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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The course of a subcutaneous weight-related infection with Strongyloides ratti was followed in rats fed diets containing either 3 mg Zn/kg diet [zinc deficient (Zn-)] or 40 mg Zn/kg diet [zinc adequate (Zn+)]. At 19 d postinfection (dpi) the proportions of larvae persisting in the intestines as adult worms were 52 +/- 2% (means +/- SEM) for Zn-, 39.5 +/- 2.5% for pair-fed Zn- (Zn-PF), and 31.6 +/- 3.2% for Zn+ (p less than 0.001, analysis of variance); some Zn- rats were then transferred to the zinc-adequate diet [This was the zinc-repleted group (ZnR).] Both groups retained a group of pair-fed controls (Zn-PF and ZnRPF). Between 19 and 28 dpi ZnR animals gained weight faster than did Zn- animals and had heavier thymuses relative to body weight. Zinc deficiency enhances the establishment of S ratti larvae in the intestine of rats and alters the characteristics of intestinal expulsion of the nematodes; however, spontaneous cure was achieved by 38 dpi in both Zn- and control groups.
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PMID:Zinc deprivation and zinc repletion: effect on the response of rats to infection with Strongyloides ratti. 236 May 47

The prevalence of marginal zinc nutriture in several populations of people in this country and the lack of reports on the effect of marginal zinc nutriture in experimental animals prompted us to look at pancreatic acinar cell function and morphology in rats fed a zinc-deficient diet ad libitum: 4 and 50 ppm zinc-supplemented diets in amounts isocaloric to a zinc-deficient diet and Rodent-Blox fed ad libitum for a period of 49 +/- 1 (SEM) days. Because of a diminished rate of energy expenditure in zinc-deficient rats, animals receiving 50 ppm zinc-supplemented diets were offered less food, resulting in decreased body weight and pancreas weight, DNA, RNA, total protein, lipase, amylase, and secretion of protein. Specific changes due to zinc deficiency included (a) further decrease in body weight and (b) increase in content, specific activity, and secretion of lipase. Both the size and volume fraction of zymogen granules were reduced in zinc deficiency. The lumina of acinar and small ducts were collapsed with paucity of secretion products. Zinc deficiency may therefore lead to a defect in discharge mechanism. A further reduction in volume fraction of zymogen granules in the 4 ppm zinc-supplemented group was associated with increased secretion of serine proteases (trypsinogen and chymotrypsinogen), which constitute approximately 46% of total secretory protein in the pancreas under normal dietary conditions. This indicated an accelerated discharge due to an unknown mechanism. Changes in the secretion of digestive enzymes in the present study simulated ethanol-induced secretory alterations that were previously observed. Because abnormal zinc nutriture and chronic alcoholism are commonly associated, it is speculated that zinc deficiency may play a role in the ethanol-induced secretory alterations.
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PMID:Pancreatic acinar cell function and morphology in rats fed zinc-deficient and marginal zinc-deficient diets. 241

Zinc deficiency was reported to lead to congenital malformations and abnormal fetal development, and zinc concentration in amniotic fluid has been found to be correlated with fetal birth weight. In the present study, zinc concentrations were estimated in 8 pregnant women at 15 gestational weeks and 68 pregnant women at term. Maternal serum zinc concentration in early and term pregnancy was significantly lower than that of the non-pregnant controls (mean values +/- SEM being 9.8 +/- 0.6, 9.3 +/- 0.2, and 11.5 +/- 0.3 mumol/l, respectively). Maternal serum zinc concentrations reached the non-pregnant level by one week post partum. The mean serum zinc concentration in cord blood was 14.4 (+/- 0.4) mumol/l. The zinc concentration in the amniotic fluid was very low both in early pregnancy and at term 1.1 and 0.8 mumol/l, respectively, and no correlation was found to the birth weight. Low serum zinc content in pregnant women occurs as a normal feature and congenital malformation as a consequence of disturbed zinc metabolism is probably only to be seen in instances of extreme zinc deficiency in conjunction with malnutrition.
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PMID:Zinc concentrations in maternal blood during pregnancy and post partum, in cord blood and amniotic fluid. 343 49

Open-chest dog preparations were used to determine divalent cation transport following acute myocardial infarction. Cardiac lymph flow, lymph and plasma protein, zinc, calcium, and magnesium content and hemodynamic measurements were recorded every 20 min before and after coronary artery occlusion in sham operated (N = 4), infarcted (N = 6), and lymph-ablated animals (N = 4). During the 4-hr occlusion period, with constant blood pressure, lymph flow increased from 1.53 +/- 0.25 to 2.15 +/- 0.44 mg/hr (SEM), P less than 0.01. Zinc decreased in plasma from 0.69 +/- 0.10 to 0.41 +/- 0.08 micrograms/ml, P less than 0.01, and in lymph from 0.69 +/- 0.08 to 0.40 +/- 0.02 micrograms/ml, P less than 0.01. Zinc to protein ratio decreased similarly to total zinc in plasma and lymph. Changes in calcium and magnesium were insignificant. Lymph to plasma concentration ratios increased for protein from 0.57 +/- 0.05 to 0.62 +/- 0.02, P less than 0.05, and for zinc from 1.10 +/- 0.26 to 1.21 +/- 0.14, P less than 0.05. Heart lymph clearance (lymph:plasma ratio X lymph flow) steadily rose for protein from 0.31 to 0.06 to 0.50 +/- 0.08, P less than 0.05, and for zinc from 0.59 +/- 0.18 to 0.92 +/- 0.15, P less than 0.05. Lymph and plasma measurements did not change significantly in sham-operated animals. Plasma zinc remained unchanged from baseline after coronary occlusion in all lymph-ablated animals. The increased clearance of protein and zinc suggests that plasma proteins are zinc carriers after acute myocardial infarction and that the reduction of plasma zinc is dependent upon an intact cardiac lymphatic circulation.
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PMID:Zinc transport by the heart lymphatic system after acute myocardial infarction. 662 Oct 29

Zinc deficiency enhances experimental esophageal tumor induction. Vitamin A supplementation inhibits carcinogenesis in animals. Plasma zinc and plasma vitamin A levels are reduced in several human squamous cancers, but have not been studied in a US population with esophageal cancer. Therefore, we measured plasma zinc and vitamin A in patients with newly diagnosed esophageal cancer. In addition, we assessed hepatic and nutritional status and attempted to control for other factors known to influence plasma zinc and vitamin A levels. Plasma zinc and vitamin A were both significantly less in esophageal carcinoma than in age-matched healthy controls (plasma zinc 65.7 +/- 3.3 micrograms/dl [mean +/- SEM] in esophageal cancer versus 80.5 +/- 2.4 micrograms/dl in controls, P less than 0.01; plasma vitamin A 32.6 +/- 3.4 micrograms/dl in esophageal cancer versus 60.2 +/- 4.2 in controls, P less than 0.001). Overall, 15 of 17 patients with esophageal cancer had decreased plasma zinc and/or decreased plasma vitamin A. Our findings are compatible with a hypothesis that zinc or vitamin A deficiency may be co-factors in the induction of human esophageal carcinoma.
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PMID:Plasma zinc and vitamin A in human squamous carcinoma of the esophagus. 683 64