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)

Monensin and lead were administered separately or concurrently at different toxic doses to broiler chicks. Administration of lead alone did not result in a significant depression of haematological parameters. Administration of higher levels of monensin caused a reduction in haematocrit and an increase in blood serum levels of alanine aminotransferase, aspartate aminotransferase and cholesterol. Concurrent administration of monensin and lead caused a severe depression of haematological profiles which indicated the existence of an interaction between the two substances. It was concluded that concurrent administration of monensin and lead potentiated the toxic effects of each other.
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PMID:Oral administration of monensin and lead to broiler chicks: effects on haematological and biochemical parameters. 781 Mar 94

The effects of protein malnutrition on haematological and serum biochemical values were evaluated in gossypol-treated rats which were simultaneously fed with ethanol. Gossypol caused anaemia, leucopenia and thrombocytopenia in malnourished animals, suggesting a depression of bone marrow activity. Gossypol also caused a significant elevation of serum alkaline phosphatase and alanine aminotransferase activities and increases in the concentrations of Mg++ and Ca++ with reduced albumin, regardless of the nutritional status. These changes were more severe with malnutrition. Ethanol alone caused a thrombocytopenia but no other significant haematological changes. However, it appeared to cause derangement of lipid and protein metabolism as reflected in serum cholesterol and urea. The toxic effects seen in gossypol-treated rats were significantly reduced in animals simultaneously given ethanol. As the livers of gossypol-treated rats were significantly heavier than in these animals, it seems possible that ethanol consumption enhances the ability of the liver to metabolize gossypol, thereby reducing its accumulation and consequently its toxicity. However, further studies are needed to determine the mechanisms responsible.
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PMID:Haematological and serum biochemical changes in the rat due to protein malnutrition and gossypol-ethanol interactions. 788 58

This study evaluated levo-alpha-acetylmethadol hydrochloride (LAAM), a long-acting morphine-like (mu) agonist approved in 1993 to treat opiate dependence. Sprague-Dawley rate (20/sex/group) were gavaged with doses of 3.0-33.5 mg kg-1 for 30 days followed by a 14-day drug-free recovery period. Treatment-related effects included dose-dependent CNS depression, decreased food consumption and body weight gain, reddish urine and abdominal staining. Tolerance developed by day 7. Mortality was dose-dependent; deaths occurred predominantly during the first week. Increased alanine aminotransferase (SGOT, AST) and lactate dehydrogenase (LDH), observed only in high-dose males, were associated with findings in liver. Decreases in spleen/brain weight and increases in brain/body weight ratios were seen in both sexes. Decreases in weights of heart, liver and kidney achieved statistical significance only for high-dose groups. Kidneys of mid- and high-dose groups displayed intertubular mineral/crystal deposition, focal corticomedullary mineralization and focal regenerative tubular epithelium. Centrilobular hypertrophy was observed in livers of high-dose males and mid- and high-dose females. Following the recovery period, decreased body weights and increased brain/body weight ratios occurred in mid-dose males and low-dose females. Weights of liver and kidney and organ/brain weight ratios were decreased in mid-dose males. Histopathological findings observed in kidneys and livers had abated. In summary, acute and repeated administration of LAAM produced a spectrum of activity consistent with its profile as a long-acting pure mu-agonist which stimulates microsomal enzymes in rodents. Renal and hepatic effects seen in initially drug-naive rats treated with morphine-type agonists are not observed in tolerant individuals stabilized on mu-agonists to treat opiate dependence.
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PMID:Toxicological evaluation of mu-agonists. Part I: Assessment of toxicity following 30 days of repeated oral dosing of male and female rats with levo-alpha-acetylmethadol HCl (LAAM). 788 49

Cytauxzoonosis is a rapidly and highly fatal disease in cats that is caused by the protozoan Cytauxzoon felis, which may be transmitted by Ixodid ticks (Dermacentor variabilis) from parasitemic bobcats (Lynx rufus). During an 8-year period, cytauxzoonosis was diagnosed in 8 cats, 7 cats within 14 months. Risk factors for these cats were warm weather, access to a wooded environment, and exposure to ticks. The most consistent clinical signs were acute lethargy, anorexia, decreased response to external stimuli (depression), icterus, dehydration, and capillary refill time > 2 seconds. Pertinent clinicopathologic findings were normocytic normochromic anemia, leukopenia, and thrombocytopenia; high serum concentrations of total bilirubin and glucose, low serum concentrations of albumin and potassium, high serum alanine transaminase activity; and, bilirubinuria. Confirmation of cytauxzoonosis was made by cytologic or histologic identification of the C felis organism. Splenic, lymph node, and bone marrow aspirates can provide an antemortem diagnosis when the number of parasitized erythrocytes is low on blood smears. Supportive treatment of 6 cats was temporarily palliative in some, but all 8 cats either died (3) or were euthanatized (5) when they became moribund. Survival time from observed onset of illness to death was < 5 days. Necropsy of 4 cats revealed predominately pulmonary involvement with venous congestion. Histologic examination revealed venous occlusion by parasitized mononuclear phagocytes in all tissue specimens, but only minimal inflammatory infiltrates.
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PMID:Cytauxzoonosis in cats: eight cases (1985-1992). 796 Oct 73

Millions of people have been exposed to silicones which are present in consumer goods such as cosmetics and toiletries, processed foods and household products. In addition, silicones have been used extensively in medical practice as a lubricant in tubing and syringes, and as implantable devices. A silicone widely used in medical practice is polydimethylsiloxane. This study was undertaken to determine the immunotoxicologic potential of long term exposure to the principal constituents of breast implants: silicone fluid, silicone gel and silicone elastomer. An alternative covering for devices containing silicone gels, polyurethane, was also included in the study. Silicone fluid and gel were injected subcutaneously into female B6C3F1 mice (1 ml/mouse) and 6 mm disks of silicone elastomer or polyurethane were implanted subcutaneously. There were no treatment-related deaths or overt signs of toxicity during the 180 day exposure. None of the tested materials had notable effects on body or organ weights, erythrocytes or leukocytes in the blood, blood chemistries such as alanine aminotransferase, urea nitrogen, glucose, albumin or total protein, or serum CH 50 or C3 levels. The cellularity of the bone marrow and responses to CSF-GM and CSF-M were normal. The tested silicones and polyurethane marginally reduced the level of Ig+ cells in the spleen but did not consistently alter the distribution of T cell surface markers. The antibody response to sheep erythrocytes was not markedly altered, nor were proliferative responses to concanavalin A, phytohemagglutinin, lipopolysaccharide or allogeneic cells. Reticuloendothelial function was normal, as was phagocytosis of chicken erythrocytes and Covaspheres by adherent peritoneal cells. Natural killer cell activity was depressed in all silicone treatment groups and in mice implanted with polyurethane. No silicone or polyurethane treatment group displayed altered susceptibility to a challenge with Listeria monocytogenes, Streptococcus pneumoniae or the B16F10 tumor. The only consistent effect of 180 day exposure to silicone materials or polyurethane was a modest depression of natural killer cell activity.
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PMID:Immunotoxicity of 180 day exposure to polydimethylsiloxane (silicone) fluid, gel and elastomer and polyurethane disks in female B6C3F1 mice. 798 84

99mTc-DTPA-galactosyl human serum albumin (99mTc-GSA) is a new liver imaging agent which binds to heptic binding protein. This study evaluated the sensitivity of 99mTc-GSA kinetics and imaging anatomy to congestive hepatic injury in rats. Regional hepatic congestion was induced by clamping the left hepatic vein for 5, 10, 20, 40, or 90 min. After recanalization, 99mTc-GSA was intravenously administered to rats. A dynamic imaging study was performed, followed by static liver imaging performed for 5 min. A hepatic accumulation index, t90, was obtained on the basis of the dynamic data. A significant difference in t90 was observed between the experimental groups and the controls (p < 0.01). A significant difference in s-GPT also was observed between the experimental groups and the controls (p < 0.01). Excellent correlations were seen between t90 and ligation time (r = 0.967, p < 0.001), and t90 and s-GPT (r = 0.907, p < 0.001). Marked depression in hepatic 99mTc-GSA uptake was observed in rats with 40 or 90 min of hepatic vein occlusion. In conclusion, 99mTc-GSA is useful for evaluating hepatic injury in rats induced by hepatic vein occlusion.
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PMID:[Usefulness of 99mTc-GSA liver scintigraphy in evaluating hepatic injury in rats induced by temporary hepatic vein occlusion]. 802 58

The physical, clinicopathologic, and survival rates of 77 cats with severe spontaneous hepatic lipidosis are detailed in this report. Cats were subdivided into groups designated as idiopathic lipidosis if no other disease process was recognized, or secondary lipidosis if another disease process was diagnosed. Cats were also subdivided into groups designated as survivors or nonsurvivors on the basis of successful recuperation at 4 months after initial diagnosis. Differences between disease and survival groups were evaluated for significance. Overall, more female cats and middle-aged cats were affected. Presenting complaints of vomiting, anorexia, weakness, and weight loss were common. Physical assessment of most cats showed obvious hepatomegaly, jaundice, dehydration, and a weight loss > or = 25% of usual body weight. Neurobehavioral signs indicative of hepatic encephalopathy, other than ptyalism and depression, were rare. Clinicopathologic features are characterized by hyperbilirubinemia and increased activities of serum ALT, AST, and ALP, with only small if any increase in gamma GT activity. Clinical features distinguishing cats with hepatic lipidosis from those with other serious cholestatic disorders include absence of hyperglobulinemia and low gamma GT activity relative to ALP activity. Although coagulation tests were abnormal in 45% of cats tested (n = 44), few cats showed clinical bleeding tendencies. Most cats received prophylactic vitamin K1 therapy. Forty two cats received aggressive nutritional and supportive care and of these 55% survived. Cats with idiopathic disease were significantly younger, had significantly higher ALP activity and bilirubin concentration, and had a slightly better survival rate than cats with secondary lipidosis. Low PCV, hypokalemia, and an older age were significantly related to nonsurvival. Because of the variety of diets and food supplements used in case management, the influence of nutritional factors on survival could not be evaluated.
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PMID:A retrospective study of 77 cats with severe hepatic lipidosis: 1975-1990. 811 31

An inverse relation is known to link blood potassium with renal synthesis and the release of ammonia. Given the liability of hyperammonemia for precipitating hepatic encephalopathy (HE), 28 patients affected by stage I HE were equally divided into two groups and maintained up to their death at the highest (5.4-5.5 mEq/l) or the lowest (3.5-3.6 mEq/l) normokalemia levels. When compared with the lowest normokalemia group, the highest one showed an early, albeit transient, improvement in the mental state (as assessed by both EEG and psychiatric investigations) and to a lesser extent in hepatic functions (as assessed by the variations in serum bilirubin, GPT, GGT and plasma prothrombin time). In the highest normokalemia group the survival was also prolonged. The cause of this improvement may be related to the induced decrease in blood pH, the consequent depression of renal ammoniagenesis and the rise in the arterial and urine NH+4/NH3 ratios. These factors reduce the entry of ammonia into the cells and enhance the urinary excretion of this metabolite, respectively.
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PMID:The importance of the highest normokalemia in the treatment of early hepatic encephalopathy. 816 17

1. The effects of simvastatin and pravastatin on measures of central nervous system activity were investigated in a double-blind, placebo-controlled, randomised crossover study. 2. Twenty-five healthy volunteers sequentially took 40 mg day-1 simvastatin, 40 mg day-1 pravastatin or placebo for 4 weeks, separated by a 4-6 week washout phase. 3. CNS measures included EEG evoked potentials, power spectral analysis, Leeds Sleep Questionnaire, Hospital Anxiety Depression (HAD) Scale, and Digit Symbol Substitution Test (DSST); biochemical measures included plasma cholesterol, liver enzymes (gamma-GT, AST, ALT) and creatine kinase. 4. Mean cholesterol concentrations with both drugs were significantly lower than with placebo, and the cholesterol-lowering effect was greater with simvastatin. There were no significant differences between treatment in EEG evoked potentials, HAD Scale, or DSST scores. On the sleep measure, subjects reported significantly greater difficulty in getting to sleep while on simvastatin than on pravastatin, but neither score differed from placebo. No significant correlations were observed between sleep ratings and either plasma cholesterol concentrations or EEG evoked potentials. 5. The study showed that, while both drugs reduced plasma cholesterol concentrations, neither exerted significant effects, compared with placebo, on EEG evoked potentials, mood, sleep, or cognitive performance after 4 weeks of chronic administration in healthy volunteers.
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PMID:Do cholesterol-lowering agents affect brain activity? A comparison of simvastatin, pravastatin, and placebo in healthy volunteers. 819 30

The effects of formaldehyde (F), m-cresol (C), guaiacol (G), ethanol (E) and their mixture (FC, FCE, FG, FGE) on erythrocytes and isolated hepatocytes from rats and surface tension in water were examined. Hypotonic hemolysis of erythrocytes was inhibited by m-cresol, while guaiacol, formaldehyde and ethanol accelerated the hemolysis. Lower concentrations of the mixture inhibited hypotonic hemolysis, but higher concentrations accelerated hemolysis. Formaldehyde caused a decrease of transaminase (GOT, GPT) in the medium and hepatocytes. GOT and GPT in the medium were increased by m-cresol, but those in the hepatocyte were decreased by this agent. FC and FCE at 10 mM increased GOT in the medium, but FG and FGE decreased GOT. All mixtures decreased GOT and GPT in hepatocytes and GPT in the medium. All mixtures and formaldehyde inhibited GOT and GPT activity. Formaldehyde and m-cresol decreased hepatocyte viability. In the all mixtures-added hepatocytes, the viability was markedly lowered. Formaldehyde, m-cresol, guaiacol and ethanol caused a depression of surface tension, but the depressive effects of FG and FGE were weaker than that of guaiacol. These results suggest that the observed effects of the drug mixtures on erythrocytes and hepatocytes were the additive effects of the component drugs.
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PMID:[Effects of disinfectants on erythrocytes and isolated hepatocytes from rats and surface tension]. 833 Aug 3


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