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

Specific pathogen-free mice were exposed to three different kinds of environmental stress during early life: (a) by infecting them with a mouse enterovirus on the second day after birth; (b) by placing the mother during pregnancy and lactation on a mildly deficient diet containing wheat gluten supplemented with See PDF for Structure small amounts of lysine and threonine; (c) by combining a (neonatal infection) and b (early malnutrition). All animals survived the three types of stresses, but all exhibited marked depressions of metabolic activity, and of body weights and organ weights. These depressions lasted throughout the experimental period even though all animals were placed under optimum conditions of nutrition and husbandry after weaning, and maintained under these same conditions thereafter. Metabolic activity was determined by measuring the turnover of (14)C-acetate and (14)C-glucose in respiratory CO(2), and their incorporation in total lipids of liver and brain. The utilization of (14)C-acetate was profoundly depressed in all experimental groups with regard to both elimination in respiratory CO(2) and their incorporation in total lipids of liver and brain. In contrast, the utilization of (14)C-glucose was much less affected; its incorporation into lipids was not decreased and its elimination in respiratory CO(2) was depressed only in animals having experienced both neonatal infection and early malnutrition. The extent of weight depression per 100 g of body weight differed according to the organ and the type of stress. Irrespective of the organ, however, depression of weight was largest in animals having experienced both neonatal infection and early malnutrition. And irrespective of the type of stress, the brain exhibited the smallest depression of weight relative to total body weight.
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PMID:Lasting biological effects of early environmental influences. VI. Effects of early environmental stresses on metabolic activity and organ weights. 554 86

This review examines the interaction of pyridoxal phosphate with select neuroendocrine and neuropharmacological systems and their health related therapeutic implications. Vitamin B6 and its vitamers can be involved in many interactions with a number of drugs as well as the actions of various endocrines and neurotransmitters. Nutritional deficiencies, particularly of vitamins and proteins, can affect the manner in which drugs undergo biotransformation and thus may modify the therapeutic efficacy of certain drugs. In addition to pyridoxine deficiency adversely affecting drug actions, improper supplementation with viatmin B6 can in some instances also adversely affect drug efficacy. A decrease by pyridocxine in the efficacy of levodopa used in the treatment of Parkinsonism is an example. The interrelationships and enzymatic interconversions amony pyridoxine vitamers, both phosphorylated and nonphosphorylated, are briefly discussed, particularly concerning their pharmacokinetic properties. The chronic administration of isoniazid for the prevention or treatment of tuberculosis can produce peripheral neuropathy which can be prevented by the concurrent administration of pyridoxine. An acute toxic overdose of isoniazid causes generalized convulsions, and the intravenous administration of pryidoxine hydrochloride prevents or stops these seizures. The acute ingestion of excessive monosodium glutamate will, in some persons, cause a group of symptoms, including headache, weakness, stiffness, and heartburn, collectively known as the "Chinese Restaurant Syndrome." These symptoms can be prevented by prior supplementation with vitamin B6. It is postulated that the intestinal absorption of zinc is facilitated by picolinic acid, a metabolite of tryptophan. The derivation of picolinic acid from tryptophan depends on the action of the enzyme kynureninase, which is dependent on pyridoxal phosphate. Therefore, the adequate absorption of zinc is indirectly dependent on an adequate supply of vitamin B6. The formation of pyridoxal phospate appears to be indirectly dependent on Zn2++ which activates pyridoxal kinase. Treatment with daily pyridoxine can reverse a state of depression induced in women who take oral contraceptives (OCs). 1 hypothesis to explain this effect is that the OC is somehow causing a deficiency of seroton serotonin in the brain and that the vitamin B6 helps to overcome this deficiency through the stimulation of 5-hydroxytryptophan decarboxylase by pyridoxal phosphate. In sum, the stimulation of 5-hydroxytryptophan decarboxylase by pyridoxal phosphate. In sum, pyridoxal phosphate in physiological concentrations seems to function as an endogenous "down regulator" of several receptor sites, including estrogen, progesterone, and androgen.
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PMID:Drug-pyridoxal phosphate interactions. 608 25

The effect of protein-energy malnutrition on biliary immunoglobulins was investigated in rats fed isocaloric diets containing 0.5%, 5%, and 18% casein, respectively. Growth was severely retarded in rats fed 0.5% casein diet and moderately in rats fed 5% casein diet, and these groups had decreases in serum albumin and total protein levels. Since the energy intake was low in rats fed protein-insufficient diets, the nutritional status was defined not as protein malnutrition but protein-energy malnutrition. Depression of systemic immune functions in protein-energy malnourished rats were demonstrated by serum IgG and IgA levels, and antibody responses to dinitrophenylated bovine gamma globulin, a T-cell dependent antigen. The depressed systemic immune functions observed in those rats were suggested to be caused by thymic atrophy. IgA levels in bile were much higher in all groups than IgG levels. IgG levels decreased in rats fed 0.5% casein diet but not in rats fed 5% casein diet, while IgA levels decreased in rats fed 5% and 0.5% casein diet relating to casein levels. The ratios of IgA to IgG in bile also decreased in rats fed protein-insufficient diets. By sucrose density gradient centrifugation secretory IgA levels in bile were shown to decrease in rats fed 0.5% casein diet, suggesting that the secretion of IgA by hepatic parenchymal cells is depressed in the protein-energy malnourished rats.
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PMID:Biliary immunoglobulins in protein-energy malnourished rats. 619 68

It has been well documented that the hospitalized child frequently is malnourished, and the considerably greater morbidity and mortality of such children, in large part, is due to the associated secondary immunodepression. To assess the mechanism of such immunodepression in acute and chronically malnourished subjects, we chose an experimental murine model of malnutrition. Immune function was assayed by lymphocyte subset population and mixed lymphocyte culture (MLC) assessment, determining whether an alteration of the T helper (TH) to T suppressor-cytotoxic (TS-C) lymphocyte ratio is the mechanism that produces immunoincompetence in malnutrition. Ten-week-old A/J mice were rendered acutely or chronically malnourished by graded protein restriction using a 2.5% protein diet. These animals were studied before and after protein depletion with the fluorescent activated cell sorter (FACS) and the MLC. FACS cell populations were defined by the monoclonal antibodies to THY 1.2, LYT 1 (TH), and LYT 2 (TS-C) antigens. MLC reactivity was assessed with A/J v C 57 BL/6 mouse lymphocytes and expressed as a stimulation index (S.I.). Results are expressed in Table 1, and suggest that these malnourished animals were significantly immunodepressed as measured in the MLC reaction. However, the mechanism of this depression is not mediated by an inversion of the TH/TS-C ratio. These data contrast with those previously reported for the immunodepression of the burned or traumatized patient in which the TH/TS-C ratios are reversed; these data suggest that a different, as yet to be elucidated, mechanism exists for the immunodepression of malnutrition.
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PMID:Immunodepression secondary to malnutrition: assay by lymphocyte subset analysis using monoclonal antibodies and the cell sorter. 624 May 29

Plasma zinc levels were measured in 95 elderly patients hospitalized in a long stay unit and in 100 healthy controls under 65 years of age. Plasma zinc concentrations were significantly lower in the elderly patients, as compared to the younger subjects (p 0.001). The correlations with serum prealbumin (p 0.05) and serum albumin (p 0.05) concentrations and the frequent association with protein-calorie malnutrition suggest that the low serum zinc levels mirror a low dietary zinc intake. Immunological tests in the elderly show moderate lymphopenia, high serum IgA and frequent depression of delayed cutaneous hypersensitivity to DNCB and PHA. We find a significant correlation between plasma zinc concentration and peripheral blood lymphocyte counts, but not the other immunological parameters. Linear discriminant analysis shows that the association of low plasma zinc values, low serum protein concentration and high serum IgG concentration implies poor prognosis.
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PMID:[Plasma zinc levels in elderly hospitalized subjects. Correlation with other nutritional and immunological markers and survival]. 632 Mar 99

Malnourished surgical patients have metabolic and functional abnormalities of skeletal muscle and it has been suggested that these are due to reduced activities of glycolytic enzymes associated with abnormalities of muscle fibres. We have measured the activities of four key enzymes of glucose utilization and the size and distribution of muscle fibre types in vastus lateralis biopsies from 14 undernourished patients awaiting surgery (mean weight loss 24 +/- 10 per cent). These results were compared with those from 14 normally nourished controls, comparable in age, sex, race and habitual activity. Fructose bisphosphatase activity was reduced in undernourished patients by 44 per cent (P less than 0.01), phosphofructokinase by 40 per cent (P = 0.005) and hexokinase by 37 per cent (P less than 0.001). Both fibre types were smaller in patients than controls (area I, 41.4 micron2 X 10(-2) +/- 0.4 vs. 73.3 micron2 X 10(-2) +/- 0.6, less than 0.001; area II, 27.7 micron2 X 10(-2) +/- 0.4 vs. 72.5 micron2 X 10(-2) +/- 0.5, P less than 0.001), and there was a smaller proportional number of type II fibres in patients (35 per cent vs. 65 per cent, P less than 0.01). This loss of type II fibre numbers and preferential type II atrophy may account for the enzyme depression associated with it and could produce the syndrome of impaired glucose tolerance, muscle weakness and fatigue seen in undernourished patients. In a subgroup of 11 patients, biopsy was repeated after 14 days of intravenous nutrition. Only phosphofructokinase activity rose significantly (19.62 +/- 1.85 to 30.74 +/- 2.99 mumol min-1 g-1, P less than 0.01) and both type II fibre size (40.6 +/- 18.5 to 47.4 micron2 +/- 20.3 X 10(-2), P less than 0.05) and number (42 per cent +/- 6 to 56 per cent +/- 5, P less than 0.05) also rose. Intravenous nutrition may therefore increase maximum glycolytic rate and improve muscle function in undernourished surgical patients.
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PMID:Abnormalities of muscle metabolism and histology in malnourished patients awaiting surgery: effects of a course of intravenous nutrition. 632 97

Plasma amino acid abnormalities are frequently reported in alcoholics, with the most common abnormalities being those of depressed branched chain amino acids (BCAA) and increased aromatic amino acids. The depression in branched chain amino acids is due to multiple factors including portal-systemic shunting, hyperinsulinemia, hyperglucagonemia (all due to advanced liver disease) as well as dietary deficiency. alpha-Amino-n-butyric acid is a nonessential amino acid derived primarily from the catabolism of methionine, threonine, and serine. Increased levels due to chronic alcohol consumption may reflect altered glutathione metabolism and lipid peroxidation due to alcohol and may be used empirically as a biochemical marker of heavy drinking. The high levels of aromatic amino acids such as tyrosine and tryptophan as well as their breakdown products may be due to impaired hepatic metabolism and appear to play a role in the pathogenesis of hepatic encephalopathy. The effects of high levels of aromatic amino acids may be potentiated by depressed BCAA; these normally compete with each other for CNS transport. Alterations in these amino acids may have implications for nutritional requirements for amino acids in these patients as well as therapeutic approaches.
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PMID:Plasma amino acids in the alcoholic: nutritional aspects. 634 43

Depressed food consumption is an early response of experimental, animals to: 1) a dietary deficiency of either protein or an individual indispensable amino acid; 2) a distortion of the dietary pattern of amino acids when protein intake is low; and 3) a substantial elevation in the protein content of the diet. In each of these conditions the change in feeding behaviour is associated with alterations in concentrations of amino acids in blood but in none of them has the biochemical basis for the depressed food intake been established. The depressed food intake of rats consuming a low protein diet in which an imbalance of amino acids has been created by adding quantities of amino acids other than the one most limiting for growth, is associated with elevations in the plasma concentrations of amino acids added to create the imbalance and usually with a depression in the plasma concentration of the growth-limiting amino acid. These changes, in turn, are associated with depression of the concentration of the growth-limiting amino acid in the brain free amino acid pool. Studies in which uptake of amino acids into brain slices has been examined support the conclusion that various distortions of the plasma amino acid pattern, as the result of dietary imbalances of amino acids, can lead to depletion of the brain pool of a specific amino acid through competition between it and other amino acids in surplus in plasma for uptake into brain. The results of studies with rats in vivo of the effects on brain amino acid pools of ingestion of diets containing supplements of amino acids that compete with the growth-limiting amino acid for uptake into brain also support this conclusion. Depletion of the brain pool of the limiting amino acid as the result of feeding a diet with an amino acid imbalance can be related to overall body protein metabolism. In the young growing animal, protein synthesis is stimulated after a meal. Thus, when the diet is limiting in a single amino acid, that amino acid will be depleted from the circulating body pool. At the same time, the activities of amino acid degrading enzymes are low in animals fed a low protein diet; hence, such animals have limited capacity to degrade surpluses of amino acids. These conditions, depletion of the blood pool of the limiting amino acid and slow removal of surpluses of competing amino acids from the blood, will increase the extent of competition between other amino acids and the limiting amino acid for uptake into brain.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Amino acid signals and food intake and preference: relation to body protein metabolism. 635 42

Infections and chronic liver injury are common causes of morbidity and mortality in alcoholics, and both of these may be related to an altered immune response. This study describes a guinea pig model of chronic ethanolism designed to selectively study the cellular immune system in a setting free from the malnutrition, socioeconomic deprivation, and severe underlying hepatic dysfunction seen in human disease. Animals were given 2.5 g/kg/day of ethanol as a 15% solution in 0.9% NaCl or isocaloric-dextrose-saline control solution intraperitoneally in 2 divided doses for 5 weeks. At 2 weeks, the mean serum ethanol level 1 hr after treatment was 20.4 mM (range 8.9-30.6) while the mean serum acetaldehyde level was 55.1 microM (range 17.0-111). At 5 weeks the serum levels for ethanol and acetaldehyde were 20.1 mM (13.3-32.9) and 41.5 microM (2.4-87.6), respectively. Weight gain was persistent throughout the study and did not differ significantly between ethanol and control groups. After 5 weeks of treatment, lymphocyte response to the mitogens, phytohemagglutinin, and concanavalin A was significantly decreased in the ethanol treated group (p less than 0.05). Response to the specific antigen, picrylated human serum albumin, T & B cell per cent and number, skin test reactivity, peripheral white blood cell count, total lymphocyte count, and migration inhibitory factor production were not significantly altered by 5 weeks of ethanol treatment. Therefore, in a controlled animal model of chronic ethanolism, we observed a significant depression of lymphocyte blastogenic response which may, in part, explain the increased propensity to infection by intracellular pathogens seen in alcoholics.
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PMID:Ethanol-induced alterations in lymphocyte function in the guinea pig. 637 25

The burn patient is in many ways the archetypical immunosuppressed host: the anatomic barriers have been breached and the host's defenses suppressed. Infection is the leading cause of death in hospitalized burn patients not having inhalation injury, being responsible for between 50 and 75 percent of the hospital deaths. Burn injury produces profound abnormalities in immunologic function. These changes are generally proportional to the degree of burn injury (surface area and depth). Cell-mediated immune function is suppressed. Anergy and depressed allograft rejection occur. Acute burn serum samples contain several factors that suppress cell-mediated immune functions. Antibody levels are usually mildly to moderately reduced. Complement, particularly the alternative complement pathway, may be massively activated and depleted, removing a critical defense mechanism against gram-negative rod infections for which preformed antibodies are absent. This depression is further exacerbated by malnutrition and infection. Fibronectin levels are also reduced. Phagocytic cell function is abnormal with burns. Neutrophil numbers may be depressed, and function is abnormal. Chemotactic responsiveness, cytoplasmic granule enzyme content, and oxygen radical generation are abnormal. Monocyte/macrophage dysfunction has similarly been demonstrated. Burn infections reflect abnormal host functions as well as changes in the hospital environment and microbial selection pressures. The burn patient is a model of cutaneous infection in the patient at risk.
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PMID:Infections in burn patients: a paradigm for cutaneous infection in the patient at risk. 637 65


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