Antioxidant vitamin levels in term and preterm infants and their relation to maternal vitamin status

BACKGROUND:Lipid peroxidation plays a vital role in the pathogenesis of many neonatal complications. Preterm babies are especially predisposed to lung diseases and retinopathy, probably due to a deficiency in their antioxidant systems. Vitamins E, A, and C are part of the natural antioxidant defense systems. We aimed to determine the levels of vitamins E, A, and C in maternal and cord blood plasma of term and preterm infants and to investigate the relationships between these levels.METHODS:In the present study we determined vitamin E, A, and C levels in the umbilical cord blood of term (n = 30) and preterm (n = 22) infants and their mothers by HPLC. Blood samples were taken during delivery.RESULTS:Levels of lipid soluble antioxidant vitamin E and A in cord blood were lower than maternal values (p &lt;0.01, p &lt;0.05, respectively). Conversely, the level of water-soluble vitamin C was higher in cord blood than in maternal level (p &lt;0.05). Significantly higher levels of vitamins E, A, and C were found in term babies as compared with those born preterm (p &lt;0.05).CONCLUSIONS:There was a positive correlation between maternal and cord blood levels of vitamins E and A (r = 0.775, r = 0.725, respectively). In conclusion, preterm babies have fewer lipid-soluble antioxidant vitamins in their serum compared to term infants. Therefore, it is possible to postulate that preterm infants are more susceptible to oxidative stress</p

Defective Treg generation and increased type 3 immune response in leukocyte adhesion deficiency 1

In 15 Turkish LAD-1 patients and controls, we assessed the impact of pathogenic ITGB2 mutations on Th17/Treg differentiation and functions, and innate lymphoid cell (ILC) subsets. The percentage of peripheral blood Treg cells, in vitro-generated induced Tregs differentiated from naive CD4+ T cells were decreased despite the elevated absolute counts of CD4+ cells in LAD-1 patients. Serum IL-23 levels were elevated in LAD-1 patients. Post-curdlan stimulation, LAD-1 patient-derived PBMCs produced more IL-17A. Additionally, the percentages of CD18-deficient Th17 cells expanded from total or naïve CD4+ T cells were higher. The blood ILC3 subset was significantly elevated in LAD-1. Finally, LAD-1 PBMCs showed defects in trans-well migration and proliferation and were more resistant to apoptosis. Defects in de novo generation of Tregs from CD18-deficient naïve T cells and elevated Th17s, and ILC3s in LAD-1 patients' peripheral blood suggest a type 3-skewed immunity and may contribute to LAD-1-associated autoimmune symptoms

Are Movers More Religious than Stayers? Religiosity of European Majority, Turks in Europe and Turkey

Turks, most of them Islamic, are establishing themselves in European countries. Studies mostly compare migrant religiosity to other migrants and to majority population in the destination societies. We add those left behind in origin country to this comparison. Using the unique possibility offered by the European Social Surveys, this study compares subjective, individual, and communal religiosity of first and second generation-Turkish origin Europeans with non-migrants in Turkey and European natives in the destination societies. Results show that the mechanisms of religiosity differ for migrants and second generation. Religion fuels the creation of ethno-religious space in the new social environment and intensifies subjective and communal manifestation of piety. However, it is also subject to the secularizing impact of the receiving society in individual religious practise. Second-generation Europeans pray less in their personal sphere but consider themselves more religious than and attend religious meetings as often as non-migrants in Turkey. European natives score much lower on all three dimensions of religiosity than first and second-generation Turkish origin Europeans

ILC3 deficiency and generalized ILC abnormalities in DOCK8‐deficient patients

BackgroundDedicator of cytokinesis 8 (DOCK8) deficiency is the main cause of the autosomal recessive hyper-IgE syndrome (HIES). We previously reported the selective loss of group 3 innate lymphoid cell (ILC) number and function in a Dock8-deficient mouse model. In this study, we sought to test whether DOCK8 is required for the function and maintenance of ILC subsets in humans

ILC3 deficiency and generalized ILC abnormalities in DOCK8-deficient patients

BackgroundDedicator of cytokinesis 8 (DOCK8) deficiency is the main cause of the autosomal recessive hyper-IgE syndrome (HIES). We previously reported the selective loss of group 3 innate lymphoid cell (ILC) number and function in a Dock8-deficient mouse model. In this study, we sought to test whether DOCK8 is required for the function and maintenance of ILC subsets in humans