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)

Cynomolgi (Macaca fascicularis) were fed diets containing 25% rapeseed oil (RSO), partially hydrogenated herring oil (PHHO), or a 3:1 mixture of lard and corn oil as control for 4 months. The RSO contained approximately 25% of the fatty acids as erucic acid; the PHHO contained a similar concentration of mainly cetoleic acid. The control diet did not include such fatty acids. At the time of necropsy, the RSO- and PHHO-fed monkeys showed myocardial and skeletal muscle lipidosis. Foci of mononuclear cell infiltration, although infrequent, occurred in all three groups and were thought to be nonspecific. The only significant intergroup difference in serum biochemical or hematologic parameters was an increase in serum glutamic-oxaloacetic transaminase activity in both RSO and PHHO groups. Ultrastructural studies confirmed the presence of lipidosis in cardiac and skeletal muscle and revealed mild mitochondrial degeneration, causing a depression of the P/O ratio of the RSO group and a State III respiratory rate depression of the PHHO group. The difference in the exposure/life span ratio represented by this experiment may account for the absence of clear intergroup differences such as are reported in rats used in similar studies, but a true species difference in regard to dietary oils containing docosenoic acids has to be considered as well.
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PMID:Morphologic effects of dietary plant and animal lipids rich in docosenoic acids on heart and skeletal muscle of cynomolgus monkeys. 41 15

The objective of this investigation was to characterize the acute and short- and long-term toxic potency of orally administered 1,2-dichloropropane (DCP). In the acute and short-term studies, male rats of 250-300 g were gavaged with 0, 100, 250, 500, or 1000 mg DCP/kg in corn oil once daily for up to 10 consecutive days. Although ingestion of DCP caused body weight loss and CNS depression, few other toxic effects were manifest 24 hr after a single dose of the chemical. Morphological changes were limited to liver centrilobular cells in 500 and 1000 mg/kg rats. Similarly, elevated activity of some serum enzymes occurred only at these two highest dose levels. Hepatic nonprotein sulfhydryl (NPS) levels were decreased and renal NPS levels increased at 24 hr. In the short-term study resistance developed to DCP hepatotoxicity over the 10 consecutive days of exposure, as reflected by progressively lower serum enzyme levels and by decreases in the severity and incidence of toxic hepatitis and periportal vacuolization. Nucleolar enlargement in hepatocytes, however, was observed at all dosage levels at 5 and 10 days. There were a number of manifestations of hemolytic anemia, including erythrophagocytosis in the liver, splenic hemosiderosis and hyperplasia of erythropoietic elements of the red pulp, renal tubular cell hemosiderosis, and hyperbilirubinemia. Urinalyses and histopathology revealed no evidence of nephrotoxicity. In the long-term study, male rats initially weighing 180-200 g were gavaged five times weekly for up to 13 weeks with 0, 100, 250, 500, or 750 mg DCP/kg. As over one-half the 750 mg/kg group died within 10 days, the survivors were sacrificed. Histopathological changes in the 750 mg/kg animals included mild hepatitis and splenic hemosiderosis, as well as adrenal medullary vacuolization and cortical lipidosis, testicular degeneration and a reduction in sperm, and increased number of degenerate spermatogonia in the epididymis in some members of the group. Similar testicular and epididymal degenerative change also were observed in some 500 mg/kg animals after 13 weeks of dosing. There was a progressive increase in the number of deaths in the 500 mg/kg group, such that more than 50% were dead by 13 weeks. No deaths occurred in the 100 or 250 mg/kg groups. The DCP dosage regimen also produced a dose-dependent decrease in body weight gain. DCP exhibited very limited hepatotoxic potential and no apparent nephrotoxic potential in the long-term study. Slight elevations in serum ornithine-carbamyltransferase activity, periportal vacuolization, and active fibroplasia in the liver were seen in the 500 mg/kg animals.
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PMID:Oral toxicity of 1,2-dichloropropane: acute, short-term, and long-term studies in rats. 274 74

Infectious bursal disease in 35-day-old specific-pathogen-free (SPF) chickens was characterized clinically by its acute onset and brief duration. Clinical signs included depression, anorexia, diarrhea, and polyuria. A detectable precipitin antibody response occurred between 3 and 5 days postinoculation. Evaluation of pooled serum samples obtained from infectious bursal disease virus (IBDV)-infected chickens revealed transient changes in potassium, cholesterol, uric acid, lactate dehydrogenase, serum glutamic-oxalic transaminase, and serum proteins. Individual serum samples analyzed for uric acid concentration indicated that several IBDV-infected chickens had serum uric acid concentrations above the normal comparison range. Histopathologic examination of lymphoid and nonlymphoid tissues from IBDV-infected SPF chickens affirmed that the predominant lesion was lymphoid necrosis in the bursa of Fabricius. Other lymphoid organs were much less severely affected and possessed greater regenerative potential. Nonspecific and relatively mild changes were found in the liver and kidney: hepatic lipidosis and necrosis, renal intratubular crystalline deposits (probably urates), and increased ectopic lymphoid foci. There was no evidence of immune-complex-mediated arteritis/vasculitis in the sartorius muscle or any other tissue examined. Histopathologic and ultrastructural evidence of glomerulonephritis was rare but compatible with acute immune complexemia.
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PMID:The pathogenesis of infectious bursal disease: serologic, histopathologic, and clinical chemical observations. 631 94

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

Administration of tetracycline was believed to be associated with an adverse drug reaction in a cat. Clinical signs consisted of anorexia, ptyalism, and signs of depression. The most noticeable biochemical abnormality was a markedly high serum alanine transaminase activity. Treatment consisted of vitamin E and selenium injections and feeding via a gastrostomy tube. Abnormalities noticed on histologic examination of hepatic tissue were centrilobular fibrosis, mild diffuse cholangiohepatitis, and mild hepatic lipidosis. The lipidosis was believed to have resulted from tetracycline administration, whereas the more chronic lesions (hepatic fibrosis and mild cholangiohepatitis) were believed to have resulted from preexisting, subclinical hepatic disease. Because serum alanine transaminase activity returned to reference ranges and the anorexia and ptyalism resolved with cessation of tetracycline administration, these abnormalities were believed to have represented an adverse drug reaction. Treatment of the cat with vitamin E and selenium was instituted on the basis of reported preventive and therapeutic effects in albino rats with tetracycline-induced hepatic lesions. Whether these compounds had any role in accelerating clinical recovery in this cat is uncertain.
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PMID:Increased alanine transaminase activity associated with tetracycline administration in a cat. 844 8

Hypophosphatemia is uncommon in cats, but it has been reported in association with diabetes mellitus and hepatic lipidosis, where it can cause hemolysis, rhabdomyopathy, depression, seizures, and coma. The purpose of this article is to describe 9 cats that developed low serum phosphorus concentrations (< 2.5 mg/dL) subsequent to enteral alimentation. Serum biochemical analyses from more than 6,000 cats were reviewed. The medical records of all cats with hypophosphatemia were examined for history of enteral alimentation; diabetic cats were excluded from the study. Nine cats, ranging in age from 3 to 17 years, were identified. All cats had normal serum phosphorus concentrations before tube feeding began. Onset of hypophosphatemia occurred 12 to 72 hours after initiation of enteral alimentation, and the nadir for phosphorus concentrations ranged from 0.4 to 2.4 mg/dL. Hemolysis occurred in 6 of the 9 cats. Hypophosphatemia secondary to enteral alimentation is an uncommon clinical finding in cats. Cats with high alanine aminotransferase activity, hyperbilirubinemia, and weight loss should be closely monitored for hypophosphatemia during the first 72 hours of enteral alimentation.
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PMID:Hypophosphatemia associated with enteral alimentation in cats. 852 19

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 forty-five Holstein Frisian dairy cows (1-6 weeks post partum; mean age: 5.1 +/- 1.2 years) the serum total bile acid concentrations (SBA) were measured enzymatically. In all cows a left sided abomasal displacement was corrected surgically by right side laparotomy and omentopexy three days before investigation. The liver fat content was determined in all cows histologically. Liver failure was assumed if typical clinical signs (ataxia, general depression, recumbency or coma), an increased venous plasma ammonia level (> 35 mumol/l) and a decreased plasma amino acid index (< 4.0) were found. Cows without liver failure (N = 29) were grouped according to the liver fat content as cows with mild (N = 5), moderate (N = 19) or severe hepatosteatosis (N = 5). Histological examination of liver biopsies in cows with liver failure (N = 16) revealed in twelve cases a severe fatty liver and in four cases a hydropic degeneration of the liver tissue. Although in cows without liver failure mean SBA concentrations were higher in the group with moderate (47.3 +/- 30.9 mumol/l) or severe fatty liver (32.9 +/- 21.7 mumol/l) than in that with mild lipidosis (18.0 (16.8 mumol/l), differences were not significant. The mean SBA concentration in cows with liver failure (70.5 +/- 49.5 mumol/l) was only significantly (p < 0.05) increased compared to cows with uncomplicated mild hepatic lipidosis. In conclusion, the determination of SBA concentrations is of little value in the recognition of fatty liver or even liver failure due to the considerable variance of SBA concentrations in dairy cows.
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PMID:Total serum bile acid concentrations in dairy cows with fatty liver and liver failure. 1002 57

In dairy cows, overfeeding during the dry period leads to overcondition at calving and to depression of appetite after calving. As a consequence, at calving overconditioned high-producing dairy cows inevitably go into a more severe negative energy balance (NEB) postpartum than cows that have a normal appetite. During the period of NEB, the energy requirements of the cow are satisfied by lipolysis and proteolysis. Lipolysis results in an increased concentration of non esterified fatty acids (NEFA) in the blood. In the liver, these NEFA are predominantly esterified to triacylglycerols (TAG) that are secreted in very low density lipoproteins (VLDL). In early lactation in cows with a severe NEB, the capacity of the liver to maintain the export of the TAG in the form of VLDL in balance with the hepatic TAG production is not always adequate. As a result, the excess amount of TAG accumulates in the liver, leading to fatty infiltration of the liver (hepatic lipidosis or fatty liver). The NEB and/or fatty liver postpartum are frequently associated with postparturient problems. In general, a severe NEB induces changes in biochemical, endocrinological, and metabolic pathways that are responsible for production, maintenance of health, and reproduction of the postparturient dairy cow. These changes include a decrease in blood glucose and insulin concentrations, and an increase in blood NEFA concentrations. High NEFA concentrations caused by intensive lipolysis are accompanied by impairment of the immune system, making the cows more vulnerable to infections. Metabolic diseases such as ketosis, milk fever, and displaced abomasum are related to overcondition at calving. The changes in biochemical, endocrinological, and metabolic pathways are associated with delay of the first visible signs of oestrus, an increase in the interval from calving to first ovulation, a decrease in conception rate, and a prolonged calving interval. It is possible that the increased blood NEFA concentration directly impairs ovarian function.
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PMID:Relationship between overfeeding and overconditioning in the dry period and the problems of high producing dairy cows during the postparturient period. 1042 30

This study was conducted with 3 objectives in mind: first, to identify the toxic fraction (aqueous or organic) in leaves and flowers; second, to identify diagnostic marker(s) of toxicosis in cats; and, third, to evaluate the morphologic effects of intoxication. The study was conducted in 2 phases. Phase 1 was to identify which extract, organic or aqueous, was nephrotoxic and also to determine the appropriate dose for use in the phase 2 studies. Results indicated that only the aqueous extracts of leaves and flowers were nephrotoxic and pancreotoxic. To identify the proximate toxic compound, cats in the phase 2 study were orally exposed to subfractions of the aqueous flower extract, 1 subfraction per cat. Results confirmed vomiting, depression, polyuria, polydipsia, azotemia, glucosuria, proteinuria, and isosthenuria as toxic effects of the Easter lily plant. Another significant finding in serum was elevated creatinine kinase. Significant histologic kidney changes included acute necrosis of proximal convoluted tubules and degeneration of pancreatic acinar cells. Renal ultrastructural changes included swollen mitochondria, megamitochondria, edema, and lipidosis. Subfraction IIa3 of the aqueous floral extract contained most of the toxic compound(s). These studies reproduced the clinical disease, identified the most toxic fraction of the Easter lily, and helped characterize the clinical pathology, histopathology, and ultrastructural pathology associated with the disease.
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PMID:A comprehensive study of Easter lily poisoning in cats. 1558 68


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