated partial thromboplastin (APTT) time remained relatively constant throughout the pre- and post parturient period.
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PMID:Evaluation of the haemostatic profile in the pre- and post parturient mare, with particular focus on the perinatal period. 155 43

Generation of coagulation factor Xa by the intrinsic pathway protease complex is essential for normal activation of the coagulation cascade in vivo. Monocytes and platelets provide membrane sites for assembly of components of this protease complex, factors IXa and VIII. Under biologically relevant conditions, expression of functional activity by this complex is associated with activation of factor VIII to VIIIa. In the present studies, autocatalytic regulatory pathways operating on monocyte and platelet membranes were investigated by comparing the cofactor function of thrombin-activated factor VIII to that of factor Xa-activated factor VIII. Reciprocal functional titrations with purified human factor VIII and factor IXa were performed at fixed concentrations of human monocytes, CaCl2, factor X, and either factor IXa or factor VIII. Factor VIII was preactivated with either thrombin or factor Xa, and reactions were initiated by addition of factor X. Rates of factor X activation were measured using chromogenic substrate specific for factor Xa. The K1/2 values, i.e., concentration of factor VIIIa at which rates were half maximal, were 0.96 nM with thrombin-activated factor VIII and 1.1 nM with factor Xa-activated factor VIII. These values are close to factor VIII concentration in plasma. The Vsat, i.e., rates at saturating concentrations of factor VIII, were 33.3 and 13.6 nM factor Xa/min, respectively. The K1/2 and Vsat values obtained in titrations with factor IXa were not significantly different from those obtained with factor VIII. In titrations with factor X, the values of Michaelis-Menten coefficients (Km) were 31.7 nM with thrombin-activated factor VIII, and 14.2 nM with factor Xa-activated factor VIII. Maximal rates were 23.4 and 4.9 nM factor Xa/min, respectively. The apparent catalytic efficiency was similar with either form of factor VIIIa. Kinetic profiles obtained with platelets as a source of membrane were comparable to those obtained with monocytes. These kinetic profiles are consistent with a 1:1 stoichiometry for the functional interaction between cofactor and enzyme on the surface of monocytes and platelets. Taken together, these results indicate that autocatalytic pathways connecting the extrinsic, intrinsic, and common coagulation pathways can operate efficiently on the monocyte membrane.
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PMID:Functional assembly of intrinsic coagulation proteases on monocytes and platelets. Comparison between cofactor activities induced by thrombin and factor Xa. 161 61

The effects of physical training on hemostatic parameters were evaluated in 56 postmyocardial infarction (MI) patients before and after one month of systematic physical training and in 30 control post-MI patients, who did not undergo such training. There were no significant changes in prothrombin time (PT) and alpha 1-antitrypsin (alpha 1AT) at the beginning and end of the study in either group. Levels of fibrinogen, Factor VIII: C (VIII:C) and von Wildebrand antigen (vWf:Ag), and activities of ATIII and plasminogen (Plg) were significantly decreased in the group with physical training (p less than 0.05), while values were unchanged in the control group. Hematocrit, platelet counts, and alpha 2-plasmin inhibitor (alpha 2PI) activities also decreased in the physical training group (p less than 0.05). In contrast, these variables increased in the control group (p less than 0.05). Activated partial thromboplastin time (aPTT) tended to be prolonged in the group with physical training, while it was shortened in the control group. In a subset of 20 patients with physical training, resting levels of plasmin-alpha 2PI complex (PIC), thrombin-antithrombin III complex (TAT), protein-C (P-C:Ag), plasminogen activator inhibitor-1 (PAI-1), VII:C, and P-C activities had significantly decreased after one month of physical training (p less than 0.05), although tissue plasminogen activator activities remained unchanged. Physical training appeared to suppress coagulability as indicated by the decrease in fibrinogen, VIII:C, vWf:Ag, VII:C, and TAT, and prolongation of aPTT. The decrease in plasminogen, t-PA:Ag, alpha 2PI, PAI-1, and PIC after physical training may result from the decreased coagulability. In conclusion, physical training appears to induce a suppression of the coagulation system in patients in the recovery phase of MI.
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PMID:Blood coagulability and fibrinolytic activity before and after physical training during the recovery phase of acute myocardial infarction. 162 56

The decay of human coagulation factor VIIIa has been studied by kinetic methods that ensure no interference through proteolytic feedback. The rate of decay of factor VIIIa activity was found to vary with the activator used to activate factor VIII. Thrombin-activated factor VIII-von Willebrand factor complex (fVIII-vWf) decayed at a rate of 0.31 min-1, whereas factor Xa-activated fVIII-vWf decayed at 0.11 min-1 under the same conditions. Factor VIII free of von Willebrand factor (factor VIII: C), although decaying at a generally slower rate after activation, still showed a dependence of decay rate on activator: thrombin-activated factor VIII:C decaying at a rate of 0.06 min-1, and factor Xa-activated factor VIII: C at 0.01 min-1. Readdition of von Willebrand factor (18 micrograms/ml) to factor VIII:C did not alter the observed activity or decay rate. The decay of the two species of factor VIIIa was studied, using the fVIIIa-vWf complex, in the presence of varying levels of factor IXa. Plots of reciprocal decay rates vs factor IXa concentration were linear, and nearly parallel for the two factor VIIIa species, with a mean slope of 0.56 min.nM-1. In addition to these studies, we have confirmed previous studies showing that the two forms of factor VIIIa differ in cofactor activity, but they do so in the same ratio as in their decay rates. We suggest that this difference and that observed in decay rate have a common cause, and incorporate this into a potential kinetic model of factor VIII activation and decay.
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PMID:Thrombin-activated and factor Xa-activated human factor VIII: differences in cofactor activity and decay rate. 163 34


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