Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.108 (TAT)
 2,389 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction of vitronectin-thrombin-antithrombin III (VN.TAT) complex with endothelial cells (EC) was investigated. Binding was specific and time- and concentration-dependent. Kinetics revealed an apparent dissociation constant of 16 nM and 1.7 x 10(5) binding sites/endothelial cell. The binding determinant of the ternary complex was located on the VN moiety. Since the association of VN to TAT adds its specific properties to the VN.TAT complex, the involvement of the heparin binding domain and the cell attachment site of VN was investigated. Neither addition of RGD peptide nor blocking of the vitronectin receptor with a monoclonal antibody interfered with VN.TAT binding to EC. Addition of heparin, a VN-derived peptide comprising two heparin binding consensus sequences or a monoclonal antibody directed against the heparin binding domain on VN, completely inhibited VN.TAT binding to EC. These results indicate that the interaction is mediated through the heparin binding domain of VN. Digestion of heparan sulfate proteoglycans resulted in a decrease of VN.TAT binding to EC, indicating the involvement of heparin-like structures on the EC surface. Our findings point to an unrecognized mechanism by which VN may act as scavenger in order to enhance the clearance of end products of the clotting system via binding of the ternary VN.TAT complex to the luminal surface of EC.
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PMID:Binding of vitronectin-thrombin-antithrombin III complex to human endothelial cells is mediated by the heparin binding site of vitronectin. 137 Aug 15

Functional antithrombin III levels were measured by factor Xa inhibition in 63 members of a large family with type 2 antithrombin III deficiency and individuals were classified as antithrombin III deficient or non-deficient according to the results. F1 + 2 and TAT complexes were measured using an ELISA and FPA levels were measured by radioimmunoassay. Thirty subjects (48%) were classified as antithrombin III deficient and 33 (52%) as antithrombin III non-deficient. The mean level of F1 + 2 was significantly higher in the deficient adults (0.87 +/- 0.26) compared to both the non-deficient adults (0.70 +/- 0.21) (p = 0.03) and the deficient adults receiving warfarin (0.16 +/- 0.01) (p less than 0.001). The differences in the mean values of TAT complexes and FPA between deficient and non-deficient individuals were not statistically significant. These findings suggest that untreated antithrombin III deficient subjects generate more thrombin than their non-deficient family members and that warfarin inhibits this thrombin formation. In this cross-sectional study, it is not possible to correlate the levels of the surrogate makers with future clinical outcome.
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PMID:Measurement of markers of activated coagulation in antithrombin III deficient subjects. 151 14

Anticoagulant activity of ionic and nonionic contrast media (CM) was investigated in vitro and in vivo. Based on the time course of FPA and TAT generations and gross examinations of the blood clots on the catheters placed in CM-blood mixtures [an 2 to 8 ratio (20% v/v)]. It was demonstrated that blood coagulation was activated during the period of 20 to 30 minutes when nonionic CM (iopamidol, iohexol) was employed, but no activation of blood coagulation was noted with ionic CM (diatrizoate, ioxaglate). Scanning electron microscopic examinations of the clots on the catheters revealed that fine fibrin meshwork fibers, in which many red blood cells were trapped in bound, were observed with nonionic CM. In contrast, no fibrin mesh was formed with ionic CM after 30 minutes. In vivo, antithrombin III and fibrinogen significantly decreased in the patients who underwent infusion of nonionic CM. Our studies confirmed that nonionic CM show weaker anticoagulant activity than do ionic CM. And these findings account for previous reported thromboembolic complications with the use of nonionic CM. Extreme caution should be therefore exercised when nonionic CM are employed during prolonged angiographic and interventional procedures.
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PMID:[Effects of uro-angiographic contrast media on blood coagulation--a scanning electron microscopic study on time dependent changes of blood clot and a clinical study]. 154 48

It has been suggested that unstable angina at rest, like acute myocardial infarction, might be associated with a thrombotic process. In order to study the hypothesis that myocardial ischemia during exercise could also be associated with an activation of blood coagulation and/or fibrinolysis, we investigated the presence of plasma markers of a prethrombotic or thrombotic state (thrombin-antithrombin III complexes TAT, prothrombin fragment F1 + 2, and D-dimers DD) in 100 consecutive patients with confirmed or suspected coronary artery disease during ergometric test with myocardial thallium-201 scintigraphy. Symptoms and scintigrams allowed to define three groups of patients: those showing no ischemia (n = 79) and those with symptomatic (n = 8) or silent myocardial ischemia (n = 13). Before exercise, DD and TAT levels were not significantly different among the three groups. On the other hand, the F1 + 2 levels were slightly albeit significantly higher in the patients without ischemia than in the patients with symptomatic or silent ischemia. After exercise, no significant difference was found between the three groups. Exercise induced a significant and parallel increase in both the TAT and the F1 + 2 levels (but not of the DD levels) in the three groups. Thus, our study does not support the hypothesis that myocardial ischemia, silent or symptomatic, is associated with an activation of plasma coagulation and fibrinolysis that can be distinguished from the exercise-induced thrombin generation.
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PMID:Effects of exercise test on plasma markers of an activation of coagulation and/or fibrinolysis in patients with symptomatic or silent myocardial ischemia. 160 40

Amidolytic chromogenic substrate assays are frequently used to determine the anticoagulant activities of various commercial heparins. With the help of a combined assay method heparin characterization is made possible using the TAT/XAT quotient under consideration of the simultaneous inhibition of the two serine proteases thrombin and factor Xa by antithrombin III. The test is primarily designed for qualitative characterization where a numerical value can be assigned to every heparin. However, quantitative aspects may also be evaluated.
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PMID:Evaluation of an amidolytic test for comparative calibration of HMW- and LMW-heparins. 166 65

In order to assess the thrombin and plasmin generation in vivo in disseminated intravascular coagulation (DIC), plasma levels of thrombin-antithrombin III (ATIII) complex (TAT) and plasmin-alpha 2-antiplasmin (a2AP) complex (PAP) were measured together with standard coagulation and fibrinolytic parameters in 80 patients with DIC. Both TAT and PAP were markedly elevated in patients with DIC. When plotted by the underlying disease categories, differences in the magnitude of the elevations of these complexes were recognized among groups. Patients with acute promyelocytic leukemia (APL) had the highest PAP, the lowest TAT/PAP ratio, low a2AP, and low fibrinogen, indicating that the most excessive fibrinolysis can occur in APL. Similar profiles, although less marked, were observed in patients with other leukemias and vascular diseases. Patients with sepsis showed the highest TAT/PAP ratio and the lowest PAP with no decrease in a2AP or fibrinogen, demonstrating a relatively impaired fibrinolysis. Patients with cancer had a relatively high TAT and high TAT/PAP ratio. In addition, both TAT and PAP were markedly elevated in patients with shock. From these, it was suggested that, although laboratory manifestations in DIC are extremely variable from patient to patient, underlying disorders are, at least in part, responsible for the observed variations. Recognition of this variable activation of coagulation and fibrinolysis would be helpful for the proper management of patients with DIC.
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PMID:Thrombin vs. plasmin generation in disseminated intravascular coagulation associated with various underlying disorders. 200 32

The present study was undertaken to determine whether the extent of Factor VII elevation correlated with the severity of coronary artery disease and whether zymogen or activated Factor VII was responsible for this elevation. A group of 69 patients with coronary artery disease with old myocardial infarction was compared with 28 control subjects. The patient groups showed elevated levels of Factor VII procoagulant activity (FVII:C) and more markedly elevated Factor VII antigen (FVII:Ag) levels than the control group; therefore they had a decreased FVII:C to FVII:Ag ratio. The increased Factor VII level in the patient groups was caused by elevated Factor VII zymogen levels, and not by activated Factor VII. Since FVII:C levels strongly correlated with the titer of thrombin-antithrombin III complexes in all patients, the hypercoagulable state accompanying severe coronary atherosclerosis seems to underlie the increase of FVII and TAT in the stable phase of myocardial infarction.
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PMID:Elevation of factor VII activity and mass in coronary artery disease of varying severity. 174 7

Increase of TAT is reflected by the generation of thrombin in hypercoagulable state. TAT might increase in DIC characterized by the formation of disseminated micro-thrombosis. DIC was classified into three groups according to the results of screening tests (FDP, platelet count, fibrinogen, prothrombin time). TAT values significantly increased in the stage of pre-DIC compared with the control group consisting of DIC prone underlying disease. Pre-DIC was easily detected by an increase of TAT during the clinical course. Management of high TAT began with the use of an anticoagulant such as heparin under the condition of sufficient ATIII level. The lowering effect of TAT was easily obtained by the anticoagulant. In ATIII-deficient DIC, the high TAT reduced with the substitution of ATIII concentrate, though a transient increase of TAT was found during the administration of ATIII. To reduce the high TAT under the deficient state of ATIII, MD805, a synthetic thrombin inhibitor, was introduced to avoid further consumption of ATIII. The TAT was decreased by the use of MD805 without administration of ATIII. MD805 could be used as an effective anticoagulant in high TAT due to DIC under an ATIII-deficient state. Although the TAT improved with an adequate anticoagulation in DIC, spontaneous bleeding sometimes appeared as a complication associated with the high level of alpha 2 plasmin inhibitor plasmin complex. In this case, the combined use of tranexamic acid relieved the bleeding.
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PMID:[Thrombin.antithrombin III complex]. 192 Aug 62

Effects of ionic and nonionic contrast media (CM) on blood coagulation, fibrinolytic system and platelet function were comparatively studied in vitro. By the gross observation of blood coagulation using mixture 2:8 of each contrast media and blood, its total coagulation time was clearly short with iopamidol and iohexol, and no complete coagulation was observed with ioxaglate and diatrizoate for 180 minutes. Anticoagulant effects of all CM were confirmed by the assays of APTT, PT, thrombin time, antithrombin III, FPA, TAT and anti-Xa activity. But, the ionic high osmolar CM (diatrizoate) and low osmolar CM (ioxaglate) showed a greater anticoagulant effect than nonionic CM. Anticoagulant effect of CM on coagulation system may be mainly caused by antithrombin effect. No effects of CM on the fibrinolytic system were observed by assays of the D-dimer, plasminogen and antiplasmin. And all the contrast media produced inhibitory effects of platelet aggregation induced by ADP. Ionic CM tended to have a little stronger inhibitory effect than non-ionic CM. In conclusion, it was suggested that a greater anticoagulant effect of ioxaglate ensures potential safety for thromboembolic complication during angiographic procedure.
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PMID:[Effects of ionic and nonionic contrast media on the blood coagulation system, the fibrinolytic system and platelets]. 194 84

The aim of the study was to evaluate if D-dimer and thrombin-antithrombin III complex determinations in patients with clinically suspected pulmonary embolism create a discrimination between patients to be further investigated with lung scanning and those who should be investigated for other diseases mimicking pulmonary embolism. The Data-Fi Dimertest Latex Assay, MAbCO Dimertest EIA, and TAT EIA were performed in 100 consecutive patients (26 percent outpatients) who were sent to our institution for lung scanning by their attending physicians because of clinically suspected pulmonary embolism. The D-dimer Latex Assay was positive (greater than 500 ng/ml) in 12 (48.0 percent) of 25 patients with high probability of pulmonary embolism and in one (11.1 percent) of nine with intermediate probability, respectively. Only one patient (1.5 percent) with a normal scan had a positive latex assay, presumably due to inapparent bleeding after a computed tomographic (CT)-guided liver biopsy. Referring to 120 ng/ml as upper limit of normal (mean +/- 2 SD of healthy controls), the D-dimer enzyme immunoassay (EIA) was positive in 21 (84.0 percent) of 25 patients with high probability, in six (66.7 percent) of nine patients with intermediate probability, and in 40 (60.6 percent) of 66 patients with normal/low probability of pulmonary embolism, respectively. The TAT EIA was positive (greater than mean +/- 2 SD of healthy controls = 3.53 ng/ml) in 18 (72.0 percent) of 25 patients with high probability, in five (55.6 percent) of nine patients with intermediate probability and in 16 (24.2 percent) of 66 patients with normal/low probability of pulmonary embolism. A normal result in one of these hemostaseologic tests did not predict a low probability of pulmonary embolism after lung scanning. Thus, it is not justified to exclude patients with clinically suspected pulmonary embolism from further investigation by lung scanning because of a normal result in one of these tests.
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PMID:Pulmonary embolism. Efficacy of D-dimer and thrombin-antithrombin III complex determinations as screening tests before lung scanning. 195 91


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