Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on a 68-year-old female patient who was admitted with abdominal pain. Elevated lipase and CRP caused us to suspect pancreatitis. Because an enlarged pancreas head was found on ultrasound, an endoscopic retrograde cholangio- and pancreaticography was performed with a pethidine-containing premedication. Thereafter, bilirubin, gamma-glutamyl transpeptidase and alkaline phosphatase increased dramatically. There was also a moderate elevation of aspartate aminotransferase and alanine aminotransferase. A second endoscopic retrograde cholangio- and pancreaticography with the same premedication was performed in order to exclude an undetected concretion. This led to a further increase of bilirubin. An association with the drugs given as premedication was therefore suspected, and in fact, a hypersensitivity reaction towards pethidine was confirmed by the lymphocyte transformation test. We thus conclude that pethidine caused an immunologically mediated hepatic injury.
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PMID:Dramatic increase in bilirubin after ERCP - pethidine as a possible cause of drug-induced hepatitis. 1466 Nov 25

Serum biochemical, hemostatic, and hematologic analytes were determined by four laboratories on dog serum or plasmas containing increasing amounts of hemolysate. From the results of testing, interferographs were prepared to aid in decision making and to enhance visualization of the effects of hemolysis on the determination of the analytes. Heniktsus consistently interfered with the analysis of creatinine phosphokinase, lactic dehydrogenase, aspartate aminotransferase, lipase, and albumin, all of which appeared to increase with increasing hemolysis. The results for the remainder of the biochemical, hemostatic, and hematologic analytes varied greatly among analyzers or methods, rarely in a predictable manner, indicating that each laboratory should evaluate the effects of hemolysis on each analyzer and for each method used, in order to make informed decisions on the use of hemolyzed but irreplaceable samples.
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PMID:Hemolysis as a factor in clinical chemistry and hematology of the dog. 1515 13

The role of 5-lipoxygenase (5-LOX) in the pathophysiology of the organ injury/dysfunction caused by endotoxin is not known. Here, we investigate the effects of treatment with 5-LOX inhibitor zileuton in rats and targeted disruption of the 5-LOX gene in mice (5-LOX(-/-)) on multiple organ injury/dysfunction caused by severe endotoxemia. We also investigate the expression of beta2-integrins CD11a/CD18 and CD11b/CD18 on rat leukocytes by flow cytometry. Zileuton [3 mg/kg intravenously (i.v.)] or vehicle (10% dimethyl sulfoxide) was administered to rats 15 min prior to lipopolysaccharide (LPS; Escherichia coli, 6 mg/kg i.v.) or vehicle (saline). 5-LOX(-/-) mice and wild-type littermate controls were treated with LPS (E. coli, 20 mg/kg intraperitoneally) or vehicle (saline). Endotoxemia for 6 h in rats or 16 h in mice resulted in liver injury/dysfunction (increase in the serum levels of aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transferase, alkaline phosphatase, bilirubin), renal dysfunction (creatinine), and pancreatic injury (lipase, amylase). Absence of functional 5-LOX (zileuton treatment or targeted disruption of the 5-LOX gene) reduced the multiple organ injury/dysfunction caused by endotoxemia. Polymorphonuclear leukocyte infiltration (myeloperoxidase activity) in the lung and ileum as well as pulmonary injury (histology) were markedly reduced in 5-LOX(-/-) mice. Zileuton also reduced the LPS-induced expression of CD11b/CD18 on rat leukocytes. We propose that endogenous 5-LOX metabolites enhance the degree of multiple organ injury/dysfunction caused by severe endotoxemia by promoting the expression of the adhesion molecule CD11b/CD18 and that inhibitors of 5-LOX may be useful in the therapy of the organ injury/dysfunction associated with endotoxic shock.
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PMID:Reduction of the multiple organ injury and dysfunction caused by endotoxemia in 5-lipoxygenase knockout mice and by the 5-lipoxygenase inhibitor zileuton. 1532 37

We investigated the efficacy of a potent inhibitor of secretory phospholipase A2 (sPLA2), S-5920/LY315920Na, in an experimental model of acute pancreatitis in rats. Combined intraductal injection of sodium taurocholate (5 mg/rat) and porcine pancreatic sPLA2-IB (300 microg/rat) caused severe hemorrhagic necrotizing pancreatitis resulting in high mortality, along with rapid increases of catalytic PLA2 and lipase activities in plasma and ascites and with gradual increases of plasma amylase and aspartate aminotransferase levels over 9 h after the pancreatitis. Prophylactic intravenous treatment with S-5920/LY315920Na significantly reduced mortality at 7 days, and strongly abrogated PLA2 activities in both plasma and ascites along with significant reduction of lipase activity, amylase, aspartate aminotransferase, and hemorrhage at 6 h. It also significantly reduced histological damage such as edema and parenchymal and fat necroses of the pancreatic tissue. This sPLA2 inhibitor could become an effective agent for the treatment of severe acute pancreatitis.
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PMID:Effect of a selective inhibitor of secretory phospholipase A2, S-5920/LY315920Na, on experimental acute pancreatitis in rats. 1546 63

Prevalence of electrolyte disturbances and biochemical changes were determined in patients admitted to the emergency room of the Department of Internal Medicine in Innsbruck, Austria during a six-month period. The value of biochemical parameters for the detection of chronic alcohol abuse was also investigated. The most frequent electrolyte disturbances found were hypernatremia (41%), hyperchloremia (21%), hypermagnesemia (17%) and hypocalcemia (15%), whereas hypokalemia and hypophosphatemia were observed quite rarely (5% and 3.4%, respectively). The most frequent biochemical changes observed were consistent with signs of cellular toxicity i.e. increased liver enzymes (elevated gamma-glutamyltransferase (GGT), aspartate aminotransferase, alanine aminotransferase and lactic dehydrogenase) as well as signs of pancreatitis (elevated serum lipase and amylase) and muscle damage (elevated creatine kinase). The most frequent changes in blood counts were leucocytosis (23%), thrombocytopenia (14%), and anemia (12%). C-reactive protein showed only minimal elevation. Male sex and level of blood alcohol were detected as major risk factors for the diagnosis of chronic alcohol abuse in the patient sample investigated. When testing the value of routinely measured parameters for predicting the presence of chronic alcohol abuse, GGT and mean corpuscular volume of red blood cells (MCV) appeared to be of equal value. A combination of elevated blood alcohol with an increase in either of these markers may be interpreted as high risk for chronic alcohol abuse in this particular group of patients.
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PMID:Disturbances of electrolytes and blood chemistry in acute alcohol intoxication. 1577 19

Hydrogen sulfide (H2S) is a naturally occurring gaseous transmitter, which may play important roles in normal physiology and disease. Here, we investigated the role of H2S in the organ injury caused by severe endotoxemia in the rat. Male Wistar rats were subjected to acute endotoxemia (Escherichia coli lipopolysaccharide (LPS) 6 mg kg(-1) intravenously (i.v.) for 6 h) and treated with vehicle (saline, 1 ml kg(-1) i.v.) or DL-propargylglycine (PAG, 10-100 mg kg(-1) i.v.), an inhibitor of the H2S-synthesizing enzyme cystathionine-gamma-lyase (CSE). PAG was administered either 30 min prior to or 60 min after the induction of endotoxemia. Endotoxemia resulted in circulatory failure (hypotension and tachycardia) and an increase in serum levels of alanine aminotransferase and aspartate aminotransferase (markers for hepatic injury), lipase (indicator of pancreatic injury) and creatine kinase (indicator of neuromuscular injury). In the liver, endotoxemia induced a significant increase in the myeloperoxidase (MPO) activity, and in the expression and activity of the H2S-synthesizing enzymes CSE and cystathionine-beta-synthase. Administration of PAG either prior to or after the injection of LPS dose-dependently reduced the hepatocellular, pancreatic and neuromuscular injury caused by endotoxemia, but not the circulatory failure. Pretreatment of rats with PAG abolished the LPS-induced increase in the MPO activity and in the formation of H2S and in the liver. These findings support the view that an enhanced formation of H2S contributes to the pathophysiology of the organ injury in endotoxemia. We propose that inhibition of H2S synthesis may be a useful therapeutic strategy against the organ injury associated with sepsis and shock.
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PMID:Inhibition of endogenous hydrogen sulfide formation reduces the organ injury caused by endotoxemia. 1610 May 27

In order to study the metabolic profile of ostriches in relation to diet, 40 animals of both sexes were divided equally into two groups and fed two diets ad libitum consisting, on a dry matter basis, of the same commercial concentrate (60%) for the two groups and of corn silage (group A) or alfalfa hay (group B). In the morning, after about 12 h of fasting, blood was collected from the wing vein. The following haematological parameters were determined with an automatic system (Ektachem 250 analyser, Kodak): glucose, cholesterol, triglycerides, lactate (LAC), total protein (TP), uric acid, total bilirubin (Tbil), creatinine (CREA), calcium (Ca), magnesium (Mg), phosphorus (P), sodium (Na), potassium (K), chloride (Cl-), iron (Fe), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), cholinesterase (ChE), alpha-amylase (Amyl), lipase (LIP) and gamma-glutamyltrasferase (GGT). Diet significantly affected some parameters of the metabolic profile. Indeed, owing to the presence of alfalfa hay in the diet, group B showed, in comparison to group A, significantly higher values of uric acid (222.5 vs 387.5 mmol/L, p < 0.01), GGT (8.50 vs 11.3 U/L, p < 0.05), Tbil (8.50 vs 10.7 mmol/L, p < 0.05), Ca (2.41 vs 2.83 micromol/L, p < 0.01), Mg (1.01 vs 1.18 micromol/L, p < 0.05) and K (2.71 vs 3.16 micromol/L, p < 0.01). The levels of creatinine (27.3 vs 32.6 mmol/L, p < 0.05) and AST (344.9 vs 461.4 U/l, p < 0.01) were also higher for group B.
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PMID:Effect of diet on the metabolic profile of ostriches (Struthio camelus var. domesticus). 1784 21

Cutaneous leishmaniasis has been recognized as a major public health problem in several countries. Pentavalent antimonies, meglumine antimoniate and sodium stibogluconate, have been considered as standard treatment for leishmaniasis. Side effects have been reported to be increased hepatic enzyme levels and electrocardiographic abnormalities. We performed this study to evaluate the influence of meglumine antimoniate on some liver, kidney, and pancreas function tests. Eighty patients fulfilled the study criteria. Forty-one (51.3%) patients were female and the mean age of the patients was 30.4 +/- 15.7 years. Blood samples were taken to evaluate liver, kidney, and pancreas function tests before and after treatment with intramuscular injections of MA at a dose of 20 mg Sb(+5)/kg/day for 15 days. Mean serum levels of blood urea nitrogen, creatinine, sodium, total and direct bilirubin, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase significantly increased after treatment, although most of them were within normal ranges. There were no significant differences in serum levels of potassium, amylase, lipase, and gamma-glutamyl transpeptidase before and after treatment. In conclusion it can be stated that one course of treatment with 20 mg Sb(+5)/kg/day MA for 15 days does not significantly alter the liver, kidney and pancreas function tests in patients with cutaneous Leishmaniasis.
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PMID:Evaluation of meglumine antimoniate effects on liver, kidney and pancreas function tests in patients with cutaneous leishmaniasis. 1795 Nov 31

The involvement of oxidative and nitrosative mediators in liver injury caused by heat stress remains unclear. This study aimed to elucidate the role of endothelial nitric oxide synthase (eNOS), and inducible NOS (iNOS)-derived NO and nitrotyrosine in the whole-body hyperthermia (WBH)-induced liver injury. Rats were anesthetized with intraperitoneal pentobarbital, and were exposed to a heating lamp for 60 min to raise the core temperature to 42.5 degrees C. The rats were maintained at the hyperthermic state for an additional 50 min. Blood urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, lactic dehydrogenase, creatine phosphokinase, amylase, lipase, nitrate/nitrite, methyl guanidine, and proinflammatory cytokines (tumor necrosis factoralpha, interleukin-1beta and interleukin-10) were measured before and 14 h after hyperthermia. Immunohistochemical staining was employed to detect the eNOS, iNOS and nitrotyrosine levels. Western blotting was used to examine the expression of heatshock protein 70 (HSP 70). Histopathological examination of the liver tissue was performed. WBH caused liver injury accompanied with significant increases in biochemical factors, nitrate/nitrite, methyl guanidine, and proinflammatory cytokines. In addition, WBH enhanced the eNOS, iNOS, nitrotyrosine and HSP 70 levels. WBH caused hepatic injury. The pathogenetic mechanism is likely mediated through the NOS-derived NO, free radical, proinflammatory cytokines and nitrotyrosine. The enhanced expression of HSP 70 may play a protective role.
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PMID:Oxidative and nitrosative mediators in hepatic injury caused by whole body hyperthermia in rats. 1866 11

The analytical performance of the selective, automatic multianalyser Olympus AU 5031 was evaluated over four months and assessed for practicability for another eight months. The evaluation followed the ECCLS guidelines. Twenty routine parameters were measured. In addition, sodium and potassium were determined on an attached flame photometric unit. Both the agreement between the eights photometers per unit and the temperature behaviour in the cuvettes was satisfactory. The imprecisions were very good. The within-run imprecision was below 1.5% for the majority of the parameters. The imprecision between days was below 5%, with the exception of creatine phosphokinase (7.4%). Glutamate dehydrogenase gave an imprecision of between 4.0% and 15.9%, which, however, is more likely due to the low activities measured rather than the fault of analyser. The recovery of the assigned values in 12 control sera was between 95% and 105% for 14 tests. Three of the remaining eight tests yielded recoveries with deviations between 10% and 18% (alanine aminotransferase, aspartate aminotransferase and bilirubin). No drift effects were observed and neither a sample carry-over nor a reagent carry-over were detected. Most tests were linear over a very wide range. Only afew tests (mainly lipase and glutamate dehydrogenase) required measurement repetitions with diluted samples. The correlation with routine instruments and tests was close. However, corrections were necessary for 14 of the 22 tests. This was not due to the performance of the analyser but, rather, to the different methodologies of compared tests, or different working temperatures on the comparison instruments, or a lack of accuracy for some of the AU tests.
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PMID:Analytical performance of the selective, automatic multianalyser Olympus AU 5031. 1892 58


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