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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relation of central haemodynamic changes to subsequent mortality and peak enzyme activity was investigated in 190 patients with acute myocardial infarction. The mean delay time from onset of symptoms to the haemodynamic study was 7.2 hours. Major exclusion criteria were heart rate less than 65 beats min-1, systolic blood pressure less than 105 mmHg and lung rales to a distance of greater than 10 cm above the lung bases. Nine patients (4.7%) died within 15 days and 16 patients (8.4%) within 90 days after the infarction. Compared to survivors, non-survivors were characterized by baseline depression of cardiac index, stroke volume index and left ventricular stroke work index, while pulmonary capillary wedge pressure and peripheral resistance were increased. However, a wide overlap between survivors and non-survivors makes the predictive value low in the individual patient. Peak serum aspartate aminotransferase (S-ASAT) activity was weakly related to baseline pulmonary capillary wedge pressure (r = 0.28; P less than 0.001) and stroke volume index (r = -0.22; P less than 0.01). The correlation to pulmonary capillary wedge pressure was only found in anterior (r = 0.34) infarcts. Peak serum lactate dehydrogenase (LD1) was not correlated with baseline haemodynamics.
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PMID:Central haemodynamics in acute myocardial infarction in relation to mortality and peak enzyme activity. 373 97

After surgical placement of end-to-side portacaval shunts (PCS), 4 adult mongrel dogs (11.8 to 18.2 kg) were fed purified diets and monitored for approximately 50 weeks for changes in body weight, neurologic status, and an array of clinically important biochemical variables. Two healthy dogs, fed the same diets and maintained in the same environment, were also observed (controls). Body weights were relatively stable over the period of observation. The branched-chain ratio ([valine] + [leucine] + [isoleucine]/[phenylalanine] + [tyrosine]), an index of the degree of change in plasma amino acid concentrations, was significantly lower in dogs with PCS than in controls. Despite this depression in branched-chain ratio, the principals (dogs with PCS) were essentially free of neurologic symptoms. Statistically significant decreases due to portacaval shunting were seen in the serum concentrations of glucose, calcium, urea nitrogen, creatinine, cholesterol, and albumin. Total protein, globulin, and triglyceride concentrations tended to be lower in the serum of principals than in serum of controls, but the differences were not statistically significant. Statistically significant increases due to portacaval shunting were seen in plasma concentrations of total conjugated bile acids and sulfobromophthalein retention. Concentrations of the following compounds tended to be higher in serum of principals than in serum of controls: phosphorus, chloride, uric acid, total bilirubin, lactate dehydrogenase, aspartate transaminase, alanine transaminase, and alkaline phosphatase. Liver biopsy at 7 months after operation showed mild-to-extensive atrophy of hepatocytes, mild-to-extensive fibrosis, and collapsed portal veins in all principals examined.
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PMID:Long-term biochemical and physiologic effects of surgically placed portacaval shunts in dogs. 395 18

A comparison of viral-induced unresponsiveness of phytohemagglutinin (PHA)-induced deoxyribonucleic acid (DNA) synthesis of mouse lymphocytes was made by culturing the cells under identical conditions in the presence of HEPES buffer in a humid-air atmosphere. The degree of PHA-induced DNA synthesis was found to vary, depending upon the type of ribonucleic acid or DNA virus treatment. Myxovirus, paramyxoviruses, Mengo virus, leukemic viruses, herpesvirus, and vaccinia virus caused a depression in responsiveness, whereas lactic dehydrogenase virus, adenovirus, and polyoma virus induced an increase in DNA synthesis. Inhibition of DNA synthesis was significant only if the virus was added at 0 h or within the first 12 h after PHA stimulation. Time studies indicated that leukemic and nonleukemic viruses caused similar patterns in the alteration of PHA-induced DNA synthesis.
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PMID:Iron-binding catechols and virulence in Escherichia coli. 457 80

Serum activities of sorbitol dehydrogenase (SDH), lactate dehydrogenase (LDH), gamma-glutamyltranspeptidase (gamma-GT), and alkaline phosphatase (ALP) were measured before, during, and after milk fat depression in 9 cows fed a high-concentrate ration during 2 experiments. In 7 of the 9 cows, increases in serum SDH and LDH activities were observed during milk fat depression. The gamma-GT activity showed only moderate changes, whereas the ALP activity remained unchanged. During recovery from milk fat depression, decreases of SDH, LDH, and gamma-GT activities were found in nearly all cows. Association of this phenomenon with changes found in beef cattle, such as ruminal lesions and liver abscesses, are discussed.
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PMID:Changes of serum enzyme activities in cows with milk fat depression. 613 78

Using histochemical techniques, the reactivities of selected enzymes and other metabolic components were examined in the myocardium, coronary arteries, and coronary arterioles of normal, two-week-sympathectomized, and sham-operated canine hearts. There were no differences in the histochemistry of coronary arteries in any of the hearts, but important differences were noted in the myocardium and especially in the arterioles. The reactivities of the enzyme glucose-6-phosphate dehydrogenase and the nucleic acids were increased in arterioles of the sympathectomized heart, possibly indicating an increased protein synthesis. The reactivities of succinate dehydrogenase, NAD-isocitrate dehydrogenase, and cytochrome oxidase were reduced in myocardium and arterioles of sympathectomized hearts as well as in arterioles of sham-operated hearts; the changes were greater in the sympathectomized arterioles where there was also observed an increase in reactivity of lactate dehydrogenase. These findings suggest a depression in aerobic metabolic capacity and, in the case of the sympathectomized arteriole, imply a possible shift in adaptation from aerobic to anaerobic metabolism.
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PMID:The myocardium and its vasculature: a histochemical comparison of the normal and chronically sympathectomized dog heart. 615 74

The effects of 12-O-tetradecanoylphorbol-13-acetate (TPA), all trans-retinoic acid (RA), 5-azacytidine (5-AC), and phenobarbital (PB) on the activities of seven enzymes and/or isozymes of a diploid rat liver epithelial cell line have been studied. At 0.1 microgram/ml, TPA depressed the specific activities of lactate dehydrogenase and gamma-glutamyl transpeptidase, whereas 2 mM PB depressed gamma-glutamyl transpeptidase and alkaline phosphatase. At 0.01 microgram/ml, RA markedly depressed the activity of NADH-diaphorase and lactate dehydrogenase but enhanced the activity of alkaline phosphatase. Only 2 microM 5-AC caused the most significant shift of lactate dehydrogenase isozyme toward the "muscle"-type isozyme. Histochemical studies revealed that PB and 5-AC induced focal areas of cells with glycogen deposits, but no significant changes in either ultrastructure or alpha-fetoprotein and albumin immunohistochemical staining pattern were observed to suggest hepatocytic differentiation. Although none of the enzymatic changes could be consistently correlated with the effects of these biological modifiers on the cellular growth rate, the effect of RA on NADH-diaphorase, lactate dehydrogenase, and alkaline phosphatase activities was the opposite of the changes observed during carcinogenesis of these rat liver epithelial cells by multiple treatments with N-methyl-N'-nitro-N-nitrosoguanidine. The depression of gamma-glutamyl transpeptidase activity by PB is contradictory to that observed histochemically in hepatocytes in vivo, but such discrepancy may be related to the differences in cell type, growth conditions, or duration of exposure.
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PMID:Biochemical effects of 12-O-tetradecanoylphorbol-13-acetate, retinoic acid, phenobarbital, and 5-azacytidine on a normal rat liver epithelial cell line. 620 84

The activity of some dehydrogenases and hydrolases was studied by cytochemical methods in the peripheral blood neutrophils of germ-free guinea pigs infected with adenoviruses. The gnotobiotic animals were obtained by hysterotomy in an operation isolation room after which they were transferred into manipulation isolation room and infected with human adenovirus type 1. A depression of enzymes of alpha-glycerophosphate shunt and NADP-H2-diaphorase in neutrophils two days after infection and activation of lactate dehydrogenase and acid phosphatase at 4 days were demonstrated. The pattern of changes in the enzymatic status of intact and infected gnotobiotic animals allowed a diagnosis of adenovirus infection in most cases.
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PMID:[Cytochemical study of granulocyte enzymes in germ-free animals with adenovirus infections]. 626 24

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 effects of nickel chloride were studied in two human cell lines, HeLa and diploid embryonic fibroblasts, as well as in V79 Chinese hamster cells and in L-A mouse fibroblasts. NiCl2 produces a dose-dependent depression of proliferation and mitotic rate. Effects on viability are accompanied by an increasing release of the intracellular enzyme lactic dehydrogenase. Lactic acid production is stimulated. The plating efficiency is reduced, as are DNA and protein synthesis and, to a lesser degree, RNA synthesis. Comparing these results with those of previous studies of the cytotoxicity of other heavy metals in the same test systems, similar effects are observed though with different intensities and slight differences between the cell lines employed. As regards lethal effects (LC50) the following rank order of cytotoxicity can be established: Ni2+ approximately equal to Pb2+ less than Mn2+ less than Hg2+ less than Cd2+; as regards growth inhibition the same rank order is observed as in the case of the LC50 in HeLa and human fibroblasts, but in L-A cells Ni2+ is more inhibitive than the other metal ions listed above with the exception of Cd2+. With respect to colony formation NiCl2 is less effective than PbCl2, MnCl2, and CdCl2. NiCl2 effects in serum-free medium are much faster and more severe than in medium containing serum or serum albumin indicating that serum constituents, notably albumin, bind the metal effectively and inhibit cellular uptake; this confirms reports of other authors on the serum binding and slow uptake of NiCl2. Synchronized cells are most sensitive in the G1 and early S phases of the cell cycle. Together with the finding that thymidine incorporation is affected to a considerable degree this contributes an explanation of the known genotoxic effects of nickel.
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PMID:Toxicity of nickel for mammalian cells in culture. 672 Jan 41

The direct myocardial protection afforded by three structurally distinct calcium antagonists (0.1 micron nifedipine, 0.1 micron verapamil and 0.4 micron diltiazem), and a calmodulin antagonist (20 micron W-7) was assessed in isolated working rat hearts subjected to 30 min global ischaemia followed by 30 min reperfusion. At these concentrations, no drug-induced cardiac depression nor coronary vasodilatation was observed prior to ischaemia. All four agents improved recovery of cardiac function (assessed as total cardiac output) on reperfusion (by 49%, 29%, 64% and 72% respectively, compared to controls), attenuated the release of lactate dehydrogenase (by 52%, 55%, 65% and 66% respectively) and inhibited intracellular 45Ca accumulation (by 42%, 35%, 49% and 45% respectively). Despite the increased tissue calcium and enzyme leakage in reperfused hearts, the [3H]inulin-impermeable space was not decreased, suggesting specific changes in membrane permeability rather than partial sarcolemmal rupture. Drug treatment did not alter the rate nor extent of high-energy phosphate depletion during ischaemia, thus eliminating ATP preservation and negative inotropy as mechanisms for the protective effects observed in this system. Improved restoration of coronary flow was obtained in treated hearts but we believe this was more likely to be a consequence of myocardial protection rather than direct coronary vasodilatation. Thus, the beneficial effects observed probably resulted from direct preservation of cellular viability. When given only during the reperfusion phase, nifedipine and W-7 were almost as effective as when given before ischaemia, whereas verapamil and diltiazem were inactive. This highlights differences between the various structural subclasses of calcium antagonists. Furthermore, the efficacy of the calmodulin antagonist, W-7, in this system suggests a possible key role for calmodulin-activated enzymes in the progression of reperfusion damage.
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PMID:Prevention of reperfusion damage in working rat hearts by calcium antagonists and calmodulin antagonists. 673 83


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