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:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinically normal Nubian goats were given the antiprotozoal drug imidocarb at single intramuscular doses of 6, 12, 18 and 24 mg/kg, and the various clinical, biochemical and pathological manifestations were recorded. At a dose of 6 mg/kg the drug produced no change in any of the parameters studied. At higher doses, the drug produced dose dependent changes which included increased heart and respiratory rates, increased defaecation, urination, depression, incoordination of movement, weakness of the hindlegs, recumbency, and finally death. Just prior to death, there was a significant decrease in the number of erythrocytes, and in packed cell volume, and haemoglobin concentration. In plasma there was an increase in the activity of aspartate transaminase, urea and creatinine concentrations and inhibition of cholinesterase activity. The main histopathological changes were associated with hepatic and renal damage. Three goats were pre-treated with atropine sulphate (1 mg/animal) and after one hour given imidocarb intramuscularly at a dose of 12 mg/kg. The changes were similar but much less severe when compared with those in animals given imidocarb alone at the same dose.
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PMID:Some effects of imidocarb in goats. 408 55

Clostridium botulinum type D intoxication was diagnosed as the cause of death of 42 of 67 lactating cows in a southeast Texas dairy herd over an 11-day period. By necessity, the diagnosis was based on clinicopathologic findings, as the toxin could not, by standard laboratory tests, be demonstrated in affected cattle. The predominant clinical findings were hindlimb weakness/ataxia rapidly progressing to persistent recumbency. Affected cattle were alert until just before death, which occurred without notable agonal movements or respirations after 6 to 72 hours' recumbency. Abnormal laboratory findings included neutrophilic leukocytosis (all affected cattle), proteinuria (most affected cattle), slight elevations of serum aspartate transaminase and low serum inorganic phosphorus (some affected cattle), and patchy areas of hyperemia/congestion of the mucosa in the small intestine (postmortem examination of 3 affected cattle). This report confirms the findings of others with regard to the difficulty of demonstrating the causative toxin in C botulinum type D-intoxicated cattle and presents available information on the clinicopathologic features of this intoxication that may aid in the differentiation of this condition from other causes of down cows.
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PMID:Catastrophic death losses in a dairy herd attributed to type D botulism. 649 May 11

A 44-year-old black male presented with fever, myalgia and weakness. He had elevated blood urea nitrogen, creatine phosphokinase and serum glutamic-oxaloacetic transaminase. During the first 6 days of this undiagnosed illness azotemia increased, a pericardial friction rub occurred, and hematuria was present. On the 7th day bilateral subconjunctival hemorrhages, anterior uveitis, and peripapillary cotton-wool spots were noted. This combination of findings suggested leptospirosis, which was subsequently confirmed by specific antibody titers. Therapeutic response was achieved with high-dose systemic steroids.
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PMID:Cotton-wool spots as a sign in leptospirosis (Weil's disease). 663 59

The clinical significance of serum aspartate aminotransferase (GOT) isozymes was studied in 18 patients with polymyositis. Abnormally high levels of mitochondrial GOT (mGOT) (6.2 +/- 1.2 IU/L, mean +/- SEM; normal, less than 2.0 IU/L) and cytosol GOT (sGOT) (95 +/- 21.6 IU/L; normal, less than 25 IU/L) were observed in sera. In polymyositic muscles, the sGOT level was significantly decreased but mGOT was not. The levels of serum sGOT and mGOT and the ratio of mGOT/tGOT before corticosteroid therapy correlated well with the severity of muscle weakness. Serial determination of CPK, sGOT, and mGOT during corticosteroid therapy revealed that mGOT most rapidly returned to normal. Exercise did not increase serum mGOT in polymyositis.
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PMID:Serum mitochondrial aspartate aminotransferase in patients with polymyositis. 683 Jan 52

Gentamicin sulfate at dosage levels of 10 and 20 mg/kg of body weight was administered twice daily IV to red-tailed hawks. Clinical signs, water consumption, and changes in blood chemical values were monitored. Tissues were examined grossly and ultrastructurally, using light and electron microscopy. Clinical signs of weakness and apnea were attributed to gentamicin-induced neuromuscular blockade in the 20-mg/kg group. Serum values of aspartate transaminase, alanine transaminase, cholesterol, inorganic phosphorus, total protein, albumin, and uric acid increased in some birds. There was a decrease in periodic acid-Schiff staining of proximal tubular brush borders. Increased numbers of cytoplasmic lysosomes, many of which contained myelin figures, in renal epithelial cells were seen at the ultrastructural level. All birds given 20 mg/kg died. Both dosage levels were considered toxic in red-tailed hawks.
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PMID:Toxicity of gentamicin in red-tailed hawks. 688 67

Megaesophagus was diagnosed in 9 adult ferrets. Clinical history of the ferrets included regurgitation, difficulty in swallowing, partial anorexia, and lethargy. Cachexia, dehydration, weakness, and ptyalism were observed on physical examination. Radiography revealed the esophagus of each ferret to be dilated in the thoracic and cervical regions. Of 4 ferrets that had lymphocytopenia, 2 had concurrent leukopenia. Serum biochemical analysis revealed high activity of alanine transaminase (4 ferrets) and aspartate transaminase (3), and hypoglycemia (4). Treatment included administration of fluid, antibiotics, and agents directed against possible primary causes of megaesophagus. Treatments were ineffective, and all of the ferrets died or were euthanatized. All 6 ferrets that were submitted for necropsy had bronchopneumonia, hepatic lipidosis, mild esophagitis, and gastritis. The etiopathogenesis of megaesophagus in the ferrets was not determined.
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PMID:Megaesophagus in nine ferrets. 796 Oct 71

1. GR95030X, a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, was administered daily to marmosets by gavage. In a Maximum Repeatable Dose (MRD) study, doses of up to 30 mg kg-1 day-1 were administered for 49 days. In a chronic study, animals received dosages equivalent to 0, 1, 2.5, 7.5 and 20 mg kg-1 day-1 for 204 or 205 days. Some animals were maintained without treatment for a recovery period of 29 or 30 days. 2. Clinical signs included poor coat condition, weakness with impaired coordination, lethargy and other behavioural changes. There was also alimentary disturbance, and some deaths occurred at doses of 20 mg kg-1 day-1 and above. 3. Adverse effects upon body weight were seen although some recovery was apparent after the cessation of treatment. 4. Serum cholesterol concentrations were reduced. Very large increases in serum ALT, AST and CK activities were recorded with CK-MM isoenzymes accounting for 80% or more of the total CK enzyme activity. 5. Treatment was associated with muscle fibre atrophy and a sarcolemmal response with little evidence of regeneration. Histological examination revealed vascular changes, glial proliferation and cell death in the brain, with no consistent distribution. Alveolar capillary congestion and alveolar proteinosis indicated that there may have been a reduction in cardiac function. 6. HMG-CoA reductase inhibitors have evident potential to cause myopathy in marmosets. This is believed to be the first report of such an effect.
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PMID:Toxicity of a novel HMG-CoA reductase inhibitor in the common marmoset (Callithrix jacchus). 804 18

The physical, clinicopathologic, and survival rates of 77 cats with severe spontaneous hepatic lipidosis are detailed in this report. Cats were subdivided into groups designated as idiopathic lipidosis if no other disease process was recognized, or secondary lipidosis if another disease process was diagnosed. Cats were also subdivided into groups designated as survivors or nonsurvivors on the basis of successful recuperation at 4 months after initial diagnosis. Differences between disease and survival groups were evaluated for significance. Overall, more female cats and middle-aged cats were affected. Presenting complaints of vomiting, anorexia, weakness, and weight loss were common. Physical assessment of most cats showed obvious hepatomegaly, jaundice, dehydration, and a weight loss > or = 25% of usual body weight. Neurobehavioral signs indicative of hepatic encephalopathy, other than ptyalism and depression, were rare. Clinicopathologic features are characterized by hyperbilirubinemia and increased activities of serum ALT, AST, and ALP, with only small if any increase in gamma GT activity. Clinical features distinguishing cats with hepatic lipidosis from those with other serious cholestatic disorders include absence of hyperglobulinemia and low gamma GT activity relative to ALP activity. Although coagulation tests were abnormal in 45% of cats tested (n = 44), few cats showed clinical bleeding tendencies. Most cats received prophylactic vitamin K1 therapy. Forty two cats received aggressive nutritional and supportive care and of these 55% survived. Cats with idiopathic disease were significantly younger, had significantly higher ALP activity and bilirubin concentration, and had a slightly better survival rate than cats with secondary lipidosis. Low PCV, hypokalemia, and an older age were significantly related to nonsurvival. Because of the variety of diets and food supplements used in case management, the influence of nutritional factors on survival could not be evaluated.
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PMID:A retrospective study of 77 cats with severe hepatic lipidosis: 1975-1990. 811 31

Clinical, diagnostic and biochemical features of generalised glycogenosis are described in 96 Brahman-type calves. Typically the calves were presented when about 6 months of age, with ill-thrift and muscular weakness as the most common signs. Acidic alpha-glucosidase activity was reduced in peripheral blood lymphocytes and skeletal muscle. Muscle glycogen concentration was consistently higher in affected animals than in clinically normal cattle. Other observations in affected calves included elevation of serum aspartate aminotransferase and creatine kinase activities and excessive amounts of high molecular weight oligosaccharides in urine. Fine cytoplasmic vacuolation of neurones in the brain and spinal cord, skeletal muscle, myocardium and of Purkinje fibres were consistent histological observations. Periodic acid-Schiff staining revealed the presence of glycogen-like material in peripheral blood lymphocytes of all affected calves, indicating that this is a useful aid for the diagnosis of glycogenosis. While 3 of the 96 calves showed somewhat different clinical signs, the similarity of pathology and the biochemical and clinical evidence in the remainder suggested that, in these animals, the disease was expressed as a single syndrome.
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PMID:Clinical, diagnostic and biochemical features of generalised glycogenosis type II in Brahman cattle. 828 22

The acute, subchronic and chronic toxicities of 2,4-dichlorophenoxyacetic acid (2,4-D) were studied ir rats. Animals were exposed acutely (600 mg/kg), subchronically (200 ppm for 30 d) and chronically (200 ppm for 180 d) to 2,4-D by the oral route. Clinical, laboratory and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased locomotor activity and induced ataxia, sedation, muscular weakness (mainly of the hind quarters) and gasping for breath; increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), amylase activities and creatinine levels; decreased total protein (TP) and glucose levels; and increased hematocrit values. Subchronic and chronic 2,4-D exposures did not induce overt clinical signs or symptoms of intoxication. However, subchronic herbicide exposure increased AST activity and albumin and hematocrit values, and chronic exposure increased AST, AP and LDH activities, decreased amylase and glucose levels, but did not change hematocrit values. Chromatographic analysis of the serum of chronically exposed rats showed the presence of the herbicide; the amount found (3.76 +/- 1.16 micrograms/ml) suggested the absence of 2,4-D accumulation within the body. Although macroscopic or histopathological lesions were not observed in acutely, subchronically or chronically 2,4-D exposed rats, the laboratory data obtained suggest tissue injuries after dosing, since the results are considered early indicators of primarily hepatic and muscle tissue damage.
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PMID:Acute, subchronic and chronic 2,4-dichlorophenoxyacetic acid (2,4-D) intoxication in rats. 888 38


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