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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four young male divers were assigned randomly to 4 treatment groups: Group I received aspirin (325 mg) three times daily; II received dipyridamole (75 mg) three times daily; III received both drug regimens; and IV received matching placebo. Double-blind procedures were followed. Treatment began 24 h prior to a 48-h saturation dive (inclusive of 17 h decompression) at a simulated depth of 18.3 m and continued throughout and for 3 days after the dive. A post-dive reduction in circulating platelet count was observed in all groups, except the group that received aspirin only. Platelet survival was shortened in all treatment groups. Five cases of Type I decompression sickness occurred and were treated by recompression, two in the aspirin plus dipyridamole group, two in the dipyridamole group, and one in the placebo group. Blood chemistry and hematology profiles showed that divers with decompression sickness had more elevated GOT, GPT, CPK, cholesterol and triglyceride levels, and greater reductions in platelet count, Platelet Factor 4 and Thrombin Clotting Time than most other subjects. Subjects receiving either aspirin or aspirin plus dipyridamole had fewer changes in these parameters. Failure of aspirin to potentiate, or add to, dipyridamole may be due to other actions of aspirin such as inhibition of prostacyclin synthesis. Further studies of the role of antiplatelet drugs in decompression sickness are warranted.
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PMID:Effects of aspirin and dipyridamole on platelet function, hematology, and blood chemistry of saturation divers. 53 93

The prognostic value of hemostatic parameters after orthotopic liver transplantation was evaluated in 37 consecutive patients. Six simple hemostatic parameters (prothrombin time, activated partial thromboplastin time, thrombin time, thrombin coagulase time, plasma fibrinogen and platelet count) were obtained for each patient pre-transplantation and daily post-transplantation for at least 8 days. Using the results of these tests, the degree of hemostatic impairment was arbitrarily scored from 0 to 6. Starting from the first day post-transplantation, hemostatic parameters improved progressively, reaching plateau values on day 7 post-transplantation. On day 8 there were significant differences in the activated partial thromboplastin time, prothrombin time, and in the overall hemostatic scores between patients who survived at least 6 months and those who died. Comparing these hemostasis parameters with such liver function tests as AST, ALT and serum bilirubin, univariate analysis showed that activated partial thromboplastin time, coagulation score and AST were significant predictors of 6-month survival, but by multivariate analysis (Cox proportional hazard rate model) only the activated partial thromboplastin time was an independent predictor. Hence, a simple coagulation test is useful for predicting the survival of patients undergoing liver transplantation.
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PMID:Prognostic value of hemostatic parameters after liver transplantation. 150 28

Fibrin glue is a topical biological adhesive, the effect of which imitates the final stages of coagulation. The glue consists of a solution of concentrated human fibrinogen which is activated by the addition of bovine thrombin and calcium chloride. The resultant clot aids haemostasis and tissue sealing and is completely absorbed during wound healing without foreign body reaction or extensive fibrosis. The fibrinogen component of fibrin glue can be produced from fresh frozen plasma obtained from single unit donations thereby reducing the risks of transfusion transmitted infections encountered by exposure to pools from large numbers of donors. Methods involving precipitation of fibrinogen by cryoprecipitation, polyethylene glycol or ammonium sulphate have been described and evaluated. The risk of transmission of infection can be further reduced by using plasma from 'accredited donors' who are plasma donors regularly tested for ALT and markers of viral infection or by use of fibrinogen prepared in advance of surgery from autologous blood. The second component, a mixture of thrombin and CaCl2, is quantitatively and qualitatively well defined and commercially available (Armour Pharmaceutical Co., Thrombinar (bovine thrombin]. Thrombin is applied to the operation site simultaneously and in equal volume to the fibrinogen but from a separate syringe. In the UK a commercial heat treated fibrin glue prepared from pooled plasma is available on a doctor/named patient basis (Tisseel, Immuno, Vienna). The haemostatic and adhesive properties of fibrin glue can be employed in virtually every surgical specialty. The usefulness of the glue is particularly well documented in the fields of cardiovascular surgery, ENT and neurosurgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fibrin glue. 178 83

The effects of soman poisoning on hematological (counts of red blood cells (RBC), white blood cells (WBC), and platelets and measurement of hematocrit) and coagulation parameters (prothrombin time, activated partial thromboplastin time, thrombin time and concentrations of fibrinogen, factor V, factor VII, and factor XI) and serum biochemistry (concentration of albumin, protein, calcium, cholesterol, triglycerides, blood urea nitrogen (BUN), magnesium, and creatinine and activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, cholinesterase, creatinine phosphokinase (CPK), hydroxybutyrate dehydrogenase, and amylase) were determined at 1, 2, 4, 24, and 48 hours after poisoning of rabbits. There were significant (p less than 0.05) decreases in the RBC counts in all treatment groups that were measured initially at 4 hours and were reflected by parallel decreases in the hematocrit values. These changes were probably due to an increase in the hemolysis of the RBC rather than a decrease in the production of RBC. There were minor changes in the coagulation parameters. Generally, the fibrinogen content increased. The activated partial thromboplastin time decreased significantly (p less than 0.05) 24 and 48 hours after soman (50 micrograms/kg) poisoning. Blood cholinesterase values were significantly reduced in all treatment groups at all time periods. The CPK activity was increased after 4 and 24 hours in the 20 and 50 micrograms/kg soman groups. There were minor changes in the other biochemistry values, but none that showed a dose-response relationship; thus, they were considered to be of limited significance with regard to the toxic manifestations of soman exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of soman poisoning on hematology and coagulation parameters and serum biochemistry in rabbits. 212 98

Fifteen Thai children, diagnosed with dengue hemorrhagic fever and admitted to the Children's Hospital in Bangkok, were studied. All cases were serologically proved to be secondary dengue infections. The clinical signs and symptoms in the first few days of the acute febrile phase were similar to those observed in cases with classical dengue fever, and included continuously high fever, headache, muscle pain, nausea, vomiting and abdominal pain, etc. In the laboratory findings we noted hypoalbuminemia and mild elevation of the GOT and GPT. The hemogram showed an increasing atypical lymphocyte count during the acute febrile period. Prolongations of the partial thromboplastin time and thrombin time were also found, especially in the severe shock cases. All patients had varying degrees of hepatomegaly and pleural effusion from their chest x-rays accompanied by a rapid increase in the hematocrit of more than 20% and a fall in the platelet count to less than 100000/microliters. During the plasma leakage period the patients easily developed shock, even leading to death, unless adequate fluid supplies were given. This is also the major pathophysiological difference between dengue hemorrhagic fever and classical dengue fever. Although some studies concerning the pathogenesis of dengue hemorrhagic fever have been reported, but the exact mechanisms need further investigation.
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PMID:[Clinical observation of 15 Thai children with dengue hemorrhagic fever]. 234 55

Stroma-free hemoglobin (SFH) is advocated as an oxygen-transporting resuscitation solution. Hemoglobin has been shown to enhance endotoxin lethality when given intraperitoneally. It is possible that SFH could interact with endotoxin when used as an oxygen-transporting resuscitation system for trauma victims with contaminating wounds. To assess the effects of these two agents when given intravascularly, rabbits were infused with SFH (1.75 gm/kg) or albumin (controls; 1.75 gm/kg) with and without endotoxin. Two doses of endotoxin were used. At 14.5 ng/kg of Salmonella enteritidis endotoxin, no effect was seen in the albumin group. However, 50% of the hemoglobin group died. At 14.5 micrograms/kg, the albumin group showed hematologic alterations, but all animals lived. All SFH-treated animals died at the higher endotoxin dose. SFH alone caused cardiac abnormalities (bradycardia in 100%, sinus arrhythmias in 30%, and ventricular arrhythmias in 20%), liver abnormalities (necrosis in 40% and 240% increase in alanine aminotransferase activity by 6 hours), and intravascular thrombi (30%). The only hemoglobin-induced abnormality that was more frequent in the presence of endotoxin was ventricular arrhythmias (up to 75% of animals). Thrombin times were approximately 20% larger in all SFH groups compared with the albumin groups. By 6 hours after infusion, endotoxin prolonged the thrombin time even further, despite the lack of fibrinogen consumption. This study shows that endotoxin and SFH exert synergistic toxicity when SFH is given in a clinically relevant dose for an oxygen-transporting resuscitation system. Only minute quantities of endotoxin are needed to produce this phenomenon. We hypothesize that this synergism is endotoxin enhancement of hemoglobin toxicity.
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PMID:Synergistic toxicity of endotoxin and hemoglobin. 352 17

The plasma values for factors (F)VII, FVIII:C, FVIIIR:Ag, FIX, FX, and FXI and the thrombin clotting time (TCT) were determined for 28 dogs with naturally occurring hepatic disease. The major morphologic type of hepatic disease present in a given dog, as determined by hepatic biopsy and histopathologic examination, was degeneration (12 dogs), inflammation (9 dogs), cirrhosis (3 dogs), or neoplasia (4 dogs). A specific morphologic diagnosis also was made for each dog in the study. Plasma coagulation factor values and screening tests were consistently abnormal in greater than 50% of the dogs with each type of hepatic disease as follows: degeneration--decreased FXI; inflammation--increased FVIIIR:Ag; cirrhosis--shortened TCT, decreased FIX, FX, and FXI, and increased FVIIIR:Ag; and neoplasia--shortened TCT, decreased FVIII:C, and increased FVIIIR:Ag. The plasma coagulation factor values were compared with serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities, fibrinogen-fibrin degradation product (FDP) concentration, and the prothrombin time (PT) and activated partial thromboplastin time (APTT) to determine the sensitivity and specificity of each test in detection of hepatic disease. Of all dogs with hepatic disease, 93% had at least 1 abnormal coagulation test value. The PT and APTT were abnormal in 50% and 75%, respectively, of these same dogs. Increased serum ALT and ALP activities were present in 61% and 50%, respectively, and FDP concentrations were increased in 14% of dogs with hepatic disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma coagulation factor abnormalities in dogs with naturally occurring hepatic disease. 666 Jun 23

Biochemical effects of acute and subacute treatments with ambrein were investigated in rats by measuring the total proteins, cholesterol, triglycerides, GOT, GPT and alkaline phosphatase in the blood plasma. Also, determinations of prothrombin time (PT), partial thrombin time (PTT), thrombin time (TT) and fibrinogen level were performed. Furthermore, changes in plasma electrolyte concentration were studied. Ambrein administered i.p. did not cause any toxic symptoms in the liver as revealed by the histology of the liver tissue both in acute and subacute treatments. Ambrein itself did not significantly affect the plasma protein, cholesterol, GOT and GPT profiles, but lowered alkaline phosphatase at high doses (50 and 250 mg/kg) after subacute treatment. Thus far, no specific pattern of action of ambrein in electrolyte control has been found. However, it increased PT, PTT and TT and decreased fibrinogen levels in both the acute and subacute studies, pointing towards its potential as an anticoagulant and antifibrinogenic agent.
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PMID:A study of ambrein treatment for the evaluation of change in plasma biochemical parameters in rats. 763 38

Rats which were infected with the gramnegative pathogen Klebsiella pneumoniae develop disseminated intravascular coagulation (DIC), multi-organ failure (MOF) and finally die in a septic shock. We investigated the therapeutic effect of antibiotic (tobramycin) treatment combined with the infusion of the highly specific thrombin inhibitor rec. hirudin. Although administration of 2 mg/kg tobramycin alone leads to a decrease of the bacterial burden, DIC could not be prevented. Infusion of rec. hirudin (0.25 mg/kg x h) for 4 h (start of treatment 1 h post infection), in addition to a bolus administration of tobramycin, led to an amelioration of DIC parameters as fibrinogen, thrombin-antithrombin complex (TAT) and platelets. Serum transaminase levels (GOT, GPT) as a marker of MOF were significantly improved by rec. hirudin, the T50 value increased from 17 h in the tobramycin group to 42 h in the tobramycin+rec. hirudin group, mortality rates were 90% or 60%, respectively. Combination of heparin (100 U/kg x h) and tobramycin was not effective on survival.
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PMID:Combination of antibiotic treatment with the thrombin inhibitor recombinant hirudin for the therapy of experimental Klebsiella pneumoniae sepsis. 797 45

Veno-occlusive disease (VOD) of the liver is a major complication of bone marrow transplantation. The clinical features are those of intrahepatic portal hypertension and while the reported frequency varies considerably, severe disease is readily identifiable and is associated with a high mortality. The single most important risk factor for the development of VOD is an elevated ALT prior to transplantation. The incidence of VOD may be reduced by prophylactic administration of anticoagulant or antiplatelet drugs and established disease can be treated by thrombolytic therapy with tissue plasminogen activator. These observations suggest that endothelial damage and thrombin generation are fundamental to the disease process. Protection of the endothelium from toxic damage and inhibition of thrombin generation are potential targets for preventing VOD.
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PMID:Veno-occlusive disease of the liver complicating bone marrow transplantation. 801 44


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