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)

Dried, milled Cestrum laevigatum plant material was drenched to 6 ewes at doses ranging from 2,5 to 10 g/kg/day for 1 to 47 days. The most noticeable clinical signs were depression, anorexia and ruminal stasis. These signs were accompanied by clinical pathological changes indicative of liver involvement such as increases in the serum activities of aspartate transaminase, lactate dehydrogenase and gamma-glutamyltransferase. Hepatosis characterized by accentuated lobulation, and centrilobular to midzonal coagulative necrosis, haemorrhage and congestion occurred in 2 of the 3 ewes given high doses of plant material. Liver lesions in the other animals included disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas. Spongy changes in the cerebral white matter were evident in the ewes of the high-dose group. Ultrastructural changes in the liver comprised degeneration and necrosis of hepatocytes and occasionally endothelial cells, and disruption of sinusoidal walls.
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PMID:Experimentally-induced Cestrum laevigatum (Schlechtd.) poisoning in sheep. 151 94

Chronic alcoholics are all too often not recognized in general practice. Diagnosis is only possible if the doctor assumes potential alcoholism in all his patients. Because of the tendency of the patient and often his family to deny alcohol dependence, diagnosis is only possible by taking psychiatric, somatic and psychosocial aspects into consideration in addition to an independent history. Questionnaires may be helpful. The severity of the dependence on alcohol is not a predictor of success in therapy. In practice, three types of alcoholics may be distinguished: (1) patients with stable social relationships; (2) patients with stable social relationships and severe anxiety or depression with alcohol abuse as an inadequate self medication; (3) patients who are not able to maintain stable relationships. The latter are unlikely to be successfully treated by a family physician. A careful classification of patients according to these simple criteria may reduce the rate of treatment failures. Therapy by the family physician is initiated with an extensive somatic, psychiatric and psychosocial work-up, and maintained by counseling and care. An important factor is close collaboration between physician and social worker. Disulfiram may be a powerful adjunct to the therapy of the family physician if supervised by a trustee. In our departments we work with alcoholics in a joint consultation service involving an internist and a psychiatrist. Two thirds of the patients who consent to supervised disulfiram remain in the program for a year. 3 months after initiation of the treatment, gamma-glutamyltransferase, ASAT, ALAT and MCV are normalized. A follow-up 5 years after treatment indicated the efficacy of this treatment.
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PMID:[What does the alcoholic patient need from his family physician?]. 158 34

Duodenitis/proximal jejunitis syndrome (DPJ) is a small intestinal disease of horses that is associated with depression and copious gastric reflux. Since an infectious cause for DPJ remains unsubstantiated, these studies were designed to investigate the possible role of Fusarium moniliforme toxins in this disease. Fusarium moniliforme was isolated by culturing 2 samples of feed that had been fed to horses with clinical signs of DPJ. These isolates (AU 2/3) were subsequently grown concurrently on autoclaved corn and their toxicity evaluated in a feeding trial utilizing horses. Isolates of F moniliforme known to be low and high producers (RRC 415 and MRC 826, respectively) of fumonisin B1 (FB1) were cultured individually on corn and each fed separately to other groups of horses. Control horses were fed autoclaved corn that was not inoculated with fungus. Production of FB1 by isolates RRC 415, MRC 826 and AU 2/3 were 19, 4360 and 1455 ppm, respectively. Each group contained 2 horses and the test diets were prepared by diluting culture material with sweet feed and clean corn. The test diets consisted of control corn that contained < 1 ppm FB1, RRC 415 diluted to < 1 ppm FB1, MRC 826 diluted to 200 ppm FB1, and AU 2/3 culture material diluted to contain 65 ppm FB1 on days 1-10 and 130 ppm on days 11-27. Horses fed either MRC 826 or AU 2/3 had elevated serum gamma-glutamyltransferase after 7 to 21 d exposure and elevated serum L-iditol dehydrogenase activity after 7 to 19 d exposure to test diets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An investigation of the role of Fusarium moniliforme in duodenitis/proximal jejunitis of horses. 770 89

Seven horses developed clinical or subclinical hepatitis 48 to 87 days after administration of tetanus antitoxin. One horse had mildly high hepatic enzyme activity 120 days after inoculation with tetanus antitoxin. The first horse developed signs of depression, lethargy, and anorexia. During hospitalization, signs of hepatoencephalopathy were noticed, and laboratory data were consistent with hepatic disease. Another horse that was found dead had gross and histologic lesions compatible with serum hepatitis. Screening of serum gamma-glutamyltransferase (GGT) and aspartate transaminase activities were used to investigate the remaining horses in the herd. High GGT activities (71 to 206 IU/L) were detected in 5 additional herd members. These horses appeared clinically normal, apart from 2 reports of nasal photosensitization and an aborted fetus. In 3 horses, high serum GGT activity persisted over a 44-day testing period. All affected horses had been given tetanus antitoxin within 12 hours of parturition, and a common source of vaccine was identified for 7 horses. Findings in this group of horses indicate that clinical and subclinical serum hepatitis can develop after administration of tetanus antitoxin.
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PMID:Hepatic disease associated with administration of tetanus antitoxin in eight horses. 778 47

The purpose of this study was to determine the effects of experimental fasciolosis at various stages of development on the daily food intake of sheep. Five male Churra sheep, 4 months of age, were infected orally with 300 Fasciola hepatica metacercariae over a 30 day period. There was a significant increase in serum glutamate dehydrogenase (GLDH) activity from 40 days post-infection and in aspartate aminotransferase (AST) activity from 60 days post-infection. Both enzyme activities reached maximum levels in the serum of infected animals at 80 days and then progressively decreased. Serum gamma-glutamyltransferase (GGT) activity was significantly increased from 80 to 120 days post-infection. Glycaemia was significantly decreased from 60 days post-infection. The average daily food intake was shown to steadily decrease until approximately 100 days. The coincidence of decreased food intake with the period of significant increase, both in AST and GLDH activities, indicated that damage caused around the time of migration of immature flukes through the liver parenchyma may be involved in appetite depression.
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PMID:Appetite depression in sheep experimentally infected with Fasciola hepatica L. 788 21

Biochemical and histochemical studies were conducted in aflatoxin B1-induced liver tumors in adult rainbow trout. Specific activities of the phase I enzymes, ethoxyresorufin-O-deethylase (EROD), microsomal and cytosolic epoxide hydrolase (mEH and cEH), aldehyde dehydrogenase (ALDH) and DT-diaphorase, and the phase II enzymes, gamma-glutamyltransferase (gamma-GT), glutathione transferase (GST) and uridine diphosphoglucuronyl transferase (UDPGT) were measured. Cryostat sections of tumor and surrounding liver from the same cohorts were analyzed immunohistochemically for cytochrome P450IA1 and histochemically for ALDH (benzaldehyde and hexanal), DT-diaphorase, gamma-GT and uridine diphosphoglucuronyl dehydrogenase (UDPGdH). In tumor tissues, the largest biochemical changes were found with benzaldehyde dehydrogenase, where activity increased from undetectable levels to 7.4 nmol/min/mg protein, and gamma-GT, where activity increased 12-fold over controls. Increases in other enzymes ranged from 1.26 to 2.84 times that of control liver, except EROD, which decreased, and cEH and mEH, which were unchanged. Histochemical analyses showed the induction of ALDH, gamma-GT, DT-diaphorase and UDPGdH, and the depression of cytochrome P450IA1 in hepatic neoplasms. In addition, marker enzyme histochemistry of neoplasms revealed heterogeneous populations of hepatocytes and absence of necrotic areas.
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PMID:Biochemical and histochemical properties of hepatic tumors of rainbow trout, Oncorhynchus mykiss. 809 46

In cattle with hepatic lipidosis, hepatic abscessation, leptospirosis, biliary calculi or fasciolosis, the progression of the disease was studied by serial measurements of serum total bile acid concentrations, plasma glutamate dehydrogenase, gamma-glutamyltransferase, 5'-nucleotidase and leucine aminopeptidase activities Terminalia avicennioides and by liver biopsy. Regardless of the cause of the hepatic disease, weight loss, anorexia, dullness and depression were consistent features. Signs of hepatic encephalopathy, such as blindness, head pressing, excitability, ataxia and weakness were less common and, together with pyrexia and jaundice, were grave prognostic signs. Plasma ammonia concentrations were significantly elevated compared to clinically normal cattle, but such changes were not always accompanied by a decline in plasma urea concentrations. In normal, healthy cattle, the plasma ammonia:urea concentration ratio is 9:1 and the plasma ammonia:glucose concentration is 11:1. In hepatic disease, a plasma ammonia:glucose ratio > 40:1 or plasma ammonia:urea ratio > 30:1, particularly with a rising total ketone body concentration and a declining glucose concentration, carried a guarded prognosis. The study suggested that other factors, such as hypokalaemia, alkalosis, short-chain volatile fatty acids, and false and true neuro-transmitters, may be important in the pathogenesis of hepatic coma in cattle.
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PMID:Clinical and pathological studies in cattle with hepatic disease. 909 45

In 1987, the National Institute for Occupational Safety and Health conducted a cross-sectional medical study to examine the long-term health effects of occupational exposure to chemicals and materials contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). This study compared living workers employed more than 15 years earlier in the production of sodium trichlorophenol (NaTCP), and 2,4,5-trichlorophenoxyacetic ester (2,4,5-T ester) with an unexposed comparison group. Health status of the worker and comparison populations was collected through a comprehensive set of standardized interviews and medical examinations. Lipid adjusted serum TCDD levels were also measured. Workers had a statistically significantly elevated mean serum lipid-adjusted TCDD level (workers = 220 pg per g of lipid [range = not detected-3,400 pg per g of lipid], and referents 7 pg per g of lipid [range not detected-20 pg per g of lipid], P < 0.001). Compared to a community-based referent population, the prevalence of chronic bronchitis, chronic obstructive pulmonary disease, peripheral neuropathy, depression, cardiovascular outcomes (myocardial infarction, angina, cardiac arrhythmias, hypertension, and abnormal peripheral arterial flow), abnormal porphyrin levels, and abnormal ventilatory function parameters FEV1.0, FVC, or FEV1.0/FVC% in workers, was not statistically significantly different. In contrast, relationships were observed between serum 2,3,7,8-TCDD levels and the enzyme gamma-glutamyltransferase (GGT), the reproductive hormones serum testosterone, luteinizing, and follicle-stimulating hormones, and abnormal high-density lipoprotein concentration, counts of CD3/Ta1 cells (helper lymphocytes), and fasting serum glucose levels. Current diagnosis of chloracne was associated with the highest levels of serum 2,3,7,8-TCDD. Analysis of other endpoints continues.
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PMID:Review and update of the results of the NIOSH medical study of workers exposed to chemicals contaminated with 2,3,7,8-tetrachlorodibenzodioxin. 950 33

Cholestatic jaundice is the major complication of total parenteral nutrition (TPN) in infancy. We have previously shown that the TPN solution is directly toxic to the liver, and that this toxicity appears to be mediated by one or more amino acids. Elevated serum methionine levels, without corresponding increases in its metabolites, suggest that accumulation of this toxic amino acid may cause TPN cholestasis. Nine-week-old rabbits (n = 28) were divided into three groups. The FED group was fed standard rabbit chow ad libitum. The TPN group was not fed and received only i.v. TPN (including methionine 121 mg.kg-1.d-1), and lipids. The EXP group was fed chow ad libitum and received i.v. methionine (121 mg.kg-1.d-1). After 14 d, we evaluated bile flow, bromosulfophthalein excretion, serum liver enzymes, liver histology, and serum amino acid levels. Bile flow was significantly depressed in the TPN and EXP groups compared with FED controls (32.9 +/- 9.4 and 45.7 +/- 14.4 versus 82.9 +/- 13.8). Excretion of the bilirubin analog bromosulfophthalein tended to be delayed by methionine infusion (p = 0.15). Serum liver enzymes (aspartate transaminase, alanine aminotransferase, gamma-glutamyltransferase, and alkaline phosphatase) were normal in all groups. Histologic liver injury in the EXP group was similar to that caused by TPN. Balloon degeneration, and portal inflammation were seen in both groups. Homocysteine, an early metabolite of methionine, was elevated in the TPN and EXP groups compared with FED controls. Intravenous methionine is hepatotoxic. Despite full oral feeding, it produces a depression of bile flow and histologic liver injury similar to that seen with TPN. Elevated homocysteine levels suggests an enzymatic block early in the pathway of methionine metabolism. We believe that methionine may be an important factor in the pathogenesis of TPN cholestasis.
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PMID:Methionine infusion reproduces liver injury of parenteral nutrition cholestasis. 1023 61

An experiment was conducted to investigate the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological parameters of starter pigs. A polymeric glucomannan mycotoxin adsorbent (GM polymer, Alltech Inc., Nicholasville, KY) was also tested for its efficacy in preventing Fusarium mycotoxicoses. A total of 150 starter pigs (initial weight of 9.3 +/- 1.1 kg) were fed one of five treatment diets (six pens of five pigs per diet) for 21 d. Diets included control, low level of contaminated grains, high level of contaminated grains, high level of contaminated grains + 0.20% GM polymer, and pair-fed control for comparison with pigs receiving the high level of contaminated grains. Feed intake and cumulative weight gain of pigs decreased linearly with the inclusion of contaminated grains in the diet throughout the experiment (P < 0.0001). Weight gains recovered, however, during wk 3 (P > 0.05). There was no difference between the pair-fed group and the pigs fed the diet containing the high level of contaminated grains in terms of weight gain or feed efficiency (P > 0.05). Feeding contaminated grains linearly increased the serum albumin:globulin ratio (P = 0.01), whereas serum urea concentrations and gamma-glutamyltransferase activities responded in a quadratic fashion (P = 0.02). When compared with the pair-fed pigs, serum concentrations of total protein (P = 0.01) and globulin (P = 0.02) were decreased in pigs fed the diet containing the high level of contaminated grains. The feeding of contaminated diets did not significantly alter organ weights expressed as a percentage of BW, serum immunoglobulin concentrations, percentages of peripheral blood lymphocyte subsets, contact hypersensitivity to dinitrochlorobenzene, or primary antibody response to sheep red blood cells (P > 0.05). It was concluded that most of the adverse effects of feeding Fusarium mycotoxin-contaminated grains to starter pigs were caused by reduced feed intake. Although supplementation of GM polymer to the contaminated diet prevented some toxin-induced changes in metabolism, it did not prevent the mycotoxin-induced growth depression under the current experimental conditions.
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PMID:Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological measurements of starter pigs, and the efficacy of a polymeric glucomannan mycotoxin adsorbent. 1460 83


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