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:2.3.1.108 (TAT)
2,389 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Selected coagulation parameters were measured in 10 women, aged 15-22, who underwent abortion induced by 15-methyl-PGF2 alpha in the 12th-14th week of pregnancy. 250 mcg of the preparation was administered i.m. every 2 hours. Parameters were measured at 6 time intervals: 5 minutes before; 30 minutes, 4 and 8 hours after the initial injection; 2 hours after the completed abortion; and 24 hours after beginning treatment. An increase in bleeding and recalcification time was observed. A significant decrease in platelet count and the number of heparinocytes was recorded until 2 hours after the completed abortion; these parameters then showed an increase 24 hours after the beginning of treatment. A significant increase in the heat fibrin level was recorded up to 4 hours after injection, followed by a significant decrease from 8 hours after injection to 2 hours after the completed abortion (p.05). After a continued decrease in prothrombin levels up to 2 hours after the completed abortion, a statistically significant increase was observed (p.01). No significant changes in the TAT or PTT were observed.
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PMID:[Determination of selected coagulation parameters in induced abortion by means of 15-methyl-PGF2 alpha]. 8 92

In order to elucidate the activation of the coagulation cascade in patients with malignant neoplasms, we measured the levels of plasma prothrombin fragment F1 + 2, which is liberated in the process of thrombin generation. Twenty healthy adults (Group A), 29 patients with malignancies not complicated with DIC (Group B) and 4 patients with DIC (Group C) were evaluated. The values of F1 + 2 in Group C (2.38 +/- 0.55 nmol/l) were significantly higher (p < 0.01) than those in Group A (0.52 +/- 0.19 nmol/l) and B (0.86 +/- 0.68 nmol/l). Many patients in Group B showed higher levels of F1 + 2 compared to normal subjects, however, no significant differences were found between Group A and B. With respect to other coagulation molecular markers such as TAT, D-Dimer and PIC, F1 + 2 levels revealed positive correlation to those levels. Concerning the clinical course of DIC, elevated levels of F1 + 2 normalized much rapidly than those of TAT and D-Dimer by continuous administration of heparin. In conclusion, the measurement of plasma F1 + 2 is important in monitoring the activation of coagulation system in patients with malignancies, especially with respect to early detection and treatment of DIC.
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PMID:[Evaluation of hypercoagulable state in patients with malignancies by using prothrombin fragment F1 + 2]. 146 81

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

Several laboratory methods are available to measure r-hirudin, including clot-based, amidolytic, immunologic, and physicochemical techniques. The global tests, such as the PT, APTT, and Heptest, did not show an adequate response to r-hirudin in the range of 0.5 to 10.0 micrograms/ml, where full anticoagulation is achieved, as determined by animal models of thrombosis. The 10 U/ml thrombin time assay was very sensitive to r-hirudin, whereas the 10 U/ml calcium thrombin time gave a dose-dependent response from 0.15 to 10.0 micrograms/ml. Whole blood clotting assays (ACT, TEG) effectively measured r-hirudin levels up to 25 micrograms/ml. The amidolytic anti-Factor IIa assay, specific for evaluating direct thrombin inhibition, was very effective, particularly when modified to decrease the sample: thrombin ratio for higher r-hirudin concentrations. This assay may be useful in quality control, since it is biochemically defined and reagents are easily standardized. Thrombin generation assays based on synthetic substrates showed limited effect of r-hirudin; however, assays based on TAT complex and prothrombin fragment F1+2 generation showed a dose-dependent response. Immunologic methods (ELISA) are under development. Since these assays measure both complexed and noncomplexed hirudin, and since they are only sensitive to submicrogram levels, they may only be useful for the direct quantitation of absolute levels of r-hirudin but not for monitoring clinical anticoagulation. Thus, thrombin-based clotting, amidolytic, and immunologic assays can be used to evaluate and measure r-hirudin. However, optimization of each assay to respond to high and low concentrations of r-hirudin and their application to clinical monitoring, batch control, and standardization needs to be determined.
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PMID:Comparative studies on various assays for the laboratory evaluation of r-hirudin. 177 8

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

Forty-eight patients with freshly diagnosed carcinoma of the lung (40 males, 8 females) were evaluated for a coagulation profile including activated partial thromboplastin time (aPTT), prothrombin time (PT), fibrinogen, F VIII R:Ag, fibrin monomers (FM), thrombin-antithrombin-III complex (TAT-III), D-dimers and the platelet count. Thirty-eight patients had a normal aPTT and 37 patients a normal PT. None of the patients had clinical or laboratory indications of serious hemorrhage or thrombosis. On the other hand, high percentages of increased values were found for fibrinogen and F VIII R:Ag, which can be seen as prethrombotic factors. The very high percentages of elevated results for the FM, TAT-III and D-dimer are strongly indicative for low-grade coagulation activation with reactive fibrinolysis. Nevertheless, most lung cancer patients are able to maintain a normal or near normal hemostatic function. The results shown here are indicative of a coagulation and fibrinolysis equilibrium at an enhanced level and demonstrate why an unbalance between the two systems can result in thrombotic complications in (lung) cancer patients as earlier reported.
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PMID:Coagulation/fibrinolysis balance and lung cancer. 195 97

The detection of TATC may inform about the presence of thrombin generation and, and hence of a pre-thrombotic status. An ELISA test (Enzygnst TAT) has been developed here in order to evaluate the predictive role played by TATC, and it was applied on 182 patients who distributed in 14 with cirrhosis of the liver, 11 with sepsis, 17 with chronic arterial insufficiency, 55 with neoplasms, 9 with thrombosis, 15 in postoperative period, 15 with pneumonia, 16 with disseminated intravascular coagulation (DIC), 14 with multiple injuries and 16 with pancreatitis. TATC levels were significantly increased in all groups with regard to the control group. Patients with thrombosis, sepsis, multiple injuries, DIC and in the postoperative period showed especially high TATC figures. No correlation between TATC and fibrinogen, platelet count, activated partial thromboplastin time or prothrombin complex assay was found in the post-operative patient-group. It was concluded that TATC are a good indicator of hypercoagulability.
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PMID:[Detection of thrombin-antithrombin complexes in hypercoagulability conditions. Analysis of 182 cases]. 229 Nov 47

We have developed a specific and sensitive ELISA for the measurement of the TAT in human plasma. The assay follows the sandwich principle and uses two different antibodies directed against human thrombin and human antithrombin III, respectively. The anti-thrombin antibody population used for coating was purified by immunoadsorption on immobilized prothrombin and thrombin, respectively. Antithrombin III antibodies were conjugated with peroxidase. Plasma samples containing TAT were incubated in polystyrene tubes coated with anti-thrombin antibodies; after washing, peroxidase-conjugated antithrombin III antibodies were added and bound enzyme activity was subsequently measured using o-phenylenediamine. The assay was calibrated with definite concentrations (2.0 to 60 micrograms/l) of preformed purified TAT added to TAT-poor plasma. Plots of absorbance at 492 nm against TAT concentrations revealed a linear correlation (r = 0.98). A reference range from 0.85 to 3.0 micrograms/l was calculated from TAT concentration in plasma samples from 88 healthy donors (mean value +/- SD: 1.45 +/- 0.4 micrograms/l). In patients with deep vein thrombosis confirmed by phlebography (n = 15), TAT was found up to 7-13 micrograms/l. Patients with septicemia associated with a consumption coagulopathy (n = 10) showed markedly increased TAT values (greater than or equal to 10 micrograms/l). From these data it can be concluded that measurement of TAT might be a parameter for detection of a latent clotting pathway activation.
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PMID:Determination of human thrombin-antithrombin III complex by enzyme immunoassay. 246 14

In a double-blind, randomized, crossover study, we investigated in 15 healthy male volunteers the effects of recombinant (r-) hirudin (HBW 023, 0.35 mg/kg body wt SC), unfractionated heparin (UFH, HeparinNovo; 150 IU/kg body wt SC), and a low-molecular-weight heparin preparation (LMWH, Fragmin; 75 IU/kg body wt SC) on coagulation and platelet activation in vivo by measuring specific coagulation-activation peptides (prothrombin fragment 1 + 2 [F1 + 2], thrombin-antithrombin-III complex [TAT], and beta-thromboglobulin [beta-TG]) in bleeding-time blood (activated state) and venous blood (basal state). In bleeding-time blood, r-hirudin and the heparin preparations significantly inhibited formation of both TAT and F1 + 2. However, the inhibitory effect of r-hirudin on F1 + 2 generation was short-lived and weaker compared with that of UFH and LMWH, and the TAT-to-F1 + 2 ratio was significantly lower after r-hirudin than after UFH or LMWH. Thus, in vivo, when the coagulation system is in an activated state, r-hirudin exerts its anticoagulant effects predominantly by inhibiting thrombin (factor IIa), whereas UFH and LMWH are directed against both factors Xa and IIa. A different mode of action for UFH and LMWH was not detectable. In venous blood, r-hirudin caused a moderate reduction in TAT formation and an increase (at 1 hour) rather than a decrease in F1 + 2 generation. Formation of TAT and F1 + 2 was suppressed at various time points following both UFH and LMWH. There was no difference in the TAT-to-F1 + 2 ratio after r-hirudin and heparin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of recombinant hirudin (r-hirudin, HBW 023) on coagulation and platelet activation in vivo. Comparison with unfractionated heparin and a low-molecular-weight heparin preparation (fragmin). 760 Jan 20

The purpose of this study is to further investigate physiologic changes in plasma coagulation-fibrinogenolysis and fibrinolysis in the utero-placental circulation in normal pregnancy, labor and puerperium, employing newly developed molecular markers for coagulation-fibrinogenolysis and fibrinolysis such as prothrombin fragment 1 + 2 (F1.2), active PAI-1, Fgfr and Fbfr. In 30 non-pregnant women and 20 normal pregnant women, the levels of plasma F1.2, TAT, FPA, Fgfr and active PAI-1 were noticeably increased from the first trimester to the full term. tPA/PAI-1/C and B beta 15-42 were also increased as gestation advanced. These findings suggested that noticeably activated states of coagulation, fibrinogenolysis and fibrinolysis exist in normal pregnancy. In 30 cases of placental circulation in healthy pregnant women and at 20-30 minutes after uteroplacental separation, the levels of plasma F1.2, TAT, FPA, tPA/PAI-1/C, PIC, B beta 15-42, Fgfr and Fbfr were noticeably increased, and the level of active PAI-1, was noticeably decreased in the uterine venous blood as compared with those of the peripheral venous blood in healthy pregnant women. At 20-30 minutes after utero-placental separation in the uterine venous blood and in peripheral venous blood, the changes in the levels of these markers were significantly increased, whereas active PAI-1 and PI were significantly depressed compared with those in healthy pregnant women. These findings suggest that further enhancement of local coagulation-fibrinolysis occurred in utero after separation of the placenta.
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PMID:[Studies on coagulation-fibrinolysis during normal pregnancy, labor and puerperium using recently developed molecular markers]. 763 33


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