Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An adult male pigeon (Columba livia) was presented to the Wildlife Service at the University of Pennsylvania School of Veterinary Medicine for depression, cachexia, and diarrhea. Five days after the initial presentation, the bird died and was necropsied. Gross lesions included opaque air sacs and multiple 1-mm yellow-white foci on the epicardial surface of the heart. Histopathologic lesions included a pericarditis, epicarditis, and multifocal hepatic necrosis accompanied by eosinophilic inclusion bodies. Ultrastructural examination of the hepatic inclusions revealed viral particles consistent with a herpesvirus. The gross, light microscopic, and electron microscopic findings are consistent with pigeon herpesvirus infection.
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PMID:Pigeon herpesvirus: inclusion body hepatitis in a free-ranging pigeon. 301 18

The relationship between circulating thyroid hormones and nutritional status was studied in sarcoma-bearing inbred C57BL/6J mice and control mice. Supplementation with exogenous thyroxine (T4) was also evaluated. Tumor-bearing animals had depressed levels of circulating thyroid hormones. This was also found in food-restricted (pair-fed and pair-weighed) controls. Plasma levels of thyroid hormones decreased with increased tumor burden. Thyrotropin-releasing hormone caused an increased response of thyroid-stimulating hormone in tumor-bearing animals. Low levels of thyroid hormones in sarcoma-bearing mice were due to depressed hormone production by the thyroid gland rather than to increased clearance rate of hormones. Plasma levels of triiodothyronine (T3) correlated to the amount of whole-body nitrogen among sarcoma-bearing mice and food-restricted controls. Exogenous T4 increased food intake by 20% in sarcoma-bearing mice. The benefit of this was probably counteracted by an increased metabolic rate, since reversal of plasma levels of T3 and free T4 had no net effect on body composition of freely eating sarcoma-bearing mice, although it had a negative effect on body and muscle composition in food-restricted controls. Exogenous T4 did not stimulate tumor growth. The results indicate that low circulating levels of thyroid hormones in experimental cancer cachexia are probably caused by the reduced food intake (anorexia), which is in agreement with findings in clinical cancer. Depression of thyroid hormones is probably a physiological means to reduce energy expenditure and to preserve substrates in progressive cancer disease.
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PMID:Thyroid hormones and experimental cancer cachexia. 309 Mar 41

Five cases of carcinoma and one case of lymphosarcoma of the pancreas in cats are reported. Duration of clinical signs ranged between three days and ten weeks, the mean age was 10.2 years. Anorexia, depression, and cachexia were the mean symptoms, in four animals a palpable mass in the cranial abdomen was noted. Laboratory evaluation was unspecific, in all cases diagnosis was performed by necropsy. Further diagnostical and therapeutical possibilities are discussed critically.
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PMID:[Tumors of the exocrine pancreas in the cat]. 318

Autonomic dysfunction was diagnosed in a 2.5-year-old spayed domestic shorthair cat. The cat had an 8-day history of progressive anorexia, signs of depression, constipation, weight loss, and intermittent regurgitation. Physical examination findings were signs of depression, dehydration, cachexia, bradycardia, bilateral nonresponsive mydriasis, prolapse of both nictitating membranes, dry oral and nasal mucous membranes, and urinary bladder atony. Thoracic radiography revealed megaesophagus. The cat lacked esophageal motility and had a decreased gastric emptying rate. Providing adequate fluid intake, electrolyte balance, and nutrition is a major problem in the management of dysautonomic cats. We were able to provide adequate nutritional support for this patient, using total parenteral feeding and, later, enteral nutrition using a nasogastric tube. Results of an ocular pharmacologic study indicated that the mydriasis and prolapse of the nictitating membrane were attributable to complete autonomic denervation of the eye. Using the method described, topical, autonomic-stimulating agents may assist the clinician in diagnosing dysautonomia in the feline. This report describes a syndrome that is well recognized in the United Kingdom and has the potential to develop in the United States.
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PMID:Dysautonomia in a cat. 339 54

Tyzzer's disease has been detected in nine unrelated, commercial rabbitries. During the acute stage of the disease, recently weaned rabbits showed profuse watery diarrhoea. Mortality was between 14.2 and 41.2% during the first three weeks of the outbreaks. In surviving animals, there was a chronic evolution with depression, anorexia, loss of weight and sometimes extreme cachexia. Reproduction animals were less badly affected. Multifocal hepatic necrosis, focal myocardial necrosis, patches of mucosal necrosis in ileum, caecum and colon and marked caecal oedema were most prominent at autopsy. In histological sections of the liver, bundles of slightly Gram-negative and Giemsa-, PAS- and silver-positive rod-shaped bacilli were established in apparently viable hepatocytes bordering foci of necrosis. They were also present in myocytes around necrotic foci in the heart and in enterocytes and smooth muscle cells of the muscularis mucosae of the intestinal mucosa. Transmission electron microscopy showed that these organisms had a similar ultrastructure as Bacillus piliformis. Most antibiotics used failed to combat the disease. Only oxytetracycline was active.
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PMID:Naturally-occurring Tyzzer's disease (Bacillus piliformis infection) in commercial rabbits: a clinical and pathological study. 401 90

Rates of synthesis of protein were measured in vivo in skeletal muscle and in the whole body of cachectic patients with cancer and in normal healthy men, using a tracer infusion of leucine labelled with a stable isotope. Synthesis of protein in muscle was significantly reduced in the patients with cancer (0.030 v 0.198%/hour; p less than 0.01), whereas whole body rates of protein synthesis and degradation did not differ significantly between the two groups. Thus depression of synthesis of protein in muscle appeared to be the immediate cause of muscle wasting in cancerous cachexia. Any therapeutic intervention that aims at preventing the onset of cachexia should be designed to stimulate the synthesis of protein in muscle, and measurement of turnover of protein may be used to evaluate such treatment provided that rates of protein synthesis are measured directly in specific tissues.
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PMID:Protein synthesis in muscle measured in vivo in cachectic patients with cancer. 608 73

An inert artificial tumor (AFT) was inflated in male F344 rats to simulate, experimentally, the growth in mass of large transplantable tumors that produce cachexia. The AFT depressed host weight gain and skeletal muscle mass up to 30% and food intake up to 20% of the depression induced by tumors of comparable size. When the growth rate of the AFT was low, there was no depression of food intake. Work-induced hypertrophy of skeletal muscles, as assessed by a gastrocnemius tenotomy model, was approximately equal to that of normal, tumor-bearing, and AFT-bearing animals. The AFT elevated host total energy expenditure by 12.5% and compartment-of-energy expenditure attributable to motor activity by 10.5%. The elevation of energy expenditure accounted for most of the depression of weight gain of AFT-bearing animals below that of intact animals. The large mass of most transplantable tumors leads to an overestimate of the malignant tissue-depletive effects of tumor and an under-estimate of the asthenic effects.
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PMID:Contribution of inert mass to experimental cancer cachexia in rats. 659 92

Protein synthesis has been measured in vivo in liver and muscle of mice bearing the XK1 tumor, an appropriate model for cancer cachexia. Two different methods were used involving measurement of tracer incorporation into tissue protein either at the end of a 4-hr constant infusion of [14C]tyrosine or 10 min after i.v. injection of a flooding dose of [3H]phenylalanine. Whole-body tyrosine flux was decreased by 60% in cachectic tumor-bearing mice, and protein synthesis was depressed by 70% in muscle and by 40% in liver. The depression of protein synthesis in muscle was due to a reduction in both RNA content (i.e., protein-synthesizing capacity) and RNA activity (i.e., protein synthesized per g of RNA per hr). In liver, the depression of protein synthesis was due entirely to a decrease in RNA activity. The results also suggest that the synthesis of export proteins was affected more than the synthesis of fixed liver protein. Restriction of food intake in normal mice by up to 50% caused a loss of body weight and reductions in protein synthesis in liver and muscle which were less severe than those caused by the presence of the tumor. It is concluded that the wasting which is associated with advanced malignant disease is brought about by a reduction in the rate of protein synthesis in the tissues, and that this cannot be explained by depression of food intake alone.
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PMID:Protein synthesis measured in vivo in muscle and liver of cachectic tumor-bearing mice. 672 6

The Walker 256 carcinosarcoma growing in Sprague-Dawley rats and the Morris 5123 hepatoma growing in Buffalo rats both produce cachexia but have widely differing patterns of host metabolism and tumor growth. Both organisms respond to exogenous insulin with increased food intake and rate of weight gain of host. The insulin treatment response of food intake was 1.5 to 2 times and of body weight gain was 2 to 3 times that of tumor-free controls. Insulin does not accelerate tumor growth. On withdrawal of insulin, the reactive hypophagia seen in tumor-free rats does not occur in tumor bearers, and the host weight does not return to the expected untreated value as it does in tumor-free rats. Most of the weight gained during insulin treatment of tumor bearers above that gained by tumor-free rats is retained after withdrawal of insulin. A computer model based on the inference from these results, that the tumor-bearing host is blind to body weight error, indicates that this abnormality of feeding control could account for only about one-third of the observed depression of host weight and food intake.
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PMID:Feeding response of tumor-bearing rats to insulin and insulin withdrawal and the contribution of autonomous tumor drain to cachectic depletion. 704 59

The potential developmental toxicity of trifluralin was evaluated in rats and rabbits. Pregnant rats and rabbits were dosed once daily by gavage on Gestation Days 6-15 and 6-18, respectively. Doses for rats were 0, 100, 225, 475, or 1000 mg/kg; doses for rabbits were 0, 100, 225, or 500 mg/kg. Cesarean sections were performed on rats and rabbits on Gestation Days 20 and 28, respectively. In rats, maternal toxicity was indicated in the 475 and 1000 mg/kg treatment groups by depression of body weights and food consumption. Fetal viability and morphology were not adversely affected at any dose level. Developmental toxicity was indicated at the 1000-mg/kg dose level by depression of fetal weight. The NOAEL for maternal toxicity in the rat was 225 mg/kg; the NOAEL for developmental toxicity in the rat was 475 mg/kg. In rabbits, maternal toxicity was indicated at the 225 and 500 mg/kg dose levels by abortions and/or deaths in conjunction with anorexia and cachexia. Developmental toxicity was indicated at the 500 mg/kg dose level by depressed fetal viability and weight. Fetal morphology was not adversely affected at any dose level. The NOAELs for maternal and developmental toxicity in the rabbit were 100 and 225 mg/kg, respectively. Based on these data, trifluralin did not exhibit selective toxicity toward the developing conceptus.
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PMID:Developmental toxicity of dinitroaniline herbicides in rats and rabbits. I. Trifluralin. 758 7


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