SUMMARYHelicobacter pylori causes a chronic gastric infection, which is usually life-long. Many epidemiological studies have shown that this is probably one of the most common bacterial infections throughout the world involving 30% of the population living in developed countries and up to 80-90% of the population in developing regions.Concomitantly, developing regions also have high prevalence of micronutrient malnutrition. In the last few years, some studies have suggested that H. pylori infection may affect the homeostasis of different micronutrients including iron, vitamin B12, folic acid, a-tocopherol, vitamin C and b-carotene. In this article, we discuss the current scientific information of the effect that H. pylori infection may produce on micronutrient malnutrition.

Zinc and iron are crucial mineral components of human diet, because their deficiency leads to several disorders, including alterations of the immune function. It has been demonstrated, in both humans and rodents, that a diminished number of lymphoid cells and a loss of lymphocyte activity accompany deprivation of these essential minerals. The aim of this work was to analyze if iron and/or zinc imbalances regulate lymphocyte activity and the intracellular signals involved in the effect. Mice from the BALB/c strain were fed with iron- and/or zinc-deficient or mineral-supplemented diets, according to the American Institute of Nutrition Rodent Diets. Levels of iron and zinc were assessed in blood, liver, or bone samples. Selective mitogen stimulation of T- and B-lymphocytes were performed. We found a diminished proliferative response in T- and B-lymphocytes from zinc- and/or iron-deficient animals with respect to controls. These effects were related to decreased mitogen-induced translocation of protein kinase C (PKC) activity to cell membranes on both cell types from all animals fed with deficient diets. Our results demonstrate that iron and zinc deficiencies affect both T- and B-lymphocyte function by PKC-dependent mechanisms.

The aim of the present work was to validate a paper chromatography system as an alternative way to determine the radiochemical purity of Na 18 F. Methods: The evaluated parameters were specificity, limit of quantification, measurement interval, linearity, precision, accuracy, and robustness. Results: The proposed method proved to be linear (P . 0.05; r 2 5 1.000), precise (relative SD, 8.6%), accurate (mean recovery, 95.9%; relative SD, 1.5%-1.8%), and robust under different conditions since no influence of the operative variables on the chromatographic performance was observed. Conclusion: This system can be used as a reliable alternative method to determine the radiochemical purity of Na 18 F samples that can be easily performed in PET radiopharmacies at low cost. TheuseofNa 18 F for bone scintigraphy dates back to the early 1960s (1). However, the unavailability of clinical cyclotrons and the development of 99m Tc-labeled agents for bone scintigraphy brought about the prompt replacement of Na 18 F with 99m Tc agents for clinical use (2). Some decades later, Na 18 F was rediscovered when, in 2000, the Food and Drug Administration approved it as a radiopharmaceutical for bone scintigraphy as part of its modernization in the handling of new drug applications (3). Since then, many reports have proposed the use of this agent as a sensitive and specific radiopharmaceutical for detection of benign and malignant osseous abnormalities that also allows the regional characterization of lesions in metabolic bone diseases (4,5).Na 18 F is a cyclotron-produced radiopharmaceutical, and the only reported and validated methodology for determining its radiochemical purity (RP) is high-performance liquid chromatography, which requires special equipment (6-8). Nevertheless, previous studies demonstrated the efficacy of a paper chromatography method for the RP determination of Na 18 F (9). This work was performed to investigate the possibility of applying the paper chromatography method as an alternative to high-performance liquid chromatography for 18 F-fluoride RP analysis. MATERIALS AND METHODS Na 18 F Production18 F-fluoride was produced on an 18-MeV cyclotron, Cyclone 18/9 (IBA), by the 18 O(p,n) 18 F nuclear reaction. The niobium target (with yield of 8.7 GBq/mA at saturation) was filled with 2 mL of enriched 18 O water, which was irradiated with protons for 10 min at anintensity of 40 mA. The solution containing 18 F 2 was transferred into an automatic synthesis module, Synthera (IBA), prepared with a commercial reagent kit and accessories for Na 18 F production. 18 F-fluoride ions were trapped in an anion exchange column (Sep-Pak Light Accell Plus QMA; Waters Corp.) and were theneluted with a 0.9% NaCl solution. Finally, the resulting 15 mL of Na 18 F were dispensed into a sterile, pyrogen-free vial through a 0.22-mm filter (Millipore) in a dispensing unit (Dispensing Hot Cell; Becquerel and Sievert Co., Ltd.). Physicochemical Quality ControlRadionuclidic purity was evaluated by g-ray spectrometry (PX4 TeCd detector; Ampt...

The aim of the study was to determine the relative bioavailability of zinc gluconate stabilized with glycine in a Petit Suisse cheese from an infant dessert. Weight gain and bone zinc content were the nutritional responses evaluated for the diets of different zinc content: 2 ppm (basal) and 5, 10, and 30 ppm from zinc gluconate stabilized with glycine and zinc sulfate. Nonlinear regression analysis of the fitted curves for weight gain determined a relative zinc bioavailability of 100% for the Ymax ratio and 96% for Ymax/t1/2 ratio for zinc gluconate stabilized with glycine (R2=0.7996 for zinc sulfate and 0.8665 for zinc gluconate stabilized with glycine). The slope ratio analysis from linear regression of femur zinc determined a relative zinc bioavailability of 93% for zinc gluconate stabilized with glycine (R2=0.8693 for zinc sulfate and 0.8307 for zinc gluconate stabilized with glycine). Zinc gluconate stabilized with glycine has similar bioavailability as zinc sulfate in a Petit Suisse cheese nutritional matrix, with the advantage that the stabilized compound does not modify the sensorial characteristics of the fortified cheese.

The iron bioavailability and acute oral toxicity in rats of a ferrous gluconate compound stabilized with glycine (SFG), designed for food fortification, was studied in this work by means of the prophylactic method and the Wilcoxon method, respectively. For the former studies, SFG was homogeneously added to a basal diet of low iron content, reaching a final iron concentration of 20.1 +/- 2.4 mg Fe/kg diet. A reference standard diet using ferrous sulfate as an iron-fortifying source (19.0 +/- 2.1 mg Fe/kg diet) and a control diet without iron additions (9.3 +/- 1.4 mg Fe/kg diet) were prepared in the laboratory in a similar way. These diets were administered to three different groups of weaning rats during 23 d as the only type of solid nourishment. The iron bioavailability of SFG was calculated as the relationship between the mass of iron incorporated into hemoglobin during the treatment and the total iron intake per animal. This parameter resulted in 36.6 +/- 6.2% for SFG, whereas a value of 35.4 +/- 8.0% was obtained for ferrous sulfate. The acute toxicological studies were performed in two groups of 70 female and 70 male Sprague-Dawley rats that were administered increasing doses of iron from SFG. The LD50 values of 1775 and 1831 mg SFG/kg body wt were obtained for female and male rats, respectively, evidencing that SFG can be considered as a safe compound from a toxicological point of view.