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)

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

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

Furazolidone (FZ) was administered to 42-day-old female Japanese quails as a feed additive at doses of 0, 200, 400, 600 and 800 ppm for a period of 28 days. Dose-dependent effects were observed. High levels of FZ (600 and 800 ppm) significantly altered growth, decreased feed consumption, caused marked atrophy of the ovaries and oviducts leading to cessation of egg laying, and resulted in higher mortality. Hepatotoxicity was evidenced by an increase in serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase and a decrease in serum total protein, in addition to degenerative changes of the hepatocytes in FZ-treated birds. A rise in serum urea was also observed. Symptoms leading to death included a loss of appetite causing emaciation followed by nervous disturbances (compulsive movements and circling). No signs of cardiomyopathy were observed. Japanese quails did not tolerate FZ at a concentration (400 ppm) recommended for the prevention of salmonellosis in poultry.
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PMID:Toxicological and biological studies on Japanese quails fed graded levels of furazolidone. 209 13

A trotter stallion showing symptoms of emaciation was suspected of disease of the liver associated with cholestasis in view of clinical symptoms (poor appetite, sluggishness, jaundice and oedema) and the results of examination of the blood (increased concentrations of gamma-glutamyl, transpeptidase, sorbitol dehydrogenase, alkaline phosphatase, aspartate aminotransferase and markedly increased conjugated bilirubin). A specimen removed at biopsy of the liver revealed the presence of portal fibrosis and severe cholestasis. At autopsy, it was found that very extensive fibrosis of the pancreas (probably due to migrating larvae of parasites) had caused extrahepatic cholestasis accompanied by fibrosis of the liver. The lesions of the coronary border, which were also present in this horse, could not be accounted for.
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PMID:[Extrahepatic cholestasis due to pancreas fibrosis in a trotter]. 397 93

Eleven adult Basenji dogs with immunoproliferative small intestinal disease (IPSID) were studied. Two items of history related to the digestive tract were characteristic: (i) chronic intractable diarrhea in most dogs, and (ii) progressive emaciation. Anorexia was intermittent in only a few dogs. In addition, skin lesions of various degrees of severity were observed, including alopecia of pinnae and ventrum, hyperpigmentation and hyperkeratosis of pinnae, and necrosis and ulcerations of margins of pinnae. The cause of the skin lesions was not determined; however, hypothyroidism did not appear to contribute to the skin changes. Standard hematologic and serum chemical values were not consistently abnormal. However, a poorly regenerative anemia, mild neutrophilia, and increased aspartate aminotransferase and alanine aminotransferase activities were generally observed in severely affected dogs. The Pelger-Huet anomaly was identified in dog 3. Maldigestion and malabsorption as determined by the N-benzoyl-L-tyrosyl-p-aminobenzoic acid and d-xylose test was documented to varying degrees in dogs with IPSID. Maldigestion was correlated with functional pancreatic exocrine insufficiency. Severe malabsorption was documented in only 3 dogs. Serum gastrin values were evaluated in these dogs because of a prior observation of parietal cell hyperplasia and gastric ulceration. Hypergastrinemia was documented in 3 dogs. Additional studies will be necessary to determine whether an acid hypersecretory state contributes to the pathogenesis of IPSID in Basenjis.
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PMID:Clinical and laboratory characterization of Basenjis with immunoproliferative small intestinal disease. 660 87

Male New Zealand White rabbits were treated with microsomal enzyme inducers, inhibitors of hemoprotein synthesis or action, and glutathione precursor and depletor before they were orally given the median lethal dose (LD50) of aflatoxin B1 (AFB1; 0.4 mg/kg) at the start of a 7-day experimental period. The drugs administered, mean duration of illness (hours), and survival percentage were as follows: controls (saline solution)-85, 50%; phenobarbital (PB)-100, 100%; phenylbutazone-115, 67%; benzoflavone-39, 17%; stanozolol-67, 67%; cobaltous chloride (CoCl2)-46, 67%; piperonyl butoxide (PBO)-88, 100% cysteine (CYS)-68, 100%; ethyl maleate-71, 83%. Signs of toxicosis included decreased feed and water consumption, weight loss, dehydration, lethargy, and emaciation; some rabbits died or were euthanatized. Clinico-pathologic changes included increased serum aspartate aminotransferase (AST) activity by 24 hours and bilirubin concentration by 48 to 72 hours after AFB1 was given. Grossly, livers were pale or tan and friable, with prominent lobular architecture. Kidneys of affected rabbits were pale to dark red. Microscopically, livers were normal or had lesions as great as extensive necrosis, hemorrhage, mineralization, and bile duct proliferation. Treatment of rabbits with PB, CoCl2, PBO, and CYS protected against AFB1 hepatic pathology, and PB, PBO, and CYS also had protective effect against lethality. Ethyl maleate provided some protection against lethality and increased serum AST activity and bilirubin concentration. Toxicosis was enhanced by benzoflavone; phenylbutazone and stanozolol had litte influence.
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PMID:Effect of enzyme inducers and inhibitors and glutathione precursor and depleter on induced acute aflatoxicosis in rabbits. 680 67

Outbreaks of ovine white liver disease (WLD) on 7 farms in eastern Victoria were investigated. Most occurred in late spring and mainly affected lambs 3 to 6 months old, with a morbidity of 20 to 100% and mortality of 8 to 15%. Clinically affected lambs showed illthrift, emaciation and bilateral, serous, ocular discharge. Clinical pathology showed mild anaemia, elevated serum liver enzymes (GGT, OCT, AST) and low levels of serum vitamin B12. Grossly, the livers were pale, fatty and friable; microscopically there was parenchymal fatty change, bile duct proliferation and ceroid pigmentation. Liver cobalt values were consistently low (mean 0.4 +/- 0.4 mumol/kg D.W.). Levels of cobalt in pasture from 2 properties were very low (0.34 mumol/kg D.W.) The diagnosis of white liver disease was made on the basis of clinical features, specific liver pathology and low cobalt status. Treatment trials established that cobalt injections or oral bullet administration resulted in clinical improvement, significant weight gains, and improved serum vitamin B12 levels. WLD did not recur in previously affected sheep using these treatments. However, when blocks containing cobalt were available continuously, WLD recurred 2 years after the initial outbreak.
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PMID:White liver disease of sheep. 713 31

From 1984 through 1992, staff at The Marine Mammal Center (TMMC, Sausalito, California, USA) examined 207 northern elephant seals (Mirounga angustirostris) with a condition of unknown etiology called northern elephant seal skin disease (NESSD). The skin lesions were characterized by patchy to extensive alopecia and hyperpigmentation, punctate or coalescing epidermal ulceration, and occasionally, massive skin necrosis. Microscopic lesions included ulcerative dermatitis with hyperkeratosis, squamous metaplasia and atrophy of sebaceous glands. All diseased seals were less than 2 years of age and suffered from emaciation, depression, and dehydration. Mortality from septicemia increased significantly with severity of skin ulceration. Compared to 14 apparently unaffected seals, diseased seals had depressed levels of circulating thyroxine, triiodothyronine, retinol, serum iron, albumin, calcium, and cholesterol. Levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transpeptidase, blood urea nitrogen, and uric acid were elevated. Morphometrically, diseased animals were approximately 15% smaller than normal seals of the same sage. Serum and blubber concentrations of 36 polychlorinated biphenyl congeners (sigma PCB) and dichloro-diphenyl-dichloroethylene (p,p'-DDE) were negatively correlated with body mass. Mean concentrations of sigma PCB and p,p'-DDE in serum in diseased seals were elevated as compared to apparently normal seals. Etiology of this syndrome remains unknown, but the possibility of PCB toxicosis cannot be ruled out.
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PMID:Clinical and pathological characterization of northern elephant seal skin disease. 924 88

Forty-six cats with clinical haemobartonellosis were studied; 75 per cent of the cats of known age were two-and-a-half years old or younger, 50 per cent were intact males and 19.5 per cent were castrated males. The predominant signs of the disease were tachypnoea, lethargy, depression, anorexia, infestation with fleas, pale mucous membranes, icterus, emaciation, dehydration, splenomegaly, anaemia, leucocytosis, increased activities of alanine aminotransferase and aspartate aminotransferase, and azotaemia. Thirty-eight per cent of the cats that were tested for feline leukaemia virus (FeLV) antigen were positive, and 22 per cent of those tested for feline immunodeficiency virus (FIV) antibodies were positive. The prevalence of both FeLV and FIV was much higher than in the general Israeli cat population. The cats infected with both Haemobartonella felis and FeLV had a significantly lower body temperature, were more anaemic and the mean cell volume of their erythrocytes was greater than in the cats with haemobartonellosis alone.
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PMID:Retrospective study of 46 cases of feline haemobartonellosis in Israel and their relationships with FeLV and FIV infections. 1216 25


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