Hypotensive Hemostasis in Patients Presenting with Ruptured Aortic Aneurysm

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Aluminium content of spanish infant formula

Aluminium toxicity has been relatively well documented in infants with impaired renal function and premature neonates. The aims of this study were to analyse the concentration of aluminium in the majority of infant formulae sold commercially in Spain, to determine the influence of aluminium content in the tap water in reconstituted powder formulae and to estimate the theoretical toxic aluminium intake in comparison with the PTWI, and lastly, to discuss the possible interactions of certain essential trace elements added to formulation with aluminium according to type or main protein based infant formula. A total of 82 different infant formulae from 9 different manufacturers were studied. Sample digestion was simulated in a closed acid-decomposition microwave system. Aluminium concentration was determined by atomic absorption spectrophotometry with graphite furnace. In general, the infant formulae studied provide an aluminium level higher than that found in human milk, especially in the case of soya, preterm or hydrolysed casein-based formulae. Standard formulae provide lower aluminium intakes amounting to about 4 % PTWI. Specialised and preterm formulae result in moderate intake (11 – 12 % and 8 – 10 % PTWI, respectively). Soya formulae contribute the highest intake (15 % PTWI). Aluminium exposure from drinking water used for powder formula reconstitution is not considered a clear potential risk. In accordance with the present state of knowledge about aluminium toxicity, it seems prudent to call for continued efforts to standardise routine quality control and reduce aluminium levels in infant formula as well as to keep the aluminium concentration under 300 g l-1 for all infant formulae, most specifically those formulae for premature and low birth neonates

Mn bioavailability by polarized Caco-2 cells: comparison between Mn gluconate and Mn oxyprolinate

<p>Abstract</p> <p>Background</p> <p>Micronutrient inadequate intake is responsible of pathological deficiencies and there is a need of assessing the effectiveness of metal supplementation, frequently proposed to rebalance poor diets. Manganese (Mn) is present in many enzymatic intracellular systems crucial for the regulation of cell metabolism, and is contained in commercially available metal supplements.</p> <p>Methods</p> <p>We compared the effects of two different commercial Mn forms, gluconate (MnGluc) and oxyprolinate (MnOxP). For this purpose we used the polarized Caco-2 cells cultured on transwell filters, an established in vitro model of intestinal epithelium. Since micronutrient deficiency may accelerate mitochondrial efficiency, the mitochondrial response of these cells, in the presence of MnGluc and MnOxP, by microscopy methods and by ATP luminescence assay was used.</p> <p>Results</p> <p>In the presence of both MnOxP and MnGluc a sustained mitochondrial activity was shown by mitoTraker labeling (indicative of mitochondrial respiration), but ATP intracellular content remained comparable to untreated cells only in the presence of MnOxP. In addition MnOxP transiently up-regulated the antioxidant enzyme Mn superoxide dismutase more efficiently than MnGluc. Both metal treatments preserved NADH and βNADPH diaphorase oxidative activity, avoided mitochondrial dysfunction, as assessed by the absence of a sustained phosphoERK activation, and were able to maintain cell viability.</p> <p>Conclusions</p> <p>Collectively, our data indicate that MnOxP and MnGluc, and primarily the former, produce a moderate and safe modification of Caco-2 cell metabolism, by activating positive enzymatic mechanisms, thus could contribute to long-term maintenance of cell homeostasis.</p

''Deferoxamine blocks death induced by glutathione depletion in PC 12 cells''

Chouraqui, E. | Leon, A. | Repesse, Y. | Prigent-Tessier, A. | Bouhallab, S. | Bougle, D. | Marie, C. | Duval, D.International audience''The purpose of the present work was to investigate the mechanisms by which glutathione depletion induced by treatment with buthionine sulfoximine (BSO) led within 24-30 h to PC 12 cells apoptosis. Our results showed that treatment by relatively low concentrations (10-30 mu M) of deferoxamine (DFx), a natural iron-specific chelator, almost completely shielded the cells from BSO-induced toxicity and that DFx still remained protective when added up to 9-12 h after BSO treatment. On the other hand, phosphopeptides derived from milk casein and known to carry iron across cell membranes, markedly potentiated the toxic action of BSO when loaded with iron but were ineffective in sodium form. Kept for 24 h in serum-free medium, the cells underwent a decrease in glutathione content after BSO treatment, but remained viable. However, these BSO-pre-treated cells showed a rapid (90-120 min) decrease in cell viability when incubated with low doses of iron, whereas a great proportion of them remained viable in the presence of higher concentrations of copper and zinc. We also observed in PC 12 cells an early (4-8 h) and transient increase in the expression of ferritin subunits following BSO addition. Taken together these results suggest that BSO-induced glutathione depletion leads to an alteration of cellular iron homeostasis, which may contribute to its toxicity. (C) 2013 Elsevier Inc. All rights reserved.'

Iron deficiency and risk factors for lower iron stores in 6-24-month-old New Zealanders.

OBJECTIVES: To determine the prevalence of biochemical iron deficiency and identify factors associated with ferritin levels among 6-24-month-old urban South Island New Zealand children. DESIGN: Cross-sectional survey conducted from May 1998 to March 1999. SETTING: The cities of Christchurch, Dunedin and Invercargill. SUBJECTS: A total of 323 randomly selected 6-24-month-old children participated (response rate 61%) of which 263 provided a blood sample. METHODS: A complete blood cell count, zinc protoporphyrin, serum ferritin and C-reactive protein were measured on nonfasting venipuncture blood samples, 3-day weighed food records and general questionnaire data were collected. RESULTS: Among children with C-reactive proteinboys), ethnicity (Caucasian>non-Caucasian), weight-for-age percentiles (negative) and birth weight (positive) were associated with ferritin after adjusting for infection and socioeconomic status. When current consumption of iron fortified formula and >500 ml of cows' milk per day were included, these were associated with a 22% increase and 25% decrease in ferritin, respectively (R2=0.28). CONCLUSIONS: The presence of suboptimal iron status (29%) among young New Zealand children is cause for concern, even though severe iron deficiency is rare, because children with marginal iron status are at risk of developing severe iron deficiency if exposed to a physiological challenge