Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013911 (emaciation)
 1,059 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

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 three-month oral subacute toxicity study of mofezolac (N-22), a non-steroidal anti-inflammatory agent, was performed using dose levels of 6, 20, 60 and 200 mg/kg in rats, and recovery was also assessed one month after withdrawal. 1. Toxic signs caused by N-22 administration, observed only in the 200 mg/kg group, were as follows: soiling around the mouth and/or nose, piloerection, anemia, diarrhea, emaciation and decreased spontaneous locomotor activity. Nine males and thirteen females in the 200 mg/kg group excreted bloody diarrhea and died of general exhaustion between weeks four and thirteen of study. 2. In the 200 mg/kg group, decrease in food consumption and suppression of body weight gain were noted in males from about week four and in females from about week six after initiation of administration, and increase in water consumption was noted in males from about week seven. 3. Urinary examination revealed a decline in urinary pH in males of the 20 mg/kg and above groups and elevation of urobilinogen levels in males of the 60 and 200 mg/kg groups. 4. Hematological examination showed decreases in erythrocyte count (RBC), hematocrit value (Ht) and hemoglobin concentration (Hb) and increase in reticulocyte rate in both sexes of the 200 mg/kg group and an increase in neutrophil rate in males of the 200 mg/kg group. 5. Biochemical examination demonstrated a decrease in chloride (Cl-) in males receiving the 20 mg/kg or above doses and a decrease in calcium (Ca++) in males of the 60 and 200 mg/kg groups. Moreover, there were decreases in cholinesterase (ChE) activity, total protein (TP) and albumin (Alb) values, as well as increases in blood urea nitrogen (BUN), uric acid (UA) and potassium (K+) in both sexes of the 200 mg/kg group, along with elevations in GOT and lactate dehydrogenase (LDH) activities in females of the 200 mg/kg group. 6. The absolute and/or relative organ weights for liver, kidneys, spleen and adrenals were increased in the 200 mg/kg group. 7. On pathological examination, perforating ulceration in the jejunum and ileum, turbid ascites, adhesion and inflammatory changes in capsules of the abdominal organs, splenomegaly, mesenteric lymph node hyperplasia and inflammatory changes in the thoracic cavity were observed in dead animals of the 200 mg/kg group. Similar pathological changes were observed in a few survival cases of the 200 mg/kg group. 8. After a one month recovery period, the above-mentioned changes had mostly recovered, indicating that they were reversible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Three-month oral subacute toxicity study of mofezolac (N-22) in rats]. 223 86

A 44-year-old man suffered from repeated impairment of consciousness associated with flapping tremor, myoclonus and generalized convulsions, and died in coma 6 months after admission. He had had a psychosomatically underdeveloped childhood, with a propensity for legumes without a family history of the same or a record of consanguinity. On admission, he had disturbed consciousness and emaciation without other physical abnormalities. The EEG revealed diffuse slow waves with occasional appearance of triphasic waves. A high level of serum citrulline (534.7 nmol/ml) was recognized and the assay of urea cycle enzymes in the liver demonstrated decreased argininosuccinate synthetase (ASS) activity (0.062 U/g liver, 7.4% of that in normal liver), although no kinetic abnormality was found. Accordingly he was diagnosed as having type II citrullinemia. In addition, this case could be classified as cluster type of localization of the ASS in the liver by immunohistochemical study. There were characteristic findings concerning his clinical picture and laboratory data, such as a significant correlation between the grade of disturbed consciousness and arterial blood gas pH (r = 0.61, p less than 0.01). However, the blood ammonia level did not always correlate with the severity of disturbed consciousness. Oral treatment with sodium citrate and sodium benzoate was very effective, though transiently, for disturbed consciousness in this case. Pathological findings of the autopsied liver were fatty change and fibrosis. Neuropathologically, characteristic findings were brain edema with cerebellar tonsilar herniation, laminar necrosis with spongy formation in cerebral cortex, and Alzheimer type II glia. The relationship between citrullinemia and other hepatic encephalopathy was also discussed.
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PMID:[An autopsied case of type II citrullinemia--transient effectiveness with either citrate or benzoate to the consciousness disturbance]. 269 30

A reproducible experimental disease model in horses using Streptococcus zooepidemicus was developed. An intravenous challenge dose of 1 X 10(10) colony-forming units (CFU), followed 24 h later with another challenge of 1 X 10(8) CFU of Strep. zooepidemicus produced the desired disease model. The disease was characterized by depression, pyrexia, anorexia, abnormal lung sounds, inflammation of joints, moderate to severe lameness, gradual loss of condition and emaciation. The effects of the disease on hematology, serum chemical profile and different protein fractions were studied. The disease state had no effect on serum glucose, sodium, potassium, chloride, urea nitrogen, creatinine, uric acid, calcium, phosphorus and enzymes SGOT or SGPT. However, the alkaline phosphatase showed a gradual decline. The serum iron levels dropped markedly and remained low to the last day of observations (post-infection day, PID 13). On serum protein electrophoresis, the albumin showed a gradual decrease; whereas, alpha II, beta and gamma globulin levels rose suggesting an immune response. The elevation of rectal temperatures and white blood cell counts related well with clinical observations. The serum iron levels proved very helpful in predicting the severity of clinical signs and often dropped before the onset of clinical signs and pyrexia.
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PMID:Standardization of an experimental disease model of Streptococcus zooepidemicus in the equine. 649 45

Camel haemonchosis is prevalent in the Sudan, especially during the rainy season, with a decrease in prevalence in the dry season possibly due to delayed maturation of the worms. The naturally occurring disease in Sudanese camels is characterized by emaciation, anaemia, oedema of the lower parts of the limbs, eosinophilia, hypoproteinaemia, hypoalbuminaemia, hyperglobulinaemia and eosinophilia, as well as elevated blood urea concentrations.
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PMID:The prevalence and pathogenesis of naturally-occurring Haemonchus longistipes infection in Sudanese camels. 673 5

Haematological and serum biochemical examinations were carried out on 12 high grade bull calves fed Gnidia latifolia (Meisn). This resulted in lymphocytopaenia, increased blood urea nitrogen and lactate dehydrogenase. There were no changes in the red blood cell counts, neutrophil counts, aspartate amino transferase, creatine phosphokinase and alkaline phosphatase. There was also no change in serum protein concentration. Post-mortem changes in the acutely intoxicated calves included petechial haemorrhages of the epicardium and submucosa of the rumen, abomasum and the intestines. The chronic cases showed a generalized emaciation with gelatinous atrophy of the body fat and accumulation of excess fluid in the body cavities. The lymph nodes and spleen showed lymphocytic degeneration with cellular depletion in the follicles. There were extensive liver fibroses in the chronic cases.
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PMID:Haematological and biochemical changes in cattle poisoned by Gnidia latifolia syn. Lasiosiphon latifolius (Thymelaeaceae). 715 95

A nondopaminergic antipsychotic agent, 5-ethyl-1,3,8-trimethyl-1H-imidazo]1,2-c]pyrazolo[3,4-e]pyrimidine (TIPP; PD 112488), has been tested for potential toxicity in rats. As part of a preclinical safety evaluation, 10 Wistar rats per sex were administered TIPP as a dietary admixture, receiving doses of 0, 5, 10, 20, 25, 50, 100, and 200 mg/kg for 2 wk. In addition, 3 groups of 6 male Wistar rats were administered TIPP (PD 114877 and PD 117498, acid hydrolysis products of TIPP) at 100 mg/kg by gavage for 5 days. All animals given 200 mg/kg were euthanatized in moribund condition or found dead after 1 wk of treatment. Clinical evidence of renal toxicity was noted and included emaciation, hematuria, urinary incontinence, and enlarged kidneys at doses of 10 mg/kg and higher. Plasma urea levels were higher than those of controls in all TIPP-treated groups. Significant pathologic changes of the urothelium were evident at all doses and were characterized by necrotizing pyelitis and cystitis. Necrosis and inflammation of the urothelium resulted in secondary hydronephrosis. No renal toxicity was noted with the acid hydrolysis products. The urothelial changes with oral administration of TIPP in rats is species-specific, and the specificity may be related to the metabolism and excretion of the drug.
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PMID:Renal toxicity of a nondopaminergic antipsychotic agent, trimethyl imidazopyrazolopyrimidine, in rats. 791 30

This paper describes a leiomyosarcoma found in the distal part of the jejunum of a 7 year old, East Friesian dairy sheep. The animal showed a progressive emaciation during 3 months, leucocytosis, neutrophilia, relative lymphocytopenia and increased levels of serum urea. On histology, the tumor was characterized by anaplasia, cellular and nuclear polymorphism and also by regressive processes and local invasion. Characteristic features such as numerous mitotic figures and giant cells were also observed.
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PMID:[Clinical and pathologico-anatomic findings in a leiomyosarcoma of the jejunum of a sheep]. 804 29


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