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:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasmin does not activate factor X into the enzyme--factor Xa. On the contrary, the enzyme inactivates factor X, rendering it incapable of conversion into factor Xa during incubation in 25% sodium citrate. After proteolysis by plasmin the prothrombin preparations contaminated with factor X lose their ability to generate thrombin. This ability is partially restored by an addition of factor X.
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PMID:[Inactivation of factor X by plasmin]. 15 77

Changes of prekallikrein in the cases with DIC were investigated, i.e., DIC cases including disseminated metastasis of gastric cancer, acute promyelocytic leukemia and endotoxin shock. Therefore, the trigger substances for this paper were the pathologic cells of the leukemia, the cultured well differentiated adenocarcinoma cells and endotoxin. (1) The lysates of the pathologic cells of the leukemia and the cultured cells showed prekallikrein activation. Endotoxin showed prekallikrein activation via factor XII. (2) Serine proteases (factor Xa, thrombin, plasmin and trypsin) activated prekallikrein in the plasma and the purified prekallikrein. (3) Antithrombin III, aprotinin and FOY inhibited prekallikrein activation. Antithrombin III was promoted by heparin in its inhibitory effect.
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PMID:Changes of prekallikrein in the cases with disseminated intravascular coagulation syndrome. 16 Jan 91

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.
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PMID:Conjugated equine oestrogens and blood clotting: a follow-up report. 19 5

The inhibitory effects of a newly synthesized protease inhibitor, Gabexate mesilate (FOY), on experimental disseminated intravascular coagulation were studied as compared with those of aprotinin or heparin. Thrombin, tissue thromboplastin, and endotoxin were used as DIC trigger substances. As parameters on DIC, platelet counts, white blood cell counts, neutrophilic leukocyte counts, fibrinogen, fibrin degradation products, platelet retention, platelet aggregation, prothrombin time, partial thromboplastin time were served. The drug efficacy in each parameter were expressed by the score system and analyzed statistically. The results were summarized as follows; (1) In thrombin-induced DIC, FOY was apparently superior to the other drugs (p less than 0.05). (2) In thromboplastin-induced DIC, heparin was slightly more effective than FOY or aprotinin. (3) In endotoxin infusion, there were no significant differences among them. In conclusion, the results of the present study suggest that FOY was more effective than heparin or aprotinin on experimental DIC.
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PMID:Inhibitory effects of gabexate mesilate (FOY) on experimental DIC. 22 8

Cyanate reacts with unchanged amino groups of various proteins in a specific irreversible carbamylation reaction. The effect of this molecule on the clotting process and the effects of carbamylation on the clotting proteins and platelet functions were investigated in vitro. An immediate effect on the clotting proteins, not related to pH, was seen in the screening tests prothrombin time, partial thromboplastin time and thrombin time at the highest concentration (100 mM), to a lesser degree at the lower concentration (10 mM). These changes reflected decreases of 19 and 36% respectively in Factor V and X activity, an inhibition of 63-75% of Factors VII, IX, X and XI activity, and 80% inhibition of thrombin activity. The inhibitory changes of carbamylation increased with time. No changes were seen in the activity of Factors I and VIII. Platelet function studies revealed no inhibition of Factor III release; aggregation was abnormal only at high concentrations with epinephrine and collagen induction and partially reversible by resuspension in normal plasma.
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PMID:The effect of cyanate on the clotting proteins and platelet function. 23 14

Initial transfusion needs aremet by type-specific rather than low titer O-negative blood. When the patient's problem approaches the magnitude of exchange transfusion (5 to 10 units) in less than 4 hours, platelet transfusion to treat dilutional thrombocytopenia is administered. Fresh frozen plasma is administered to provide clotting factors. When five units have been exceeded, platelet, pro-thrombin, and partial thromboplastin are measured. A blood clot is checked for clotting, retraction, and lysis. These tests screen platelet quantity and the intrinsic and extrinsic clotting system. Administered blood is warmed in a water bath or heating coil. Blood gas analysis (pH, pO2, and pCO2) is performed every five units to allow for precise administration of bicarbonate. The electrocardiogram is used to monitor potassium and calcium abnormalities. Hyperkalemia is seldom a problem. Hypocalcemia may be present transiently and is treated with calcium choride. Component therapy is the standard recommended practice. Fresh blood is recommended for the patient who has had an acute exchange transfusion and continues to require large quantities of blood. Fresh blood obviates the need for combining components and allows one transfusion unit to address itself to the multiple needs of the patient.
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PMID:The use of fresh blood in the treatment of critically injured patients. 23 51

A purified preparation of bovine thrombokinase (activated Factor X) loses the ability to hydrolyze TAME (p-toluenesulfonyl-L-arginine methyl ester) when it is incubated at 37 degrees in 0.25 M Tris. HCl buffer, pH 7.4 with lauroxypropyl biguanide, N1, N5-dimethyl, N1-lauroxypropyl biguanide, N1-p-chlorophenethyl, N5-phenethyl biguanide, or N1-methyl, N1-p-chlorobenzyl, N5-o,p-dichlorobenzyl biguanide. Activity is lost much more slowly when 0.15 M NaCl is also present. Lauroxypropyl biguanide is the most potent of the compounds tested, 0.22 mM causing thrombokinase to lose almost all of its activity in about 30 minutes at 37 degrees in pH 7.4 buffered saline. Topical bovine thrombin also loses activity when incubated with either of the lauroxypropyl biguanides but not with the diphenethyl or the dibenzyl compound. Instead, the latter biguanides accelerate thrombin's hydrolysis of TAME. The percent acceleration is not affected or only slightly decreased by the presence of 0.15 M NaCl or KCl, and it is also unaffected by incubating the enzyme with the compounds in buffered saline for 4 to 120 minutes. Purified bovine trypsin is stabilized by both lauroxypropyl and the diphenethyl biguanide when incubated at 37 degrees in pH 7.4 buffered saline for the 60 minute test period but neither compounds has any effect on its rate of hydrolysis of TAME. It is postulated that the enzymes first react rapidly and reversibly with all of the test biguanides and, depending upon the enzyme and the substrate, the rate of hydrolysis of the substrate is unaffected, accelerated or inhibited. The lauroxypropyl biguanides also undergo a second, slower reaction with both thrombokinase and thrombin that produces loss of enzymatic activity. The dibenzyl and diphenethyl biguanides also undergo this second slow reaction with thrombokinase but not with thrombin, and none of the biguanides undergo this second reaction with trypsin.
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PMID:The effects of biguanides on thrombokinase, thrombin and trypsin. 24 90

Serial coagulation studies were performed in 26 pediatric patients with acute lymphoblastic leukemia during initial induction therapy with vincristine, prednisone, and L-asparaginase. Prolongation of screening coagulation tests was frequent: prothrombin time (in 16 of 26 patients), partial thromboplastin time (23/26) and thrombin time (21/26). In all 26 patients fibrinogen levels fell below .20 g/100 ml and 16 had levels below .10 g/100 ml. Sixteen patients had plasma coagulation factor assays performed. In these 16 patients, Factor XI was less than 40% in 14 and Factor XI was less than 70% in 9, with only a few scattered low levels of other factors. There were no clinical bleeding episodes. Coagulation abnormalities returned to normal at the completion of L-asparaginase therapy while the patients remained on vincristine and prednisone.
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PMID:The effect of L-asparaginase of plasma coagulation factors in acute lymphoblastic leukemia. 26 3

An episode of disseminated intravascular coagulation following therapeutic gelfoam embolization to control bleeding from esophageal varices in a patient with liver disease is presented. We have since followed 13 patients prospectively (six control and seven gelfoam/autologous clot) to determine the effect of this procedure on clotting. We were unable to show significant differences between the two groups as measured by the prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen and platelet count. However, fibrin (ogen) degradation products were significantly elevated (p less than .01) in the gelfoam/autologous clot group. We suspect this occurred secondary to clot lysis at the site of embolization. No subsequent bleeding diathesis attributable to this abnormality occurred in any of the patients.
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PMID:Gelfoam and autologous clot embolization: effect on coagulation. 30 83

The diagnosis of defibrination syndrome in shock, sepsis and neonatal hypoxia is based, in addition to the clinical picture, upon a few parameters of the hemostatic system, which, in part as global tests, provide information about the course of coagulation. The parameters measured are partial thromboplastin time, thromboplastin time, plasma thrombin time, fibrinogen, thrombin-coagulase and reptilase times as well as platelet count. Normal values of these laboratory parameters were established for healthy newborns 1--5 days of age, and for healthy adults. It is suggested that especially partial thromboplastin time, the thrombin-coagulase and reptilase times, the latter influenced by fibrinolysis cleavage products, are representative for the tentative diagnosis of disseminated intravascular coagulation with fibrinolysis syndrome (DICFS). The platelet fall often lags 1--2 days behind the event. Moreover normal values for newborns, are markedly higher than those for older children or adults. In the presence of DICFS, a low-dose heparin therapy is immediately initiated. If completed defibrination is manifest, therapy is supplemented with urokinase and streptokinase, For DICFS with congenital sepsis, an exchange transfusion with heparinized fresh blood is the treatment of choice.
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PMID:[Diagnostic therapeutic problems of defibrination syndrome in shock, sepsis, and neonatal hypoxia (author's transl)]. 32 24


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