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

---

Query: EC:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Determination of the complement titer in the serum and plasm of 120 patients with chronic liver diseases showed that in eight (7%) patients with cirrhosis of the liver, chronic active or chronic inactive hepatitis complement in the serum was less than half in the plasma. The dissociation of complement serum and plasma was due to cold activation of the classical pathway of complement in vitro since serum drawn from these patients at 37 degrees C lost hemolytic activity in 4 hours when transferred to a cold environment. Neither HB antigen nor cryoglobulin participated in this phenomenon. The activation of complement in the cold could be prevented by increasing the ionic strength, or by adding vitamin E or, to a lesser extent its vehicle HCO-60, while heparin, Trasylol, soybean trypsin inhibitor, or hirudin had no effect. Trans-AMCHA prevented activation in one case. It is speculated that a factor appearing as a result of blood clotting is able to activate the classical pathway of complement in the cold; it is probably not related to Hageman factor (factor XII), factor VII, thrombin, kallikrein.
...
PMID:Cold activation of complement i. presence of coagulation-related activator. 5 81

Antithrombin III, purified to homogeneity according to polyacrylamide gel disc electrophoresis and immunoelectrophoresis, inhibited the activity of purified factor IXa and Xa, whereas factor VII was not inhibited either in the active or in the native form. Antithrombin III is the single most important inhibitor of factor Xa in plasma. Factor Xa does not, however, reduce the activity of antithrombin III against thrombin.
...
PMID:The effect of antithrombin III on the activity of the coagulation factors VII, IX and X. 6 31

A follow-up study of blood clotting and platelet aggregation was performed on 21 women who had received long-term hormone replacement treatment with conjugated equine oestrogens. The prothrombin time and factor VII and X values were significantly accelerated after three months, but there was no further increase with continual administration for 18 months. After 12 to 18 months' treatment, however, thrombin-induced platelet aggregation (Chandler's tube) was also significantly accelerated, which suggested a widening spectrum of effect. No overall acceleration of "intrinsic" clotting (partial thromboplastin time and thromboelastography) was found during the study, but the relatively small numbers may have been responsible. Further efforts are therefore required to find formulations and doses of oestrogens which, while relieving menopausal symptoms, cause less acceleration of blood clotting and platelet aggregation.
...
PMID:Conjugated equine oestrogens and blood clotting: a follow-up report. 19 5

Thirty patients in whom all aorta-coronary artery vein grafts became occluded within one year of operation, as demonstrated by cardiac catheterization, were evaluated for hypercoagulability. A total of 59 grafts were constructed in these patients. At operation, blood flows of 35 to 90 c.c. per minute were measured through the grafts. In 23 of the 30 patients, the blood was to be hypercoagulable, as evidenced by a low level of antithrombin III activity, high thrombin generation index, high factor VII values, or high platelet adhesivity. Another group of 11 patients (total number of grafts, 23) had all grafts patent at cardiac catheterization. These patients had flows through the grafts ranging from 20 to 125 c.c. per minute. None of the patients with patent grafts had hypercoagulable blood. The status of runoff was comparable between the patients with open grafts and those with occluded grafts.
...
PMID:Coagulation factors influencing thrombosis of aorta-coronary bypass grafts. 29 8

The activated parial thromboplastin time is susceptible to changing concentrations of factor VII even in the presence of heparin. Heparin delays, but does not abolisn, thrombin generation, and this delay is obviated by factor VIII. It is not known if activated parial thromboplastin time shortened by increased factor VIII demands an increase in heparin administration.
...
PMID:Heparin monitoring and thrombosis. 44 97

Evidence of developmental evolution of coagulation can be seen when the studies of 10 thriving extremely premature (EPT) infants are compared to normal full-term (FT) infants. The prothrombin time, partial thromboplastin time, and thrombin time all became shorter with increasing gestational age. Fibrinogen levels and platelet counts appear to be comparable to term infant and adult levels. Fibrin degradation products (FDP) of 10 micrograms/ml or less were found in the thriving EPT infants. When compared to healthy full-term infants, there is a definite gestational dependency of anti-thrombin III levels. Factors II and VII appear to be related to intrauterine maturation after the age of viability (24 wk), but factor VII-X complex does not. The contact factors XI, XII, high molecular weight kininogen (Fitzgerald factor), and prekallikrein (Fletcher factor) are all markedly decreased in thriving EPT infants. The mean factor V level is lower than that found in FT infants. This study confirms a gestational age dependency of factor VIII activity. The ratio of factor VIII antigen to factor VIII clotting activity is increased (2.8 vs 1.01 in FT and adults). Thriving small for gestational age (SGA) infants had coagulation studies which were not statistically different from those of thriving EPT infants. The coagulation changes which occurred in severely ill EPT were mainly in the factors which decrease during intravascular coagulation (factors I, V, and VIII). The present study suggests that because of the high antigen to activity ratio seen in thriving EPT infants, a dysfunctional or fetal factor VIII may have been produced. However, the further elevation of this ratio in the severely ill EPT infants is in keeping with a pathologic proteolysis or increased endothelial release of factor VIII antigen.
...
PMID:Coagulation studies in extremely premature infants. 52 93

Factor IX concentrate was obtained using DEAE-Sephadex A-50 as an adsorbent. The yield of factor IX in vitro averaged 81%. Each bottle of the concentrate contained 288-512 u. of factor II, 96--360 u. of factor VII, 440--660 u. of factor IX and 256--680 u. of factor X. The results of studies showed trace amounts of factor Xa in the final product, in the range of 0.01--0.04 u/ml. The concentrate was found to be free of thrombin. In the years 1976--1977 the new concentrate was administered 48 times to 10 patients with severe haemophilia B. The in vivo recovery of factor IX was 27--65%. Clinical results of treatment were satisfactory in all patients. No significant changes were observed in platelet count, fibrinogen level and the concentration of fibrinogen degradation products after infusion of the concentrate. The ethanol gelation test was negative in all cases.
...
PMID:[Preparation and clinical use of a new factor IX concentrate]. 66 30

A 15-year-old girl with severe factor VII deficiency and chronic arthropathy showed an excessively prolonged bleeding time. Further studies demonstrated low platelet adhesiveness and abnormal platelet aggregation with ADP, collagen and epinephrine. Release of 14C-serotonin was deficient after aggregation with ADP and epinephrine, but was normal with thrombin. Transfusion of plasma or prothrombin complex concentrate resulted in a partial or complete correction of the bleeding time, respectively, but had no effect on in vitro platelet function tests. Both parents and the only sister had factor VII activities of 42%-72% and factor VII antigen levels of 45%-66% of normal and may thus be heterozygotes with respect to factor VII deficiency. All three had normal bleeding times in spite of abnormal in vitro platelet functions. The observations are interpreted to mean that in this family with factor VII deficiency and abnormal platelet release reaction the platelet abnormality as such was not sufficiently severe to prolong the bleeding time unless the factor VII activity was also very low.
...
PMID:A syndrome of factor VII deficiency and abnormal platelet release reaction. 71 73

Highly purified bovine factor VII prepared according to our technique and having a specific activity of 500 U/mg protein has been studied. The chemical analysis of the preparation revealed it to be composed of amino acids, lipids (8-10%) and carbohydrates (7%). The lipid moiety can be removed by chromatography. Different mechanism of inactivation of bovine factor VII and the possible molecular changes induced by the inactivating agents were studied. EDTA and EGTA provoke a weakening of the bonds linking the structural elements of the molecule, which allows for the separation of two different components of the molecule by gel filtration. Upon treatment with thrombin, the carbohydrate content of bovine factor VIII decreases without any apparent degradation of the protein moiety of the molecule. The fact that precipitating and neutralizing antisera against factor VIII were obtained, shows that the molecules modified by EDTA and thrombin still have the antigenic properties of factor VIII. The inhibitor developed by hemophiliacs transfused with human factor VIII is bound to bovine factor VIII, forming a complex reveal that it is composed of bovine factor VIII and human gamma-globulin. Bovine factor VIII in the complex retains some antigenic determinants which bind rabbit antiserum against bovine factor VIII, as shown by neutralization of the antiserum and by precipitation studies.
...
PMID:Physical, chemical and immunological studies on bovine factor VIII. 81 87

A simple chromatographic technique for rapid adsorption of heparin and protamine from plasma samples is described, allowing accurate interpretation of coagulation screening tests and specific clotting factor assays. With the use of columns of ECTEOLA-cellulose, up to 300 U. of heparin could be completely adsorbed from a 1 ml. plasma sample. When citrated nonheparinized plasma was passed over the ECTEOLA-cellulose columns, the thrombin, prothrombin, and partial thromboplastin times were unaffected. Levels of fibrinogen, prothrombin, and factors V, VII, VIII, IX, and XI average within 90 per cent of control, nonchromatographed samples. When heparinized plasma samples (0.1 and 1.0 U. per milliliter) were passed over columns, heparin was completely removed and the results of the screening tests and the specific factor assays were the same as for the chromatographed nonheparinized samples. In addition, heparinized samples with decreased factor VIII activity maintained their pretreatment factor VII activities after heparin removal. Blood samples containing heparin were obtained from two patients during open-heart surgery. Following heparin adsorption on ECTEOLA-cellulose columns, factor VIII activity levels remained above 60 per cent during cardiopulmonary by-pass. The presence of protamine sulfate in plasma samples prolonged the prothrombin and partial thromboplastin times while slightly shortening the thrombin time. The protamine effect persisted after ECTEOLA-cellulose, but could be removed by a similar column of carboxymethyl-cellulose. The latter resin had no effect on screening tests or on assays of factors VIII or IX activity. The combination of the two resins was then used to remove the separate inhibitory effects from heparinized plasma samples to which protamine had been added.
...
PMID:Removal of heparin and protamine from plasma. 99 45


1 2 3 4 5 6 7 8 9 10 Next >>

---