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)

Blood coagulation and fibrinolytic activities were studied in rats with hepatic injury induced by carbon tetrachloride (CCl4). Acute hepatic injury was induced by single oral administration of 0.5, 1.0, 2.0 and 3.0 ml/kg of CCl4. Experiments were performed on the parameters of blood coagulation activities (TEG, HPT, TT, PRCT, PT, PTT, fibrinogen, factor XIII and AT III) and those of fibrinolytic activities (PLG, alpha 2PI) and plasma total protein, GOT, GPT, Ht, L/B ratio. All determinations were measured at 24 hr after administration of CCl4. Blood coagulation and fibrinolytic activities in rats were weakened in accordance with the dosage of CCl4 administration. Below CCl4 administration of 1.0 ml/kg, the GOT and GPT values increased in accordance with the dosage. However, with CCl4 administration of above 1.0 ml/kg, these values stayed at almost the same level. On the other hand, the relationship between the dosage of CCl4 and logarithmic values of HPT, PT, PTT, factor XIII and PLG all showed a good straight line.
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PMID:[Effect of carbon tetrachloride on blood coagulation and fibrinolytic activities in rats]. 379 59

A polymethylmethacrylate total artificial heart (kinetic components made of polyetherurethane) of TNS Brno II type was implanted into seven calves (2-5 months of age) surviving for the average of 152.4 +/- 19.1 days after the implantation. During the entire post-operative period the animals received oral warfarin-sodium, acetylsalicylic acid, dipyridamole and alpha-tocopherol. Blood was taken for biochemical and hematological examinations twice a week from the jugular vein. During the experiments there were decreases in the number of red blood cells, hematocrit and hemoglobin levels. Plasma free hemoglobin and serum enzymes (alkaline phosphatase, AST, ALT, LDH) increased. Coagulation tests were abnormal because anticoagulation therapy was used. There were minimal changes in the number of white blood cells and platelets, fibrinogen, blood pH, blood glucose, serum electrolytes, bilirubin (total and direct), creatinine, blood urea, and lactate. Possible reasons for observed changes include the gradual rise in the central venous pressure and damaged function of the liver parenchyma. Other factors playing a possible role in inducing changes in laboratory findings are also discussed.
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PMID:Hematological and biochemical studies in calves living over 100 days with the polymethylmethacrylate total artificial heart TNS Brno II. 395 54

The influence of long term plasmapheresis on the health of donors was examined in two groups of plasma donors that donated mean volume of 411 ml of plasma during 176 weeks and 670 ml of plasma during 123 weeks (p less than 0,05). The control group consisted of 27 whole blood donors. Statistically no significant differences (p greater than 0,05) were found in the concentrations of total proteins, albumin, gammaglobulins, immunoglobulins, alpha 1 antitrypsin, alpha 2 macroglobulin, plasminogen, fibrinogen, factor V, factor VIII, GPT and alkaline phosphatase. Although the difference was significant for bilirubin and GOT the mean values were within the normal range. Significant elevations were found in alpha 1 globulins, and alpha 2 globulins in the group that donated 411 ml of plasma/week after 35 sessions. In this latter group of donors the elevation of beta globulins was observed after 100 sessions. On the basis of these results we suggest that plasma donors should not donate more than 500 ml of plasma per week and that the maximal number of regular plasmapheresis should not exceed 70. The yearly number of sessions should therefore not exceed 50 and the yearly donated volume of plasma should be not more than 25 liters.
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PMID:Observation of the changes of plasma proteins after long term plasmapheresis. 616 6

Two chimpanzees (Pan troglodytes) were inoculated and cross-challenged with a fibrinogen and factor VIII preparation, respectively. Successful non-A, non-B (NANB) infection was documented by biphasic elevations of aminotransferases (ALT), concomitant hepatitic reactions and typical electron microscopic alterations, the most consistent being dilatation of the endoplasmic reticulum, as well as tubular and sponge-like cytoplasmic inclusions in the absence of nuclear virus-like particles. An anti-nuclear (anti-DNA) antibody of the IgM class in one of the chimpanzees simulating an antiviral antibody is described.
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PMID:Experimental non-A, non-B hepatitis in chimpanzees: light, electron and immune microscopical observations. 630 79

A prospective study of post-transfusion hepatitis was conducted in 97 adult patients undergoing open heart surgery. Twelve patients developed presumed non-A, non-B hepatitis (five of these were hospitalized and three were jaundiced), and all 12 had received clotting factors from pooled plasma (fibrinogen, factor VIII, factor IX complex) from different manufacturers. Of the remaining 85 patients none received these high risk plasma derivatives and none developed hepatitis. Multiple peak ALT elevation seems to be an indication of development of chronic non-A, non-B hepatitis. In addition to the 12 cases of presumed non-A, non-B hepatitis, nine cases of serological changes related to hepatitis B virus were observed as follows: six early booster reactions of anti-HBs, but not anti-HBc, in anti-HBs and anti-HBc positive persons; one late immunization-like response for anti-HBs and two serological hepatitis B infections without transaminase elevation. Five of the nine cases were also associated with the administration of pooled clotting factors.
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PMID:Post-transfusion hepatitis and its association with pooled clotting factors. 640 30

The authors evaluated hematological side effects in 410 epileptic patients under chronic therapy. The aim of the study was to find out the most suitable parametres for preliminary screening. Values outside the normal range were seen in patients treated with multiple drug therapy and in patients receiving antiepileptic drugs from 3 years at least. The following tests were the most frequently influenced: GOT, GPT, alcaline phosphatase, protrombin time, fibrinogen.
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PMID:[Retrospective study on side effects in 410 patients in antiepileptic therapy. Proposal for new biochemical screening]. 652 8

Carbon tetrachloride (CCl4) produces hepatic necrosis and Galactosamine (GALN) causes acute hepatocellular injury in dogs. 8 Beagle dogs were treated orally twice with 0.4 ml/kg CCl4 and 12 Beagle dogs with 200 mg/kg GALN i.v. After intoxication, groups of dogs were given antithrombin III (AT III) (Kybernin) from human plasma (25-100 U/kg i.v., days 1-3). Serum enzymes (GOT, GPT) were elevated, alkaline phosphatase values and serum bilirubin were increased in all animals. Dogs developed severe coagulation disorders reflecting intravascular coagulation and depressed levels of factors produced by the liver, such as AT III or fibrinogen. First toxic symptoms were seen after 48 h. Untreated dogs died between 48 and 72 h after GALN. AT III reduced the toxic effects on the coagulation system dose-dependently (minimal effective dose 3 X 50 U/kg). Decrease of fibrinogen and of platelet count were less pronounced, coagulation tests (Quick, TEG) less altered than in untreated dogs. Death rate was reduced. In CCl4 intoxicated animals also serum enzyme levels normalized after AT III. In GALN treated animals serum glucose levels were decreased in control dogs. These experimental results confirmed clinical effects of AT III in acute hepatic intoxications of humans.
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PMID:[Effect of antithrombin III on experimental hepatotoxin poisoning in dogs]. 653 7

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

Male New Zealand White rabbits were orally given 0.05 mg of aflatoxin B1 (AFB1)/kg of body weight daily for 10 days and were treated with glutathione-precursors and depletor, antibacterial agents, or sodium thiosulfate. The drug administered, the mortality, and the mean survival time were as follows: corn-oil controls (0), euthanatized at 25 days; AFB1-controls (2), 21 days; AFB1 and saline controls (2), 22 days; cysteine and AFB1 (5), 13 days; methionine and AFB1 (5), 12 days; sodium thiosulfate and AFB1 (2), 21 days; sulfadimethoxine and AFB1 (1), 24 days; oxytetracycline and AFB1 (0), euthanatized at 25 days; and ethyl maleate and AFB1 (3), 21 days. Clinical signs of toxicosis included decreased feed consumption during AFB1 administration, loss of body weight or failure to gain, and death. Clinicopathologic changes included increases in serum bilirubin concentration and alanine aminotransferase and aspartate aminotransferase activities. Prothrombin and activated partial thromboplastin times were lengthened. Plasma fibrinogen concentration was decreased. Changes in PCV, hemoglobin concentration, and serum alkaline phosphatase were unremarkable. Oxytetracycline had protective effects against chronic aflatoxicosis in rabbits. Cysteine and methionine enhanced chronic aflatoxicosis.
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PMID:Effects of various treatments on induced chronic aflatoxicosis in rabbits. 680 40

Blood concentrations of six acute phase reactants (ESR, neutrophil count, fibrinogen, haptoglobin, alpha 1-antitrypsin, and ferritin), parameters of muscle necrosis (myoglobin, CK, ALT, and AST) as well as hemopexin, iron, and TIBC were determined before and for 7 consecutive days after muscle biopsy in patients and in a control group. A muscle biopsy was chosen as a standardized surgical procedure that induces a mild transient inflammatory response. After muscle biopsy, a significant increase occurred in five (ESR, neutrophil count, fibrinogen, haptoglobin, and alpha 1-antitrypsin) of the six acute phase reactants. The concentration of serum ferritin did not show a significant change. A significant decrease was noted in the serum iron concentration and a significant increase occurred with CK and myoglobin secondary to the muscle biopsy. Thus the inflammation of a muscle biopsy produces a significant acute phase reaction.
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PMID:Quantification of acute phase reactants after muscle biopsy. 711 53


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