Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 2-month-old boy was admitted to our hospital because of poor sucking and jaundice. There were no abnormalities during the whole period of pregnancy and at birth. His mother was a HBeAb positive HBsAg carrier, but prophylactic maneuver such as anti-HB immunoglobulin and HB vaccine was not performed on him at birth. Physical examination on admission revealed mild disturbance of consciousness. The laboratory findings showed marked increments of serum bilirubin, GOT, GPT, and NH3, and prolongation of prothrombin time, activated partial thromboplastin time and hepaplastin test. Thus, he was diagnosed as fulminant hepatitis and treated with exchange transfusion once or twice a day. Biochemical data improved gradually, but hypocoagulable states remained unchanged. At that time we decided to use Factor VII concentrate, because we found that, among several coagulation factors, factor VII activity decreased most rapidly after exchange transfusion. The alternate therapy of exchange transfusion and Factor VII concentrate improved his coagulation abnormality without any side effects. Our experience suggests that the combination therapy of exchange transfusion and Factor VII concentrate may be useful for management of fulminant hepatitis, particularly for uncontrollable coagulopathy.
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PMID:[Successful treatment of an infant with fulminant hepatitis by factor VII concentrate]. 260 16

Zinc is essential to numerous metabolic processes in the organism, multiform symptoms being found especially in deficiencies. In addition to nutritional factors, diseases such as cirrhosis of the liver. Crohn's disease and chronic renal diseases are relevant in this context. In the present work, serum zinc levels were investigated in 109 patients with various chronic liver diseases. The lowest serum zinc concentrations were seen in patients with decompensated hepatic cirrhosis with coma. Patients with decompensated alcoholic cirrhosis had lower zinc levels as subjects with nonalcoholic cirrhosis. None of the groups exhibited a significant change in serum zinc levels during the treatment period. Laboratory data (such as transaminases, thromboplastin time, alkaline phosphatase, total proteins) did not correlate with the serum zinc concentrations. The concentration of plasma ammonia, however, appeared to be inversely related to the serum zinc levels. Thus, patients with coma had maximum ammonia and minimum zinc levels.
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PMID:Clinical studies on zinc in chronic liver diseases. 321 83

Medical records of 151 dogs with chronic hepatitis were reviewed. Corticosteroid treatment had a statistically significant (P less than 0.005) effect on improving survival time when corticosteroid-treated dogs were compared with untreated dogs. Dogs dying within 1 week of examination represented 37.1% of the cases, and when compared with those living more than 1 week, serum glucose concentration was significantly lower (P less than 0.001); prothrombin time and partial thromboplastin time were significantly longer (P less than 0.001); blood ammonia concentration after oral administration of ammonium chloride was significantly higher (P less than 0.05); and necrosis severity and fibrosis severity were significantly greater (P less than 0.05 and P less than 0.022, respectively). The best predictors of early death were low normal serum glucose concentration (P less than 0.001) and prolonged prothrombin time (P less than 0.030), which was abnormal in 60.0% of dogs dying early. Partial thromboplastin time, which was increased in 92.0% of dogs dying early and in 42.6% of dogs living more than 1 week, was a less reliable predictor. Plasma ammonia concentration after oral administration of NH4Cl was least reliable in predicting early death. In dogs living more than 1 week, hypoalbuminemia was a predictor of shorter survival time (P less than 0.003). Of all the histologic features evaluated, only necrosis severity and fibrosis severity were accurate predictors of early death. The presence of bridging fibrosis was a predictor of shorter survival time in dogs living more than 1 week (P less than 0.0002).
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PMID:Effects of corticosteroid treatment on survival time in dogs with chronic hepatitis: 151 cases (1977-1985) 291 83

Protein C inhibitor isolated from human plasma inhibited thrombin, factor Xa, trypsin and chymotrypsin as well as activated protein C, but had very little effect on urokinase and plasmin. The inhibition constants (K1) of protein C inhibitor for activated protein C, thrombin and factor Xa were 5.6 X 10(-8) M, 6.7 X 10(-8) M and 3.1 X 10(-7) M, respectively. The second-order rate constant for inhibition of activated protein C by the inhibitor increased about 30-fold in the presence of an optimal heparin concentration (5-10 units/ml). The inhibition of activated protein C by plasma protein C inhibitor was also accelerated by heparin. When activated protein C (Mr = 62,000) was incubated with protein C inhibitor (Mr = 57,000), enzyme-inhibitor complexes with apparent Mr = 102,000 and 88,000 were observed in the nonreduced and the reduced samples, respectively, on SDS-polyacrylamide gel electrophoresis. In addition to these complexes, a band of unbound enzyme and a band with Mr = 54,000 were detected. When 125I-labeled protein C inhibitor was exposed to activated protein C, the inhibitor band was converted to bands with apparent Mr = 102,000 and 54,000 in the nonreduced samples, as determined by autoradiography after gel electrophoresis in SDS. The band with Mr = 54,000 also appeared when the inhibitor reacted with other serine proteases. The activated protein C was released from the inactive complex by treatment with 1 M ammonia or hydroxylamine. This phenomenon was found by SDS-polyacrylamide gel electrophoresis to represent the dissociation of the enzyme-inhibitor complex by ammonia or hydroxylamine into the free enzyme and the proteolytically modified inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of inhibition of activated protein C by protein C inhibitor. 632 92

Eight foals, 2 to 5 days of age, with similar clinical signs and laboratory and pathologic findings, died from hepatic failure. The predominant clinical signs were depression and icterus. Abnormally high values were found for plasma ammonia content, aromatic-to-branch-chain amino acid ratio, total serum bilirubin content, gamma glutamyl transferase activity, alkaline phosphatase activity, and PCV; partial thromboplastin time and prothrombin time were prolonged. Some foals had high sorbitol dehydrogenase activity. These laboratory findings were suggestive of subacute hepatic disease and failure. Predominant pathologic findings were limited to the liver and brain. The livers were less than half the expected size for 2- to 5-day-old foals, had prominent bile ductule proliferation, hepatic cell necrosis, and mild periportal fibrosis. These findings suggested both prenatal and postnatal diseases caused by exposure to a hepatoxin. The predominant lesion in the brain was the presence of Alzheimer type II astrocytes, which are characteristic of hepatoencephalopathy. Although the periportal fibrosis was suggestive of in utero exposure to a toxin, epidemiologic information suggested that the hepatic failure more likely resulted from oral inoculation of a microorganism culture product at birth. The same disease was reproduced in 2 newborn foals by feeding this product.
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PMID:Toxic hepatic failure in newborn foals. 665 19

The current liver allocation system has been criticized, since available organs go to those who are the most critically ill. These recipients have the poorest overall survival. Identification of pretransplant risk factors for mortality would allow better allocation of donor livers. This study was a retrospective analysis of pretransplant clinical and laboratory parameters and subsequent postoperative liver transplant mortality to identify high-risk subgroups. Of 347 consecutive consecutive primary liver transplant recipients, 59 (17%) met United Network for Organ Sharing (UNOS) criteria for status 4. Pretransplant factors included liver function, coagulation, albumin and ammonia levels, renal function, the presence of ascites, and etiology of liver disease. Overall 1-year patient survival was significantly worse for the status 4 recipients (89.0% vs. 67.7%; P = 0.01). In a univariate analysis of pretransplant risk factors for all recipients, elevated creatinine (P = 0.008) and ammonia (P = 0.009), and UNOS status 4 (P = 0.01) significantly affected postoperative survival. In multivariate analysis of pretransplant risk factors for all recipients, elevated creatinine (P = 0.003) was the only factor to significantly affect postoperative survival. In UNOS status 4 patients, univariate analysis of pretransplant risk factors and their influence on patient survival demonstrated that prolonged coagulation partial thromboplastin time (P = 0.04) and a higher grade of encephalopathy (P = 0.02) significantly affected postoperative survival. Advanced encephalopathy (P = 0.009) and prolonged partial thromboplastin time (P = 0.01) were the only significant risk factors by multivariate analysis in status 4 patients. In status 4 and non-status 4 patients, we identified risk factors that adversely affected patient survival, but their predictive power was insufficient to deny transplantation. Despite the higher mortality in status 4 recipients, their long-term survival is only slightly worse than that of non-status 4 patients. Until better predictors of survival are ascertained, our data do not support limiting the use of donor livers in UNOS status 4 recipients.
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PMID:Pretransplant status and patient survival following liver transplantation. 749 94

1. Crude salivary gland extract of the giant Amazon leech, Haementeria ghilianii, contains an inhibitor of plasma factor XIIIa. 2. The inhibitory agent was purified to homogeneity by anion-exchange, cation-exchange, gel-filtration and reverse-phase chromatography to yield a single band on SDS/PAGE with an apparent molecular mass of 7.3 kDa. It has been named tridegin. 3. Micro-sequencing of proteolytic fragments showed tridegin to be a peptide of 66 amino acids. The sequence is unique with little similarity to other leech-derived proteins. 4. Inhibition of plasma factor XIIIa activity was confirmed by four independent methods: tridegin increased the solubility of fibrin clots in urea, inhibited ammonia produced from the incorporation of ethylamine into casein, inhibited the incorporation of 5'-(biotinamido)pentylamine into casein and prevented gamma-dimer formation in clotting fibrinogen. 5. The IC50 of tridegin (approx. 9.2 nM) is very close to the concentration of factor XIIIa used in the assay and in fact depends on its concentration. This is the most potent inhibitor of factor XIIIa yet described. 6. Tridegin also inhibits platelet factor XIIIa (factor XIIIAa) with a similar potency to that of the plasma enzyme. 7. Tridegin also inhibits tissue transglutaminase but with lower potency and independently of the enzyme concentration. 8. Tridegin appears to be specific for transglutaminases, since it has no effect on the coagulation times of human plasma, on thrombin or factor Xa. Moreover it has no effect on other thiol-containing enzymes and has no ability to digest fibrinogen or cleave the isopeptide substrate, L-gamma-glutamyl-4-nitroanilide.
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PMID:Tridegin, a new peptidic inhibitor of factor XIIIa, from the blood-sucking leech Haementeria ghilianii. 921 Apr 3

Asparaginase (ASNase) is a widely used and successful agent against childhood acute lymphoblastic leukemia (ALL). Asparaginase cleaves asparagine (Asn) to give aspartic acid and ammonia, thereby depleting free Asn in the blood. However, treatment with ASNase has been implicated in significant reduction of plasma levels of the coagulation serine protease inhibitor (serpin) antithrombin III (AT3), predisposing patients to thromboembolic complications. Our investigation was designed to delineate the biochemical mechanism of AT3 depletion that can occur in the plasma of ALL patients undergoing ASNase therapy. SDS-PAGE showed no cleavage of purified AT3 following treatment with ASNase. Furthermore, purified AT3 treated with ASNase demonstrated no decrease in inhibitory activity. Human plasma and whole blood treated with approximate therapeutic concentrations of ASNase showed no loss of AT3 activity as detected by a plasma-based factor Xa inhibition assay. Treatment of a confluent monolayer of HepG2 (hepatocarcinoma) cells with ASNase showed no gross loss in AT3 message levels detected by rtPCR. However, a decrease of cell viability was observed in cultures treated with ASNase. Interestingly, medium from HepG2 cells treated with ASNase showed a marked decrease in secretion of AT3 and another serpin, heparin cofactor II. Collectively, these data show that ASNase has no direct effect on AT3 in blood or plasma, but that ASNase may affect plasma levels of AT3 by interfering with translation and/or secretion of the protein in liver cells.
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PMID:Insight into the mechanism of asparaginase-induced depletion of antithrombin III in treatment of childhood acute lymphoblastic leukemia. 1086 29

Regioselective derivatization was carried out introducing sulfate, phosphate or quaternary ammonia groups in C2-, C3- and C6-position of the anhydroglycose unit of cellulose. The anticoagulant potential of these derivatives was estimated with common clotting assays, such as thrombin time and partial thromboplastin time. It was found that a pronounced anticoagulant activity of cellulose derivatives could be achieved if the degree of substitution (DS) with sulfate was above 1.0. The anticoagulant activity was maximal at a DS of about 1.5 and then decreased again. Further, it was detected that particularly sulfation in C2-position resulted in a pronounced anticoagulant activity of cellulose derivatives. Development and application of assays specific for thrombin and factor Xa indicated that the anticoagulant potential of these cellulose derivatives was mainly due to anti-thrombin activity. The comparison of cellulose sulfates and cellulose derivatized with phosphate and quaternary ammonium groups demonstrated that the negative charge and type of the substituent is an important prerequisite for the anticoagulant activity of cellulose derivatives. Indeed, derivatization with sulfate produced superior activity in comparison with phosphate.
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PMID:Anticoagulant potential of regioselective derivatized cellulose. 1154 6

We examined the blood compatibility and protein adsorption on hydroxyapatite and hydroxy-carbonate apatite. Those apatites were synthesized under a 0, 5, or 15% CO(2)-containing N(2) atmosphere by a wet-chemical method with a strong ammonia alkali solution of calcium nitrate and diammonium hydrogen phosphate (5:3 in molar ratio) and subsequent calcination in the range of 105-700 degrees C. From infrared (IR) analysis, the carbonate ions substituted both phosphate ions and hydroxyl ions in the hydroxyapatite lattice; the intensities of IR bands assignable to phosphate ions and hydroxyl ions were reduced on calcinations. The specific surface areas of synthesized apatites decreased with increasing calcination temperature. Blood-clotting properties were evaluated in terms of active partial thromboplastin time, prothrombin time, and the amount of fibrinogen for the plasma in contact with the apatites, indicating that all the apatites barely influenced the blood clotting system. The apatites were in contact with a solution containing both bovine serum albumin (BSA) and beta(2)-microglobulin (beta(2)-MG), and the amounts of those proteins adsorbed on them were examined: the amount of absorbed BSA and beta(2)-MG gradually increased with the calcination temperature below 500 degrees C, while it showed a sudden increase when more than 600 degrees C. Hydroxy-carbonate apatite synthesized under a 15% CO(2)-containing N(2) atmosphere and calcined below 400 degrees C had the greatest selectivity in adsorbing beta(2)-MG. Thus, a higher selectivity for beta(2)-MG adsorption was empirically correlated to carbonate ions incorporated in the hydroxyapatite lattice.
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PMID:Selective protein adsorption and blood compatibility of hydroxy-carbonate apatites. 1512 1


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