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)

Toxicosis was induced in pregnant Holstein-Friesian heifers by giving polybrominated biphenyls a in gelatin capsules at the rate of 25 g/day. Initially, this dosage was approximately 67 mg/kg of body weight. Clinical signs were anorexia, excessive lacrimation and salivation, diarrhea, emaciation, dehydration, depression, and abortion. Fever was not evident during the experiment. Values for serum glutamic-oxalacetic transaminase, lactic dehydrogenase, blood urea nitrogen, and bilirubin were increased. Changes in packed cell volume, hemoglobin content, total erythrocyte and leukocyte counts, and differential leukocyte counts were minimal and reflected dehydration and secondary infection. The principal urine changes were decreased specific gravity and moderate proteinuria. Gross necropsy findings included dehydration; subcutaneous emphysema and hemorrhage; atrophy of the thymus; fetal death with concomitant necrosis of cotyledons; kidneys that were enlarged, pale tan to gray; thickened wall of the gallbladder; inspissated bile; edema of abomasal folds; mucoid enteritis; linear hemorrhage and edema of the rectal mucosa; and secondary pneumonia. Microscopic changes were most marked in the kidneys, gallbladder, and eyelid. In the kidney, the principal changes were extreme dilatation of collecting ducts and convoluted tubules, with epithelial degenerative changes of cloudy swelling, hydropic degeneration, and separation from the basement membrane. Common changes in the gallbladder were moderate to marked hyperplasia and cystic dilatation of the mucous glands in the lamina propria. The changes in the eyelids were characterized by hyperkeratosis, with accumulations of keratin in hair follicles of the epidermis and squamous metaplasia with keratin cysts in the tarsal glands. Clinical signs and lesions of toxicosis did not develop in heifers given the polybrominated biphenyls at the rate of 0.25 mg and 250 mg/day for 60 days. Initially these rates were approximately 0.00065 mg/kg and 0.65 mg/kg of body weight, respectively.
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PMID:Pathology of experimentally induced polybrominated biphenyl toxicosis in pregnant heifers. 18 92

Toxicosis was induced in pregnant heifers by feeding 25,000 mg/head/day of FireMaster BP-6, a commercial blend of polybrominated biphenyls (PBB). The PBB feeding decreased dry matter intake approximately 50% by 4 days exposure. Emaciated animals became anorexic a few days prior to death at 33 to 66 days. Weight losses of heifers average 80 kg. Other clinical signs observed were dehydration, diarrhea, excessive salivation and lacrimation, fetal death, abortion, and general depression as evidenced by depressed heart and respiratory rates. Clinical signs were apparent after 10 days exposure and progressively intensified along with loss of condition until death. Clinicopathologic changes included significantly increased serum glutamic-oxaloacetic transaminase and decreased serum calcium by 30 days exposure. Lactate dehydrogenase, urea nitrogen, and bilirubin were elevated, and serum albumin decreased by 36 to 40 days. Principal urine changes were decreased specific gravity and moderate proteinuria. Pregnant heifers fed 0.25 or 250 mg/head/day for 60 days and nonpregnant heifers fed 250 mg/head/day for 180 days displayed neither clinical signs nor clinicopathologic changes indicating adverse effects from PBB exposure. Post-exposure, all heifers exposed to PBB for 60 days calved normally with zero calf mortality and were successfully rebred. Milk production was not different from control animals. Birth weights of calves from dams exposed to 250 mg PBB/head/day were significantly greater than calves of dams exposed to 0 mg or 0.25 mg/head/day. PBB exposure of dams produced no detrimental effects on calves as indicated by clinical signs, clinicopathologic changes, or performance.
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PMID:Effects of PBBs on cattle. I. Clinical evaluations and clinical chemistry. 21 5

Jatropha curcas seed was fed to six calves at doses of 2.5, 1 and 0.25 g/kg once and to two other calves at 0.025 g/kg up to 14 days. The onset of toxic manifestations in the six calves was rapid and death occurred within 19 hours of administration. The two calves that received daily the lowest dose of J. curcas showed signs of poisoning and died within 10 to 14 days. The clinical signs of diarrhoea, dyspnoea, dehydration and loss of condition were well correlated with the pathological findings. There was an increase in aspartate aminotransferase, ammonia and potassium and a decrease in total protein and calcium in the serum of jatropha-poisoned calves.
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PMID:Effects of Jatropha curcas on calves. 45 22

The sequential development of the clinical signs and lesions in the organs of desert sheep and Nubian goats dosed with Jatropha curcas seeds at 0.05, 0.5 and 1 g/kg/day was studied. Diarrhoea, reduced water consumption, dehydration, sunken eyes, inappetence and loss in condition were the important signs of J curcas poisoning in sheep and goats. The main pathological changes were haemorrhage in the rumen, reticulum, lungs, kidneys and heart, catarrhal and/or haemorrhagic enteritis, hepatic fatty change, pulmonary congestion and oedema and straw-coloured fluid in serous cavities. An increase in the concentrations of AST, ammonia, potassium and sodium and a decrease in total protein and calcium were detected in the serum. Haematological changes were haemoconcentration and leucocytosis.
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PMID:Toxicity of Jatropha curcas in sheep and goats. 50 10

Infection of pigs by the whipworm (Trichuris suis) resulted in profuse diarrhea on postinfection days 17 to 21. Anorexia, retardation of growth, dehydration, and emaciation were observed in infected pigs. Scanning electron micrography showed nematodes embedded in the mucosa of the cecum and colon, with resultant disruption of the mucosa. Infected pigs had decreased values of albumin, amylase, calcium and creatine phosphokinase, but increased values of alpha-, beta-, and gamma- globulins, total iron-binding capacity, copper, potassium, uric acid, and aspartate aminotransferase.
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PMID:Pathophysiology of swine trichuriasis. 88 15

Twenty-six 3-week-old genetically obese pigs were fed in two experiments to determine the serum chemistry profile during severe protein malnutrition and repletion. Severe protein deficiency was produced in pigs fed the high-fat, low-protein diet (growth failure, rough hair, low serum total protein and albumin). In Experiment 1, blood was sampled from the anterior vena cava of each pig five times during depletion and three times during repletion to determine serum total cholesterol, high density lipoprotein (HDL)-cholesterol, triglycerides, total protein, albumin, glucose, Ca, inorganic P, Mg, Na, K, Cl, total bilirubin, urea N, creatinine, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltransferase. In Experiment 2, blood was sampled weekly for 8 weeks for serum total cholesterol, HDL-cholesterol, triglycerides, albumin, glucose, Ca, P, Mg and alkaline phosphatase. HDL-cholesterol was increased (P less than 0.01) and albumin was decreased (P less than 0.01) in protein-deficient pigs in both experiments. Creatinine, total bilirubin, gamma-glutamyltransferase, alanine aminotransferase, and aspartate aminotransferase were elevated in protein-deficient pigs compared with controls after 7 weeks of depletion. Inorganic P (P less than 0.01), Ca (P less than 0.01), and Mg (P less than 0.05) concentrations were depressed in protein-depleted pigs compared with controls in both experiments. After 8 weeks of repletion in Experiment 1, all elements except inorganic P were similar in the two groups. Short-term, severe, protein malnutrition affected lipid, electrolyte, and structural mineral metabolism and indices of liver function in the absence of parasites, diarrhea, and infection. The effects were reversed after 8 weeks of repletion. We conclude that the elevated serum cholesterol in protein deficiency is related primarily to an increase in the HDL fraction.
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PMID:Response of blood serum constituents to production of and recovery from a kwashiorkor-like syndrome in the young pig. 135 73

The historical and clinical features and the haematological and biochemical changes in 126 cats with hyperthyroidism are described; 125 of the cats were domestic short- or longhaired, and one was a chinchilla. There were 62 males and 64 females with a mean age of 13.0 years. The duration of signs ranged from two days to two years with a mean of 5.4 months. The historical and clinical features were weight loss, polyphagia, polyuria/polydipsia, tachycardia, hyperactivity, diarrhoea, respiratory abnormalities, other cardiac abnormalities, skin lesions, vomiting, moderately raised temperature, decreased activity, decreased appetite, congestive cardiac failure, haematuria and intermittently decreased appetite. Goitre was palpable in 123 cats. The serum total thyroxine concentrations of the cats were more than three standard deviations above the mean of the reference range. Serum total tri-iodothyronine concentrations ranged from 0.78 to 14.96 nmol/litre and were within the reference range in 11 of the cats. Mild hyperthyroidism was a much commoner cause of high normal or marginally above normal thyroid hormone concentrations than severe, concurrent, non-thyroidal illness. Other common biochemical changes were increased of serum alanine aminotransferase, urea, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase. There were minimal changes in the red cell parameters. Leucocyte changes showed two trends: a mature neutrophilia, either with or without an accompanying leucocytosis often in association with a lymphopenia, or an eosinophilia, either with or without a lymphocytosis.
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PMID:Historical, clinical and laboratory features of 126 hyperthyroid cats. 141 11

Medical records of 11 cats with lymphoma involving large granular lymphocytes were reviewed. All 9 cats tested were FeLV-negative. Ten cats had a history of anorexia, lethargy, vomiting, or diarrhea, and had lymphoma involving abdominal viscera. The most common site of tumor in these cats was the jejunum. One cat had cutaneous masses caused by dermal and epidermal infiltration with neoplastic large granular lymphocytes. The most common hematologic abnormality was leukocytosis, characterized by neutrophilia with a left shift (7 cats); 2 cats had a left shift without neutrophilia. None of the cats had lymphocytosis, but immature large granular lymphocytes were found in the blood of 4 cats. The most common serum biochemical abnormalities were hypoalbuminemia (10 cats), hypocalcemia (10 cats), hypoproteinemia (9 cats), high aspartate transaminase activity (9 cats), and hyperbilirubinemia (8 cats). Large granular lymphocytes were characterized by abundant cytoplasm containing distinct azurophilic granules that varied in size and number. The most common cytochemical staining pattern included detection of alpha-naphthyl butyrate esterase, acid phosphatase, and beta-glucuronidase activities. On examination of histologic sections, granules stained weakly eosinophilic with Giemsa and moderately with periodic acid-Schiff reaction. Ultrastructurally, the granules appeared membrane bound and contained an electron-dense matrix in 4 cats.
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PMID:Lymphoma involving large granular lymphocytes in cats: 11 cases (1982-1991). 142 72

Three residents of New Jersey suddenly developed vomiting, abdominal pain, and watery diarrhea 12 h after ingesting five to 13 hand-picked Amanita phalloides-type mushrooms. The group was led by an amateur mycologist who had been eating hand-picked mushrooms without complications for 20 years. The patients developed mild to severe acute hepatic injury, with a peak serum aspartate aminotransferase level ranging from 133 to 826 Karmen U/L, and a peak serum alanine amino-transferase level ranging from 163 to 1176 Karmen U/L. One of the patients developed a transient severe coagulopathy, but no one developed renal failure or hepatic coma, and all rapidly improved. These three cases demonstrate that mycetismus can occur in the heavily urbanized northeastern United States, that consuming hand-picked mushrooms even under the guidance of an experienced amateur may be dangerous, and that Amanita phalloides ingestion produces a biphasic illness with early gastrointestinal symptoms and subsequent hepatic injury.
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PMID:Gastrointestinal and hepatic effects of Amanita phalloides ingestion. 147 67

The efficacy and safety of ursodeoxycholic acid for the treatment of primary sclerosing cholangitis were evaluated in a prospective, randomized, double-blind, placebo-controlled trial. Fourteen patients with primary sclerosing cholangitis documented by cholestatic serum enzyme pattern, liver histological appearance and endoscopic retrograde cholangiography were included in the trial. Six patients received ursodeoxycholic acid (13 to 15 mg/kg body wt/day), and eight patients received placebo. Two patients had to be withdrawn from the study, one because of UDCA-related diarrhea and the other because of worsening of the disease during placebo treatment. Patients in the ursodeoxycholic acid group improved significantly during 1 yr of treatment with respect to serum levels of bilirubin (median = -50%), alkaline phosphatase (median = -67%), gamma-glutamyltransferase (median = -53%), AST (median = -54%) and ALT (median = -36%) compared with the placebo group, but not with respect to serum levels of hydrophobic bile acids. During ursodeoxycholic acid treatment, histopathological features also improved significantly, as evaluated by multiparametric score. Expression of human leukocyte antigen class I molecules appeared to be markedly reduced on liver cells after ursodeoxycholic acid treatment. We conclude that ursodeoxycholic acid is beneficial in reducing disease activity in patients with primary sclerosing cholangitis.
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PMID:Ursodeoxycholic acid for treatment of primary sclerosing cholangitis: a placebo-controlled trial. 150 13


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