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)

Data were obtained and analyzed in 229 patients admitted to the coronary care unit from November 1988 through July 1989. The patients were classified into 2 groups: patients without or with only mild left ventricular failure (Killip class I or II) during their hospital stay (group I), and patients who were in Killip class I or II on admission but developed cardiogenic shock during hospitalization (group II). Discriminant function analysis was performed using the following variables: patients' age, history of previous myocardial infarction, diabetes mellitus, blood lactate, urea, creatinine, creatine kinase, aspartate aminotransferase, lactate dehydrogenase concentrations, and chest x-ray cardiothoracic ratio. Variables that were found to significantly discriminate the 2 groups of patients were age, previous infarction, x-ray cardiothoracic ratio, blood urea and lactate concentrations. The risk index was computed, and blood lactate was the variable with the greatest predictive power for shock development. The sensitivity, specificity and predictive value of the risk index, taking various cutoff points, were calculated. With a cutoff value of 1, sensitivity was 65%, specificity 91%, positive predictive value 36% and negative predictive value 97%. With a cutoff value of 2, sensitivity was 53%, specificity 99%, positive predictive value 82% and negative predictive value 96%.
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PMID:Usefulness of blood lactate as a predictor of shock development in acute myocardial infarction. 200 Jul 87

This study explored myocardial protective effects of allopurinol at various doses. Ninety patients undergoing coronary artery bypass or repair or replacement of cardiac valves were divided into three groups of 30 patients each in accordance with the amount of allopurinol administered to patients in each group. Patients in group I received no allopurinol, those in group II received low-dose allopurinol (total dose 1200 mg), and those in group III received high-dose allopurinol (total dose 2400 mg). Aspartate aminotransferase, cardiac isoenzyme of creatine kinase, and lactic dehydrogenase levels were measured up to 5 days after operation. Concentrations of allopurinol and oxypurinol were also measured before initiation of cardiopulmonary bypass and at the start and at the end of aortic crossclamping. Postoperative aspartate aminotransferase, creatine kinase, and lactate dehydrogenase 1 plus lactate dehydrogenase 2 levels in group III were significantly lower than those in groups I and II. Aspartate aminotransferase, creatine kinase, and lactate dehydrogenase 1 plus lactate dehydrogenase 2 levels in group II were lower than those in group I, without statistically significant differences. Plasma oxypurinol concentrations were significantly higher in group III than in group II. It was concluded that allopurinol had resultant high myocardial protective effects in dose-related fashion, but its effect might be attributed to oxypurinol levels formed by its degradation.
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PMID:A clinical trial of allopurinol (Zyloric) for myocardial protection. 200 10

Thirty-two volunteers participated in a two-period crossover study in which ibuprofen was tested against an identical placebo for its effectiveness in reducing muscle soreness and damage after two bouts of downhill running. Subjective soreness, quadriceps isometric strength and isometric endurance time at 50 percent of maximum strength, serum activities of creatine kinase, lactate dehydrogenase and aspartate transaminase and serum levels of creatinine and urea were recorded at intervals up to 72 hours after exercise. Each downhill run produced muscle soreness, and a decline in muscle strength and 50 percent endurance time, although these parameters were unaffected by ibuprofen treatment. All serum parameters measured increased after both runs, but for the three enzymes this increase was smaller after the second run. Serum creatine kinase and urea levels were higher in the ibuprofen group after both runs. These results indicate that ibuprofen is not an appropriate treatment for delayed onset muscle soreness and damage.
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PMID:Effects of ibuprofen on exercise-induced muscle soreness and indices of muscle damage. 207 6

The purpose of the present study was to investigate the effects of 8 months of a specific and controlled sprint training programme on three groups of young athletes (two groups of males and one of females). Biopsies of vastus lateralis were taken before and after the period of training. The type percentage and diameter of the fibres, as well as the glycogen content and the activities of the enzymes of glycogen metabolism (glycogen synthase and glycogen phosphorylase), glycolysis (phosphofructokinase, pyruvate kinase, aldolase and lactate dehydrogenase), oxidative metabolism (succinate dehydrogenase) and creatine kinase and aminotransferases were studied. The results show an increase in the percentage of type I fibres and an increase in the diameter of both fibre types. A significant increase was also observed in glycogen content, and in the activities of glycogen synthase, glycogen phosphorylase, phosphofructokinase, pyruvate kinase, succinate dehydrogenase, aspartate aminotransferase and alanine aminotransferase. We conclude that a long period of sprint training induces a biochemical muscle adaptation to anaerobic exercise. This metabolic adaptation is followed by a morphological adaptation, although this is probably not as specific as the biochemical one.
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PMID:Biochemical and histochemical adaptation to sprint training in young athletes. 208 3

A correlation study was performed on the degree of muscle weakness in 36 patients with dermatomyositis and 69 with polymyositis in relation to muscle biopsy findings, electromyography (EMG) abnormalities, and serum concentrations of creatine kinase (CK), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymes. Statistically significant correlations were found between muscle weakness and EMG results in patients with polymyositis, and between muscle weakness and serum CK and AST levels in dermatomyositis. As expected, correlations were found between the results of the three enzyme determinations in both groups of patients.
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PMID:Correlation between tests of muscle involvement and clinical muscle weakness in polymyositis and dermatomyositis. 208 50

Acute muscle pain with stiffness developed in a patient with latent hypothyroidism after administration of clofibrate. Serum creatine kinase (CK), aspartate aminotransferase, and lactate dehydrogenase were markedly elevated, but returned to normal one and a half months after the discontinuation of clofibrate. Clofibrate challenge (750 mg/day) for three days caused muscle pain and an elevation in serum CK. Hypothyroidism may be a predisposing factor in the development of clofibrate-induced myopathy.
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PMID:Clofibrate-induced myopathy in a patient with primary hypothyroidism. 208 82

The mitochondrial isoenzyme of aspartate aminotransferase showed only slight increases in serum of twenty-seven patients after uncomplicated coronary bypass surgery, which contrasted the rapid and substantial increases in creatine kinase MB. In seven patients suffering perioperative infarction or serious complications, substantial increases in mitochondrial aspartate aminotransferase were detected and the elevations in creatine kinase MB were prolonged. Mitochondrial aspartate aminotransferase may appear as a specific marker of myocardial necrosis following coronary bypass surgery. The elevations of creatine kinase and creatine kinase MB were detected as early as 5 minutes after onset of coronary reperfusion and slightly higher activities were measured in coronary sinus blood than in systemic blood sampled simultaneously. Increases in mitochondrial aspartate aminotransferase, however, could first be measured 8 hours after reperfusion.
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PMID:Activities of mitochondrial aspartate aminotransferase and creatine kinase isoenzyme MB in serum following coronary bypass surgery. 209 76

The effect of differences in sympathoadrenomedullary and pituitary-adrenocortical responses of individual animals to 35% hemorrhage on severity of shock induction has been studied in unanesthetized unrestrained rats by measuring plasma concentrations of adrenaline (A), noradrenaline (NA), corticosterone (CS) and adrenocorticotropin (ACTH). The responses of A, CS and ACTH were related to the decrease of blood volume and mean arterial pressure (MAP), whereas plasma NA remained unchanged. Higher susceptibility to blood loss was characterized by more pronounced hemorrhage-induced increase in blood lactate concentration and plasma enzyme activities as well as lethal outcome of hemorrhagic shock. In animals with irreversible hemorrhagic shock, enhanced catecholamine secretion and reduced ACTH release was observed. Furthermore, a revealed direct correlation between A and blood lactate concentration and plasma enzyme activities (aspartate aminotransferase, isocitric dehydrogenase, creatine kinase, lipase and glutathione-S-transferase) may indicate its possible participation in the mechanism of shock induction. In contrast, an inverse relationship of plasma CS to the indicators of shock severity was demonstrated. In conclusion, non-optimal neuroendocrine regulation of cardiovascular adjustments to hemorrhage in shock-prone animals might cause an exaggerated compensatory activation of adrenomedullary catecholamine secretion, which in turn has been shown to exert deleterious vascular and metabolic effects. The mechanisms responsible for reduced ACTH secretion in shock-prone animals remain to be established.
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PMID:Hormonal responses to hemorrhage and their relationship to individual hemorrhagic shock susceptibility. 216 2

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

Recent advances in methodology allow the mass concentration of creatine kinase MB isoenzyme (CK-MB), and of lactate dehydrogenase isoenzyme 1 (LD1) to be determined quickly and easily as routine, emergency tests. We evaluated these tests as diagnostic criteria of perioperative myocardial infarction (PMI) after coronary bypass surgery. These tests were compared with the usual measurements of CK-MB activity by immunoinhibition and LD1 by electrophoresis and with other biological markers of myocardial infarction such as total CK, total LD, and aspartate aminotransferase. Sixty-one patients who underwent coronary bypass grafting were followed pre- and postoperatively by enzyme determinations and electrocardiography; a subgroup was monitored by myocardial scintigraphy. CK-MB mass appeared to be the best marker of PMI during the first 48 h, although LD1 was the marker of choice from days 2 to 4.
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PMID:Mass concentration of creatine kinase MB isoenzyme and lactate dehydrogenase isoenzyme 1 in diagnosis of perioperative myocardial infarction after coronary bypass surgery. 220 55


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