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

Manganese, zinc and copper are essential for normal prenatal and neonatal development. Manganese deficiency causes skeletal abnormalities, congenital ataxia due to abnormal inner ear development, and abnormal brain function. Depression of mucopolysaccharide synthesis and manganese superoxide dismutase activity may be fundamental to ultrastructural and other defects. In copper deficiency, neurological and skeletal abnormalities are due to impairment of phospholipid synthesis and collagen crosslinking, and possibly to low activity of copper metalloenzymes. The fundamental defect leading to the extremely teratogenic effects of zinc deficiency is related to depressed synthesis of DNA. In the neonatal period, poor survival and growth and depressed function of the immune system are salient features. Developmental patterns of trace element concentrations in various tissues suggest that important changes in metabolic regulation of trace elements may occur during the neonatal period. This hypothesis is being investigated by studies of molecular localization of trace elements in certain neonatal tissues, in conjunction with similar observations in milk.
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PMID:The roles of trace elements in foetal and neonatal development. 611 92

Applications of pulse-labeling techniques to the study of axonal transport have provided new insights into certain types of peripheral nerve disease. In normal neurons, many of the newly synthesized proteins that are rapidly transported to distal parts of the cell eventually undergo a process of "turnaround," after which they are carried back to the cell bodies for degradation. This turnaround is selectively impaired in rat nerves early in the course of streptozotocin-induced diabetes and of experimental neuropathies induced by exposure to acrylamide, zinc pyridinethione, or p-bromophenylacetylurea. In the neuropathy of p-bromo-phenylacetylurea, depression of turnaround precedes the clinical signs of neurologic dysfunction, is later proportional to the severity of the disability, and may account for the characteristic accumulation of debris in preterminal axons.
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PMID:Abnormalities of axonal transport: are they a cause of peripheral nerve disease? 618 27

Alcohol has at least two actions on essential fatty acid (EFA) and Prostaglandin (PG) metabolism. It enhances the conversion of dihomogammalinolenic acid (DGLA) to PGE1 but it blocks the activity of the delta-6-desaturase, an enzyme necessary for replenishment of DGLA stores from dietary precursors. The acute effect of ethanol is therefore an increased production of PGE1 but chronic consumption will lead to depletion of DGLA and PGE1. Withdrawal from alcohol will lead to a precipitous fall in PGE1. PGE1 is known to have profound effects on the nervous system and behaviour. Patients with mania produce more PGE1 than normal while those with depression make less. Alcoholics may drink to maintain a normal PGE1 level, something which will require more and more ethanol as DGLA is depleted. In both animals and humans PGE1 or its precursor, gamma-linolenic acid (GLA) have been shown to attenuate the acute withdrawal syndrome. PGE1 injections prevent the development of fatty liver in alcohol-treated animals. Defective EFA and PGE1 metabolism are known to lead to increased fibrosis, reproductive failure, cardiomyopathy, cardiovascular disorders, gastritis and pancreatitis and could therefore be the basis for these disorders in alcoholics. A PGE1 deficiency could also be responsible for the fetal alcohol syndrome. Three other agents are known to produce constellations of fetal defects very similar to those found in the alcohol syndrome. These other factors are dihphenylhydantoin, lithium, and a deficiency of zinc. These three factors and excessive alcohol consumption all lead to PGE1 deficiency by different routes. If this concept is correct, the key to the management of alcoholism and its medical complications lies in the provision of GLA or DGLA, fatty acids which by-pass the alcohol blocked step and which are unfortunately unlikely to be present in any normal diet. Unlike many concepts of alcoholism and alcohol damage, the EFA/PGE1 idea is very readily testable and already has considerable experimental support.
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PMID:A biochemical basis for alcoholism and alcohol-induced damage including the fetal alcohol syndrome and cirrhosis: interference with essential fatty acid and prostaglandin metabolism. 625 73

Effects of therapeutic and pulp protecting dental materials on nervous tissue were studied in an in vitro model utilizing the isolated left rat phrenic nerve. The nerve was placed in a buffer bath between two suction electrodes, one for electrical stimulation and one for recording. Evoked compound action potentials (cAP) were monitored in an oscilloscope. Fresh mixes of six commonly used pulp-dentin materials were placed in contact with the nerve, and the cAP registered. Formocresol, zinc oxide-eugenol (ZOE), Calasept and Dycal caused a complete depression of the nerve activity within 0.5 to 5 min of contact. The depression appeared irreversible with Formocresol and Calasept, reversible with Dycal, and reversible with ZOE when applied to nerves surrounded by adherent fatty tissue. De Trey Zinc and Durelon caused only a minor depression of the cAP within 30 min of contact.
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PMID:Effects of therapeutic and pulp protecting materials on nerve transmission in vitro. 630 26

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

1. Zinc deficiency was studied in mice infected with Trypanosoma musculi. 2. In all dietary groups, the infected animals consumed more food and gained more weight than the uninfected controls. 3. In all studies, at the peak of parasitemia, the zinc-deficient animals showed three times the number of trypanosomes as that of the complete and pair-fed mice. 4. The average coefficients of variation in body lengths of T.musculi cells indicated that the formation of the reproductive-inhibiting antibody (ablastin) occurred later in zinc-deficient animals compared to animals fed complete diets. The degree and duration of parasitemia in the zinc-deficient animals indicated a delay in the synthesis of the terminal lytic antibody. 5. Irrespective of diets, severe depression in the primary and secondary antibody responses to in vivo immunization of sheep erythrocytes was observed in infected animals over non-infected controls.
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PMID:Interaction of nutrition and infection: effect of zinc deficiency on resistance to Trypanosoma musculi. 634 33

Many of the features of the premenstrual syndrome are similar to the effects produced by the injection of prolactin. Some women with the premenstrual syndrome have elevated prolactin levels, but in most the prolactin concentrations are normal. It is possible that women with the syndrome are abnormally sensitive to normal amounts of prolactin. There is evidence that prostaglandin E1, derived from dietary essential fatty acids, is able to attenuate the biologic actions of prolactin and that in the absence of prostaglandin E1 prolactin has exaggerated effects. Attempts were made, therefore, to treat women who had the premenstrual syndrome with gamma-linolenic acid, an essential fatty acid precursor of prostaglandin E1. Gamma-linolenic acid is found in human, but not cows', milk and in evening primrose oil, the preparation used in these studies. Three double-blind, placebo-controlled studies, one large open study on women who had failed other kinds of therapy for the premenstrual syndrome and one large open study on new patients all demonstrated that evening primrose oil is a highly effective treatment for the depression and irritability, the breast pain and tenderness, and the fluid retention associated with the premenstrual syndrome. Nutrients known to increase the conversion of essential fatty acids to prostaglandin E1 include magnesium, pyridoxine, zinc, niacin and ascorbic acid. The clinical success obtained with some of these nutrients may in part relate to their effects on essential fatty acid metabolism.
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PMID:The role of essential fatty acids and prostaglandins in the premenstrual syndrome. 635 May 79

X-ray studies on human insulins prepared by semisynthetic and biosynthetic methods have recently been undertaken. Human insulin differs from porcine insulin only at the COOH terminus of the B-chain. The present study reports the crystal structure of 4-zinc human insulin, which is used clinically as a slow-acting preparation. The structure has been refined, using 1.85-A resolution data, to a residual of 0.173. The unit cell is rhombohedral, space group R3, with hexagonal cell constants a = 80.953 and c = 37.636 A, and it is nearly isomorphous with that of 4-zinc porcine insulin. As a result of a conformational change of the first eight residues of the B-chain of molecule 1 from an extended conformation observed in the 2-zinc structure to an alpha-helical one, the coordination around one of the zinc ions on the 3-fold axis has changed, an additional zinc ion in a general position is bound by the hexamer, and additional hydrogen-bonded interactions help stabilize dimer and hexamer formation. Unlike the surface of the 2-zinc insulin hexamer, which possesses a shallow depression containing a zinc ion and its coordinating water molecules, the 4-zinc human insulin hexamer contains a zinc and chloride ion at the bottom of an 8-A tunnel produced by three parallel alpha-helices. These alpha-helices shield the zinc ion from the environment, decreasing the rate of dissociation of the hexamer, and provide an explanation for the slow-acting aspect of the 4-zinc crystalline form.
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PMID:Structural stability in the 4-zinc human insulin hexamer. 639 Apr 30

The case of a surgical patient with a full blown syndrome of zinc deficiency is presented and the various implications related to a deficiency of this trace mineral are discussed. The symptomatology involved mental depression, visual disturbances, glucose intolerance, decreased serum alkaline phosphatase levels, wound healing impairment, eczematoid dermatitis and reduced humoral and cellular immune defences. Oral supplementation with zinc sulphate dramatically reversed the signs and symptoms of the syndrome and resulted in rapid wound healing. This case seems to have exhibited most of the different signs and symptoms reported from time to time in the literature. Awareness of zinc deficiency is being brought to light in many medical and surgical conditions. Total parenteral nutrition (T.P.N.) can exacerbate the lack of this trace metal and supplementation with fresh blood derivate are, as demonstrated, useless in these cases. Zinc, as component of various metalloenzymes, accounts for the clinical manifestations of its deficiency.
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PMID:First full blown syndrome of acute zinc deficiency in course of long term total parenteral nutrition: a clinical case. 643 15

Several experiments were performed with young chicks to evaluate lead (Pb) toxicity and its effect upon copper (Cu) and zinc (Zn) toxicosis in the presence or absence of Eimeria acervulina infection. Toxic levels of Pb (3300 mg/kg) and Cu (500 mg/kg) or Zn (2000 and 4000 mg/kg) were added to completely adequate corn-soybean meal diets, while duodenal coccidiosis was produced by multiple crop inoculations of 4 X 10(5) sporulated E. acervulina oocysts. Both Pb and Cu depressed gain and feed efficiency while concomitant coccidial infection reduced these parameters further. Moreover, E. acervulina increased the concentration of liver Cu and kidney Pb. Although Pb supplementation slightly decreased the accumulation of liver Cu, additional Cu tended to increase the deposition of Pb in the kidney in both infected and uninfected birds. Similarly, chick performance was significantly reduced by excess dietary Pb or Zn, although coccidiosis slightly ameliorated the growth depression caused by toxic levels (4000 mg/kg) of Zn. Although 4000 ppm Zn and coccidial infection reduced the deposition of Pb in the kidney, this interaction was not evident when 2000 mg/kg Zn was fed to infected chicks. It is evident that Pb toxicosis in the chick is affected little by excess dietary levels of either Cu or Zn.
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PMID:Lead toxicity in the chick as affected by excess copper and zinc and by Eimeria acervulina infection. 648 23


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