scholarly journals The Measurement of the Ratio of Factor VII Activity Utilizing Bovine Tissue Thromboplastin and Human Tissue Thromboplastin in Hypercoagulable State

1993 ◽  
Vol 4 (1) ◽  
pp. 15-22
Author(s):  
Osamu TAKAMIYA ◽  
Nobuo OKUMURA ◽  
Kenichi FURIHATA
Keyword(s):  
Human Tissue ◽  
Hypercoagulable State ◽  
Factor Vii ◽  
Bovine Tissue ◽  
Tissue Thromboplastin

The Activation of Human Factor IX

1975 ◽  
Vol 33 (03) ◽  
pp. 553-563 ◽  
Author(s):  
B Østerud ◽  
K Laake ◽  
H Prydz
Keyword(s):  
Molecular Weight ◽  
Sodium Dodecyl ◽  
Apparent Molecular Weight ◽  
Factor Ix ◽  
Factor Vii ◽  
Activate Factor ◽  
Human Factor Ix ◽  
Factor Xia ◽  
Tissue Thromboplastin ◽  
Native Factor

SummaryThe activation of factor IX purified from human plasma has been studied. Factor XIa and kallikrein separately activated factor IX to factor IXa. In both cases factor IX a had an apparent molecular weight of about 42–45000 in sodium dodecyl sul-phate-polyacrylamide disc gel electrophoresis compared with a molecular weight of about 70000 for the native factor IX. The activation by XIa required Ca2+-ions whereas Ca2+-ions did not influence the activation by kallikrein. A mixture of tissue thromboplastin and factor VII or RusselPs-viper venom alone did not activate factor IX. Trypsin activated and plasmin inactivated factor IX.

Ultramicroscopic and Coagulation-Fibrinolytic Findings Induced by Tissue Thromboplastin

1979 ◽  
Author(s):  
H Nagata ◽  
T Seya ◽  
Y Oguma ◽  
M Yamauchi ◽  
T Murakoshi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Electron Microscope ◽  
Transmission Electron Microscope ◽  
Hypercoagulable State ◽  
Membrane Structures ◽  
Transmission Electron ◽  
Single Sheet ◽  
Tissue Thromboplastin ◽  
Short Time

We have studied the ultrastructures of tissue thromboplastin (T.Tbp) to demonstrate how It changes during coagulation.[Materials and Methods] T.Tbp from lungs of rabbits was used for these studies. It was injected into ear veins of rabbits. Lungs were resected at several seconds, 10sec, 1 min, 5 min, 24 hrs or 48 hrs after the injection. They were examined by transmission electron microscope.[Results] Concentrically arranged membrane structures of the injected T.Tbp disappeared in extremely short time after the injection. 1 min after the injection, fibrin fibers were seen between single sheet of membrane and endothelial cells of capillaries. In the rabbit which had died suddenly after the injection of T.Tbp, multiple pulmonary thrombi made of fibrin and platelets were seen in capillaries. The endothelial cells of capillaries were destroyed and interstitial tissues were edematous.The hypercoagulable state was seen 10~30sec after the start of the injection, indicating the shortening of r of TEG. Then, it gradually returned the level before injection. Moreover, changes of the measurements of fibrinogen, antiplasmin and prekallikrein were also seen after the injection.

Thrombotic Events in Homozygotes with a Proven or Highly Probable Arg304Gln Factor VII Mutation (FVII Padua)1): Only Limited Replacement Therapy is Needed in Case of Surgery

2019 ◽  
Vol 19 (3) ◽  
pp. 233-238
Author(s):  
Antonio Girolami ◽  
Elisabetta Cosi ◽  
Silvia Ferrari ◽  
Bruno Girolami ◽  
Maria L. Randi
Keyword(s):  
Replacement Therapy ◽  
Thrombotic Event ◽  
Factor Vii ◽  
Compound Heterozygous ◽  
Activity Levels ◽  
High Prevalence ◽  
Molecular Studies ◽  
Tissue Thromboplastin ◽  
The Difference ◽  
Compound Heterozygotes

Objective: To investigate the prevalence of thrombotic events among patients with proven or highly probable homozygosis for the Arg304Gln (Factor VII Padua) defect or compound heterozygosis containing the Arg304Gln mutation. Methods: Homozygotes and compound heterozygotes proven by molecular studies to have the Arg304Gln mutation were gathered from personal files and from two PubMed searches. In addition, patients with probable homozygosis on the basis of clotting tests (discrepancies among Factor VII activity levels according to the tissue thromboplastin used) were also gathered. Results: 30 proven homozygotes and 17 probable ones were gathered together with 8 compound heterozygotes. In the latter use, the associated mutation was Cys135Arg (twice), Gly180Arg, Arg304Trp, Arg315Trp, His348Gln, Gly365Cys. The prevalence of venous thrombotic events was 16.6, 11.8 and 11.1 percent, respectively for the three groups of patients. Heterozygotes showed no thrombotic event. The difference for proven homozygotes was statistically significant, while for the other groups only a trend was present. Conclusion: proven homozygous or compound heterozygous patients with the Arg304Gln mutation showed a higher than expected incidence of thrombotic events. The same is true for probable cases gathered only on the basis of clotting tests. These patients, because of their frequent lack of bleeding and for their relatively high prevalence of thrombosis should probably receive only limited replacement therapy in case of surgical procedures.

Involvement Of Human Factor IX In Tissue Thromboplastin Induced Coagulation

1981 ◽  
Author(s):  
A M H P van den Besselaar ◽  
I E Ram ◽  
R M Bertina
Keyword(s):  
Tissue Factor ◽  
Polyacrylamide Gel Electrophoresis ◽  
Fold Increase ◽  
Factor Ix ◽  
Factor Vii ◽  
Factor Xii ◽  
Free System ◽  
Plasma Coagulation ◽  
Human Factor Ix ◽  
Tissue Thromboplastin

This study is concerned with the question whether activation of factor IX by factor VII - tissue thromboplastin contributes to the rate of plasma coagulation. The protein component of tissue factor was partially purified from human brain. Its molecular weight as deduced from SDS - polyacrylamide gel electrophoresis was about 48,000. Reconstitution of thromboplastin activity was obtained by mixing apoprotein and phospholipids in the presence of Triton X-100 and subsequent removal of Triton by adsorption to Biobeads SM-2. Reconstituted tissue factor greatly accelerated the activation of factor IX by isolated factor VII in the presence of calcium ions. In a contact free system (plasma from a patient with congenital factor XII deficiency; factor XII<0.001 Unit/ml) plasma coagulation times (tc) were determined as a function of apoprotein concentration (at constant phospholipid) both in the presence and absence of factor IX. At high apoprotein concentration tc showed to be independent of factor IX, whereas at low apoprotein concentration the removal of factor IX resulted in a 2 - 3 fold increase of tc. The involvement of the tissue factor - factor VII complex in this phenomenon was evaluated using a specific anti-factor VII serum. The results indicate that activation of factor IX by factor VII - tissue thromboplastin does not significantly contribute to the rate of plasma coagulation.

THE EPIDEMIOLOGY OF HAEMOSTATIC AND OTHER VARIABLES IN CORONARY ARTERY DISEASE

1987 ◽  
Author(s):  
T W Meade
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Fibrinogen Level ◽  
Plasma Fibrinogen ◽  
Blood Cholesterol ◽  
Hypercoagulable State ◽  
Factor Vii ◽  
Plasma Fibrinogen Level ◽  
Increased Risk ◽  
Artery Disease

The increase in the clinical manifestations of coronary artery disease (CAD) since the 1920s cannot be explained solely in terms of atheroma. Another major process such as thrombogenesis must also be involved. Pathological studies show that thrombosis contributes not only to myocardial infarction but to nearly all cases of sudden coronary death as well. Epidemiologically, it is the coagulation system rather than platelet function that has so far been more rewarding in attempting to identify characteristics of the haemostatic system that are associated with the subsequent risk of CAD. In particular, two clotting factors - factor VII coagulant activity, VIIc, and fibrinogen - may be involved. Factor VII has several characteristics that are required for a system to secure rapid haemostasis after injury. The question is whether an exaggeration of the physiological state of readiness implied by these features may predispose to thrombosis. There are at least four pathways through which high fibrinogen levels, however they are determined, may operate to increase the risk of CAD - involvement in atherogenesis, determination of blood and plasma viscosity, effects on platelet aggregability and an influence on the amount of fibrin formed. The prospective Northwick Park Heart Study (NPHS) has shown an association between high VIIc levels and an increased risk of CAD. NPHS and three other prospective studies have also demonstrated a clear association between high levels of plasma fibrinogen and an increased risk of CAD, this association generally being stronger than for more familiar markers of risk such as the blood cholesterol level. There may well be an interaction between fibrinogen and blood pressure, the occurrence of high levels of both increasing CAD or stroke risk to a greater extent than would be expected from the sum of their separate effects. Several pathological and clinical observations support a “hypercoagulable state” not simply as a concept but as a demonstrable abnormality in which characteristics of the circulating blood influence the course of events. These include the effects of anti-thrombotic agents (particularly oral anticoagulants) on re—infarction rates and the likelihood that high VIIc levels lead to increased levels of thrombin production. The general epidemiology of VIIc and fibrinogen is consistent with the view that high levels of each are of pathogenetic significance. Thus, increasing age, obesity, oral contraceptive usage, the occurrence of the menopause and diabetes are all associated with high levels of VIIc and fibrinogen and with an increased risk of CAD. Psychosocial influences may increase the risk of CAD through effects on the plasma fibrinogen level. There is strong evidence that dietary habit, particularly the consumption of fat, is a leading determinant of the VIIc level. A substantial proportion of the relationship between cigarette smoking and CAD is probably mediated through the plasma fibrinogen level. The most radical implication of a “hypercoagulable state” is for the pharmacological prophylaxis of CAD which, it may turn out, is better approached by anti—thrombotic measures than by the use of lipid-lowering agents.

scholarly journals Immunologic Identification of Tissue Factor (Thromboplastin) Synthesized by Cultured Fibroblasts

Blood ◽  
1973 ◽  
Vol 41 (5) ◽  
pp. 671-678 ◽  
Author(s):  
Leo R. Zacharski ◽  
Leon W. Hoyer ◽  
O. Ross McIntyre
Keyword(s):  
Factor Viii ◽  
Tissue Factor ◽  
Coagulation Factors ◽  
Procoagulant Activity ◽  
Factor Vii ◽  
Cultured Fibroblasts ◽  
Procoagulant Effect ◽  
Tissue Thromboplastin ◽  
Thromboplastin Factor

Abstract Immunologic methods were employed in an attempt to identify a potent procoagulant present in homogenates of human skin fibroblasts cultured in vitro. The activity of this procoagulant was restricted to the early stages of coagulation and was heretofore considered to be due to tissue factor (tissue thromboplastin, factor III) either alone or in combination with one or more of the first-stage coagulation factors (VIII, IX, XI, XII). The present studies demonstrated that procoagulant activity was not diminished by incubation with anti-VIII or anti-IX antibodies of human origin or with anti-VIII antibody of rabbit origin. Furthermore, cell culture homogenates failed to bind antifactor VIII antibody and did not contain an inhibitor of the reaction between factor VIII and its antibody. By contrast, procoagulant activity was obliterated by an antibody to tissue factor protein regardless of whether plasmas deficient in factor VIII, IX, XI, or XII were used in the assay system. The antitissue factor antibody failed to block the procoagulant effect after tissue factor had complexed factor VII. The procoagulant, therefore, consisted entirely of tissue factor.

Multicentric Evaluation of a New PT Reagent Based on Recombinant Human Tissue Factor and Synthetic Phospholipids

1994 ◽  
Vol 71 (03) ◽  
pp. 292-299 ◽  
Author(s):  
R Bader ◽  
P M M Mannucci ◽  
A Tripodi ◽  
J Hirsh ◽  
F Keller ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Human Tissue ◽  
Regression Line ◽  
Coagulation Factor ◽  
Phosphatidyl Serine ◽  
Factor Vii ◽  
Rabbit Brain ◽  
Sensitivity Index ◽  
Mean Values ◽  
Automated Instrument

SummaryA new PT reagent based on recombinant human tissue factor and synthetic phospholipids (phosphatidyl choline and phosphatidyl serine) with defined fatty acid side chains was calibrated against BCT/253 and CRM 149R. A small but consistent bias in the International Sensitivity Index (ISI) value was obtained using either the human or rabbit brain reference material. ISI values were around 1.0 or slightly lower depending on the respective instrument. Mixing studies with factor deficient plasmas showed a high factor sensitivity especially for factor VII as compared to commercial rabbit brain or human placenta thromboplastin. In an international field trial the reagent was tested using fully or semi automated Electra™ coagulometers in 4 different laboratories. Results with normal samples were in excellent agreement among the different laboratories. Mean values were 10.9, 10.9, 11.0, 11,7 s with a range of 9.5 to 12.5 s. Results of males and females were not different. In patients with liver disease very similar PT activities were found as compared to sensitive rabbit brain or human placental thromboplastins. In normals and patients with oral anticoagulation INR values correlated very well against BCT (r = 0.98, regression line y =-0.07 + 0.9 x). The distribution of samples was linear over the whole range. In the comparison against sensitive rabbit brain thromboplastin or human placental thromboplastin similar correlations were found. In a few cases higher INR values were observed for the recombinant reagent especially in patients with intensive treatment. Factor assays in those patients showed at least the strong reduction of one vitamin Independent coagulation factor. Over all the linearity was better against the rabbit brain reagent than against the human placental reagent which is slightly less factor VII sensitive as shown in mixing studies with normal and factor VII deficient plasma. Precision studies in the 4 laboratories showed excellent reproducibility of lyophilised controls or local patient plasma pools for all reagents with a better performance of the recombinant reagent. C. V. values from day to day ranged from 1.3% to 5% for normal and abnormal controls.These results show that the recombinant PT reagent, especially in conjunction with a precise automated instrument, may improve the results of PT testing and thus may lead to better patient care.

The Role of Vitamins in Hemostasis

1975 ◽  
Vol 33 (02) ◽  
pp. 191-198
Author(s):  
Armand J Quick
Keyword(s):  
Vitamin K ◽  
Physiological Mechanism ◽  
Factor Vii ◽  
Clotting Factors ◽  
The Third ◽  
Abnormal Bleeding ◽  
Vitamin Q ◽  
Tissue Thromboplastin ◽  
And Control

SummaryThe physiological mechanism to prevent and control abnormal bleeding is dependent on three vitamins (C, K, and Q). Two of these are unequivocally established as essential for hemostasis while the existence of the third (Q) is supported by experimental evidence and by clinical and therapeutic observations (Quick 1972; Quick 1974). The interrelationship of these three vitamins has remained moot except for clue observations. Both vitamins C and K have a key structure in their molecules which supplies a redox mechanism, ascorbic acid and 2-methyl, 1,4-naphthoquinone, respectively. Both vitamins are concerned with growth. Lack of vitamin C, which clinically is the basic defect in scurvy, does not appear to cause a defect in blood coagulation while vitamin K affects the clotting mechanism by being essential for the production of four distinct clotting factors: prothrombin, factors VII, IX and X.In this presentation an attempt is made to correlate the action of the vitamin K-dependent clotting factors grouping them in a diagram to show how two systems of thrombin formation exist, one being essentially intrinsic, the second extrinsic requiring tissue thromboplastin and factor VII. The possible interlocking of vitamin Q in this mechanism is presented.

Treatment of Tissue Thromboplastin Membranes with Phospholipase C

1973 ◽  
Vol 30 (03) ◽  
pp. 509-518 ◽  
Author(s):  
E Bjørklid ◽  
A.-B Otnæss ◽  
E Storm ◽  
H Prydz ◽  
B. V Johansen ◽  
...  
Keyword(s):  
Human Brain ◽  
Phospholipase C ◽  
Morphological Changes ◽  
Phospholipid Fraction ◽  
Enzyme Treatment ◽  
Factor Vii ◽  
Gel Chromatography ◽  
Coagulation Activity ◽  
Binding Factor ◽  
Tissue Thromboplastin

SummaryTissue thromboplastin from human brain, partially purified by extraction with deoxycholate, gel chromatography and recombination of the protein (fraction A) and phospholipid (fraction B) fractions, was examined after treatment with phospholipase C (E.C. 3.1.4.3). Various morphological changes accompanied the loss in coagulation activity caused by the enzyme. All concentrically arranged vesicles (spherulites) disappeared. Instead, a large number of quite small vesicles and many big “blebs”, probably containing diglycerides, were seen. Fused membranes appeared after treatment with the enzyme. The phospholipid fraction (fraction B) showed similar structures as thromboplastin, but not quite the same morphological changes after enzyme treatment.Phospholipase C treatment probably caused a splitting of the concentrically arranged tissue thromboplastin membranes, which spontaneously rearranged to form new vesicles or were fused to other membranes. The hydrophilic parts of the phospholipids are required for coagulation activity, either because they impart a certain ultrastructure to the membrane, or because they participate in the coagulation process in a more direct way, e.g. by forming complexes with factor VII or by binding factor VII through calcium bridges.

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