Socioeconomic disparities in diet vary according to migration status among adolescents in Belgium

Little information concerning social disparities in adolescent dietary habits is currently available, especially regarding migration status. The aim of the present study was to estimate socioeconomic disparities in dietary habits of school adolescents from different migration backgrounds. In the 2014 cross-sectional Health Behavior in School-Aged Children survey in Belgium, food consumption was estimated using a self-administrated short food frequency questionnaire. In total, 19,172 school adolescents aged 10-19 years were included in analyses. Multilevel multiple binary and multinomial logistic regressions were performed, stratified by migration status (natives, 2nd- and 1st-generation immigrants). Overall, immigrants more frequently consumed both healthy and unhealthy foods. Indeed, 32.4% of 1st-generation immigrants, 26.5% of 2nd-generation immigrants, and 16.7% of natives consumed fish two days a week. Compared to those having a high family affluence scale (FAS), adolescents with a low FAS were more likely to consume chips and fries once a day (vs. <once a day: Natives aRRR = 1.39 (95%CI: 1.12-1.73); NS in immigrants). Immigrants at schools in Flanders were less likely than those in Brussels to consume sugar-sweetened beverages 2-6 days a week (vs. once a week: Natives aRRR = 1.86 (95%CI: 1.32-2.62); 2nd-generation immigrants aRRR = 1.52 (1.11-2.09); NS in 1st-generation immigrants). The migration gradient observed here underlines a process of acculturation. Narrower socioeconomic disparities in immigrant dietary habits compared with natives suggest that such habits are primarily defined by culture of origin. Nutrition interventions should thus include cultural components of dietary habits

Psychosocial work and home stressors predict sickness absence from work

info:eu-repo/semantics/nonPublishe

Computer simulations reveal novel properties of the cell-cell signaling network at the shoot apex in /Arabidopsis

The active transport of the plant hormone auxin plays a major role in the initiation of organs at the shoot apex. Polar localized membrane proteins of the PIN1 family facilitate this transport, and recent observations suggest that auxin maxima created by these proteins are at the basis of organ initiation. This hypothesis is based on the visual, qualitative characterization of the complex distribution patterns of the PIN1 protein in Arabidopsis. To take these analyses further, we investigated the properties of the patterns using computational modeling. The simulations reveal previously undescribed properties of PIN1 distribution. In particular, they suggest an important role for the meristem summit in the distribution of auxin. We confirm these predictions by further experimentation and propose a detailed model for the dynamics of auxin fluxes at the shoot apex

Bcl-2–Modifying Factor Induces Renal Proximal Tubular Cell Apoptosis in Diabetic Mice

This study investigated the mechanisms underlying tubular apoptosis in diabetes by identifying proapoptotic genes that are differentially upregulated by reactive oxygen species in renal proximal tubular cells (RPTCs) in models of diabetes. Total RNAs isolated from renal proximal tubules (RPTs) of 20-week-old heterozygous db/m+, db/db, and db/db catalase (CAT)-transgenic (Tg) mice were used for DNA chip microarray analysis. Real-time quantitative PCR assays, immunohistochemistry, and mice rendered diabetic with streptozotocin were used to validate the proapoptotic gene expression in RPTs. Cultured rat RPTCs were used to confirm the apoptotic activity and regulation of proapoptotic gene expression. Additionally, studies in kidney tissues from patients with and without diabetes were used to confirm enhanced proapoptotic gene expression in RPTs. Bcl-2–modifying factor (Bmf) was differentially upregulated (P < 0.01) in RPTs of db/db mice compared with db/m+ and db/db CAT-Tg mice and in RPTs of streptozotocin-induced diabetic mice in which insulin reversed this finding. In vitro, Bmf cDNA overexpression in rat RPTCs coimmunoprecipated with Bcl-2, enhanced caspase-3 activity, and promoted apoptosis. High glucose (25 mmol/L) induced Bmf mRNA expression in RPTCs, whereas rotenone, catalase, diphenylene iodinium, and apocynin decreased it. Knockdown of Bmf with small interfering RNA reduced high glucose–induced apoptosis in RPTCs. More important, enhanced Bmf expression was detected in RPTs of kidneys from patients with diabetes. These data demonstrate differential upregulation of Bmf in diabetic RPTs and suggest a potential role for Bmf in regulating RPTC apoptosis and tubular atrophy in diabetes

Rethinking the anti-FGM zero-tolerance policy: From intellectual concerns to empirical challenges

Abstract Purpose of Review Based on the discussions of a symposium co-organized by the Université Libre de Bruxelles (ULB) and the University of Lausanne (UNIL) in Brussels in 2019, this paper critically reflects upon the zero-tolerance strategy on “Female Genital Mutilation” (FGM) and its socio-political, legal and moral repercussions. We ask whether the strategy is effective given the empirical challenges highlighted during the symposium, and also whether it is credible. Recent Findings The anti-FGM zero-tolerance policy, first launched in 2003, aims to eliminate all types of “female genital mutilation” worldwide. The FGM definition of the World Health Organization condemns all forms of genital cutting (FGC) on the basis that they are harmful and degrading to women and infringe upon their rights to physical integrity. Yet, the zero-tolerance policy only applies to traditional and customary forms of genital cutting and not to cosmetic alterations of the female genitalia. Recent publications have shown that various popular forms of cosmetic genital surgery remove the same tissue as some forms of “FGM”. In response to the zero-tolerance policy, national laws banning traditional forms of FGC are enforced and increasingly scrutinize the performance of FGC as well as non-invasive rituals that are culturally meaningful to migrants. At the same time, cosmetic procedures such as labiaplasty have become more popular than ever before and are increasingly performed on adolescents. Summary This review shows that the socio-legal and ethical inconsistencies between “FGM” and cosmetic genital modification pose concrete dilemmas for professionals in the field that need to be addressed and researched

Gene transfer to pre-hematopoietic and committed hematopoietic precursors in the early mouse Yolk Sac: a comparative study between in situ electroporation and retroviral transduction

<p>Abstract</p> <p>Background</p> <p>Hematopoietic development in vertebrate embryos results from the sequential contribution of two pools of precursors independently generated. While intra-embryonic precursors harbour the features of hematopoietic stem cells (HSC), precursors formed earlier in the yolk sac (YS) display limited differentiation and self-renewal potentials. The mechanisms leading to the generation of the precursors in both sites are still largely unknown, as are the molecular basis underlying their different potential. A possible approach to assess the role of candidate genes is to transfer or modulate their expression/activity in both sites. We thus designed and compared transduction protocols to target either native extra-embryonic precursors, or hematopoietic precursors.</p> <p>Results</p> <p>One transduction protocol involves transient modification of gene expression through <it>in situ </it>electroporation of the prospective blood islands, which allows the evolution of transfected mesodermal cells in their "normal" environment, upon organ culture. Following <it>in situ </it>electroporation of a GFP reporter construct into the YS cavity of embryos at post-streak (mesodermal/pre-hematopoietic precursors) or early somite (hematopoietic precursors) stages, high GFP expression levels as well as a good preservation of cell viability is observed in YS explants. Moreover, the erythro-myeloid progeny typical of the YS arises from GFP⁺mesodermal cells or hematopoietic precursors, even if the number of targeted precursors is low. The second approach, based on retroviral transduction allows a very efficient transduction of large precursor numbers, but may only be used to target 8 dpc YS hematopoietic precursors. Again, transduced cells generate a progeny quantitatively and qualitatively similar to that of control YS.</p> <p>Conclusion</p> <p>We thus provide two protocols whose combination may allow a thorough study of both early and late events of hematopoietic development in the murine YS. <it>In situ </it>electroporation constitutes the only possible gene transfer method to transduce mesodermal/pre-hematopoietic precursors and analyze the earliest steps of hematopoietic development. Both <it>in situ </it>electroporation and retroviral transduction may be used to target early hematopoietic precursors, but the latter appears more convenient if a large pool of stably transduced cells is required. We discuss the assets and limitation of both methods, which may be alternatively chosen depending on scientific constraints.</p

Lyl-1 regulates primitive macrophages and microglia development

During ontogeny, macrophage populations emerge in the Yolk Sac (YS) via two distinct progenitor waves, prior to hematopoietic stem cell development. Macrophage progenitors from the primitive/ early EMP and transient-definitive/ late EMP waves both contribute to various resident primitive macrophage populations in the developing embryonic organs. Identifying factors that modulates early stages of macrophage progenitor development may lead to a better understanding of defective function of specific resident macrophage subsets. Here we show that YS primitive macrophage progenitors express Lyl-1, a bHLH transcription factor related to SCL/Tal-1. Transcriptomic analysis of YS macrophage progenitors indicate that primitive macrophage progenitors present at embryonic day 9 are clearly distinct from those present at later stages. Disruption of Lyl-1 basic helix-loop-helix domain leads initially to an increased emergence of primitive macrophage progenitors, and later to their defective differentiation. These defects are associated with a disrupted expression of gene sets related to embryonic patterning and neurodevelopment. Lyl-1-deficiency also induce a reduced production of mature macrophages/microglia in the early brain, as well as a transient reduction of the microglia pool at midgestation and in the newborn. We thus identify Lyl-1 as a critical regulator of primitive macrophages and microglia development, which disruption may impair resident-macrophage function during organogenesis