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)

Data from the 1976 and 1977 CAP surveys were analyzed for response of the activated partial thromboplastin time (APTT) to heparin. Different sources and concentrations of heparin were used. The results indicate that the precision of the APTT is more dependent on instrumentation than on partial thromboplastin. This was true for all four of the heparinized specimens evaluated. A single exception was found with the "old" Dade reagent activated cephaloplastin. The mean difference in the activated partial thromboplastin times obtained with differing concentrations of heparin was entirely dependent on the partial thromboplastin reagent used. No significant difference in the results was found when equal concentrations of bovine lung and porcine intestinal mucosal heparin were compared.
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PMID:The effect of heparin on the activated partial thromboplastin time. 56 81

Analysis of the data for the 1969 to 1973 CAP Surveys of proficiency in partial thromboplastin time (PTT) determination indicates more than desirable variability in this measurement. Non-activated procedures show greater interlaboratory variability than activated methods; therefore, they may be preferable for routine use. It is likely that many laboratories have not determined their own upper limit of normal for their PTT system and thus have received unacceptable evaluations in the Surveys. It also was determined that many laboratories do not closely follow the manufacturer's directions, especially in regard to incubation times and calcium concentration of the recalcification solution.
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PMID:The partial thromboplastin time in the CAP survey program. 114 70

Prothrombin time was measured in three different plasma samples by 2580 laboratories in the 1977 CAP Proficiency Testing Program. Analysis of variance was used to show that instrument, as well as thromboplastin, has a significant effect upon observed prothrombin time. In addition, the instrument and thromboplastin effects were estimated, and all were shown to be linearly related to the prothrombin time of the plasma sample. This linear relationship was used to develop a formula for adjusting/correcting an observed prothrombin time for both the thromboplastin and instrument effect. This adjustment/correction method seems promising on the basis of its use in four different sets of data.
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PMID:Effect of thromboplastin and instrumentation on the prothrombin time test. 733 64

Data from the 1978 CAP Hematology Survey were analyzed for the effect of sodium and calcium salts of heparin on the activated partial thromboplastin time (APTT). The results indicate that the sodium salt of heparin prolongs the APTT more than the calcium salt at a heparin concentration of 0.2 units/ml. Furthermore, there was a variable response of the different APTT reagents to the different heparin salts. Data from the 1979 CAP Hematology Survey showed a greater sensitivity of the Automated APTT reagent and the Platelin Plus Activator of General Diagnostics compared with Actin (Dade) and Thrombofax (Ortho) at therapeutic heparin levels of 0.2 units/ml to 0.4 units/ml. The 1979 CAP heparin questionnaire results are presented and analyzed.
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PMID:Laboratory monitoring of heparin therapy--the effect of different salts of heparin on the activated partial thromboplastin time. 743 50

Investigation of the 1978 CAP Hematology Survey results for hemoglobin, hematocrit, erythrocyte count, leukocyte count, prothrombin time, and partial thromboplastin time with respect to the assumption of normality and the method for detecting outliers was performed. The findings indicate that the assumption of normality, while not exactly valid, is reasonable for the purposes of the Survey, but that the method of determining outliers may be too stringent in the case of hemoglobin, hematocrit, erythrocyte count, and leukocyte count, and not appropriate for prothrombin time and partial thromboplastin time. These findings are similar to those reported earlier for selected chemistry and immunology constituents in the CAP Survey.
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PMID:The distribution of selected hematology measurements in the CAP survey. 743 55

Endotoxin(lipopolysaccharide = LPS), cell wall component of gram-negative bacteria, activates monocytes and macrophages to release cytokines, reactive nitrogen intermediates (RNI), and to generate tissue factor(TF) which initiate coagulation. We have purified 7kDa and 18kDa cationic antibacterial proteins (CAP-7 and CAP-18) with LPS-binding and LPS-neutralizing activities from rabbit granulocytes using as an assay the agglutination of erythrocytes coated with Re-LPS. From protein sequencing, CAP-7 was identified as the C-terminal 37 amino acid fragment of CAP-18. Synthetic peptide #197 (identical sequence to CAP-7, Gly1-Try37) and #36-1 (a truncation of CAP consisting of 32 amino acid residues, Gly1-Ala32) showed LPS-binding activity. Each peptide inhibited LPS-induced tissue factor(TF) generation by murine peritoneal macrophages, even added 1-3 hours after stimulation of cells with LPS. C57BL/6 mice treated with #197 were significantly protected from lethal LPS challenge. Peptide #36 also blocked the LPS-induced lethality. These peptides had antibacterial activity to gram-negative bacteria, such as E.coli, S.typhimurium, K.pneumonia, Ps.aeruginosa and also to gram-positive S.aureus (Methicillin sensitive and resistant strains). Both peptides inhibited TF- and Xa-induced plasma clotting. Using synthetic chromotogenic substrates, both CAP7 peptides blocked the coagulation cascade at two sites, activation of factor X to Xa and conversion of Factor II (prothrombin) to factor IIa (thrombin). In vivo treatment of peptide #197 prevented acute lethality in mice injected with tissue factor (rabbit brain thromboplastin). Two other peptides, #32(Gly1-Phe9) and #50(Ile13-Typ37) failed to demonstrate LPS-binding, LPS-neutralizing, antibacterial and anticoagulant activities. The active peptides but not the inactive peptide maintain a putative heparin binding domain at their N-termini. This heparin binding domain is participate in the LPS-binding, LPS neutralizing, antibacterial and anticoagulant activities of CAP7. These active peptides may have a therapeutic potential for treatment for DIC due to sepsis and endotoxin shock.
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PMID:Endotoxin-binding synthetic peptides with endotoxin-neutralizing, antibacterial and anticoagulant activities. 783 55

Antiphospholipid syndrome (APS) is characterized by recurrent thromboembolic phenomena, recurrent fetal loss and thrombocytopenia associated with high titers of IgG anticardiolipin antibodies and/or lupus anticoagulant. There is an increased platelet aggregation in these patients and thus aspirin was found to be effective in abrogating some of the clinical findings. The purpose of this study was to employ the experimentally induced APS in mice infused with anticardiolipin antibodies, to study the effect of a thromboxane receptor antagonist (BMS, 180, 291) on the various overt manifestations of APS. Experimental APS was induced in pregnant female mice by iv infusion of a pathogenic anticardiolipin antibody (CAM). The mice were then treated daily with 300 micrograms/mouse of BMS. The study group and the untreated group were killed on day 17 of pregnancy. Live and absorbed fetuses and the mean weight of the placentae, fetuses and platelet counts were recorded. BMS treated mice had a significant reduction in fetal resorption rate from 45% to 19.8% and an increase in mean placental and embryo weights (182 vs 104, 1043 vs 721 mg, respectively). In parallel, an increase in platelet count (from 597,100 to 1075,000 platelets/mm3) and decrease in activated thromboplastin time (95 to 44s) was seen. It seems that thromboxane receptor antagonist may be effective in abrogating the diverse manifestations seen in APLS. Increased platelet aggregation may be one of the pathogenetic mechanisms in APS.
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PMID:Effect of long-acting thromboxane receptor antagonist (BMS 180,291) on experimental antiphospholipid syndrome. 784 93

Antiphospholipid syndrome is characterized by the presence of high titers of anti-beta(2)-glycoprotein I (beta(2)GPI) antibodies, lupus anticoagulant associated with thromboembolic phenomena, thrombocytopenia and recurrent fetal loss. Single-chain Fv (scFv) were prepared from four anti-beta(2)GPI mAb, CAM, CAL, CAR and 2C4C2, and one anti-ssDNA. All five scFv showed the same antigen binding properties as the original mAb. Replacement of the pathogenic CAM V(H) domain with the non-pathogenic CAL V(H) or anti-ssDNA V(H) decreased the binding affinity of the scFv to beta(2)GPI and completely abrogated the anticoagulant activity. Exchanging the CAM V(H) with anti-DNA V(H) resulted in a shift from anti-beta(2)GPI to anti-ssDNA binding of the scFv. Replacement of the CAM V(L) with CAL V(L) did not affect the binding and activity. BALB/c mice were immunized with the anti-beta(2)GPI scFv, and the scFv resulting from the substitution of the heavy (H) and light (L) chains. The mice which were immunized with CAM, 2C4C2 and CAR scFv developed clinical manifestations of experimental anti-phospholipid syndrome. Elevated titers of mouse anti-cardiolipin (aCL), anti-beta(2)GPI, associated with lupus anticoagulant activity, thrombocytopenia, prolonged activated partial thromboplastin time and a high percentage of fetal resorptions were detected, in the CAM scFv group and in the scFv composed of CAM V(H) groups. High titers of aCL, anti-beta(2)GPI, anti-ss/dsDNA and anti-histone associated with lupus findings were observed in the sera of the 2C4C2 scFv-immunized mice. Immunization with CAL scFv did not lead to any clinical findings. The current study shows that scFv of pathogenic antibodies are capable of inducing the same clinical manifestations as the whole antibody molecule upon active immunization. Replacement of H/L chains point to the importance of the V(H) domains in the pathogenic potential of anti-beta(2)GPI.
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PMID:Characteristics and pathogenic role of anti-beta2-glycoprotein I single-chain Fv domains: induction of experimental antiphospholipid syndrome. 1059 Feb 57

Clinical and experimental data have recently accumulated for antithrombotic action of angiotensin-converting enzyme inhibitors (ACE-1s). We have shown previously that captopril (which contains a thiol group in the moiety) exerts more pronounced antithrombotic activity than does an equipotent dose of enalapril (the drug devoid of the thiol group). To clarify the relative importance of the presence of the thiol group in the molecule versus angiotensin-converting enzyme (ACE) inhibitory properties in the antithrombotic action of captopril, rats were treated with captopril (5 mg/kg twice daily; CAP), epicaptopril (stereoisomer of captopril devoid of ACE-inhibitory properties; 5 mg/kg twice daily; EPI), N-acetylcysteine (3.75 mg/kg twice daily; ACC), enalapril (3 mg/kg once daily; ENA), or distilled water (VEH) for 10 days, per os. After ligation of the vena cava, the incidence of the venous thrombosis and/or the thrombus weight decreased significantly in all but the ENA-treated groups when compared with control rats. The effect of CAP, EPI, and ACC was accompanied by a marked reduction of euglobulin clot lysis time and, with the exception of ACC, by an increase in prothrombin time in the blood collected from the site of the thrombus formation. Antithrombotic activity of EPI was completely abolished by nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) or indomethacin, with the parallel reversal of fibrinolytic and coagulation parameters toward normal. Activated partial thromboplastin time, mean blood pressure, and bleeding time were not altered by either of the administered drugs. Thus, we demonstrated that thiol compounds exert antithrombotic activity by increasing fibrinolysis and/or suppression of the extrinsic pathway of the coagulation cascade in a nitric oxide/prostacyclin-dependent manner.
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PMID:Thiol repletion prevents venous thrombosis in rats by nitric oxide/prostacyclin-dependent mechanism: relation to the antithrombotic action of captopril. 1102 53