20 research outputs found

    L’appropriation du changement de politiques universitaires par les Ă©tudiants en Afrique subsaharienne : le cas de la rĂ©forme Licence-Master-Doctorat au Burkina Faso

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    Faced with the imperative to adapt to an environment marked by the internationalization of higher education and education policy transfers, universities in French-speaking sub-Saharan African countries adopted in 2006 a new policy called “Bachelor-Master-Doctorate (BMD) reform.” Given the importance of the role of the actors in the implementation of a public policy, this study was designed to analyse the appropriation of the BMD reform by students in Burkina Faso. Based on a definition of appropriation consistent with the sociology of public action, we examine how students interpret the BMD reform and their attitude and behaviour towards it. Data gathering involved a survey questionnaire administered to 531 students. The findings show that students have limited knowledge of the reform, and moderate adherence and low commitment to its implementation.Les universitĂ©s d’Afrique subsaharienne francophone ont dĂ» s’adapter Ă  un environnement marquĂ© par l’internationalisation de l’enseignement supĂ©rieur et les transferts des politiques Ă©ducatives en s’alignant sur le processus de Bologne par une nouvelle politique dite « rĂ©forme Licence-Master-Doctorat (LMD) ». Cette Ă©tude a pour objectif d’analyser et de comprendre l’appropriation de la rĂ©forme LMD par les Ă©tudiants au Burkina Faso. À partir d’une dĂ©finition de l’appropriation cohĂ©rente avec la sociologie de l’action publique et de donnĂ©es recueillies par questionnaire auprĂšs de 531 Ă©tudiants, nous examinons la maniĂšre dont les Ă©tudiants interprĂštent la rĂ©forme LMD, leur attitude et leur comportement Ă  son Ă©gard. Les rĂ©sultats montrent que les Ă©tudiants ont une connaissance limitĂ©e de la rĂ©forme, une adhĂ©sion modĂ©rĂ©e et un engagement faible pour son implantation. En outre, les indices de l’appropriation chez les Ă©tudiants sont reliĂ©s Ă  leurs caractĂ©ristiques sociodĂ©mographiques

    Transcriptomic Analysis of Murine Embryos Lacking Endogenous Retinoic Acid Signaling

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    <div><p></p><p>Retinoic acid (RA), an active derivative of the liposoluble vitamin A (retinol), acts as an important signaling molecule during embryonic development, regulating phenomenons as diverse as anterior-posterior axial patterning, forebrain and optic vesicle development, specification of hindbrain rhombomeres, pharyngeal arches and second heart field, somitogenesis, and differentiation of spinal cord neurons. This small molecule directly triggers gene activation by binding to nuclear receptors (RARs), switching them from potential repressors to transcriptional activators. The repertoire of RA-regulated genes in embryonic tissues is poorly characterized. We performed a comparative analysis of the transcriptomes of murine wild-type and <i>Retinaldehyde Dehydrogenase 2</i> null-mutant (<i>Raldh2</i><sup>−/−</sup>) embryos — unable to synthesize RA from maternally-derived retinol — using Affymetrix DNA microarrays. Transcriptomic changes were analyzed in two embryonic regions: anterior tissues including forebrain and optic vesicle, and posterior (trunk) tissues, at early stages preceding the appearance of overt phenotypic abnormalities. Several genes expected to be downregulated under RA deficiency appeared in the transcriptome data (e.g. <i>Emx2</i>, <i>Foxg1</i> anteriorly, <i>Cdx1</i>, <i>Hoxa1</i>, <i>Rarb</i> posteriorly), whereas reverse-transcriptase-PCR and in situ hybridization performed for additional selected genes validated the changes identified through microarray analysis. Altogether, the affected genes belonged to numerous molecular pathways and cellular/organismal functions, demonstrating the pleiotropic nature of RA-dependent events. In both tissue samples, genes upregulated were more numerous than those downregulated, probably due to feedback regulatory loops. Bioinformatic analyses highlighted groups (clusters) of genes displaying similar behaviors in mutant tissues, and biological functions most significantly affected (e.g. mTOR, VEGF, ILK signaling in forebrain tissues; pyrimidine and purine metabolism, calcium signaling, one carbon metabolism in posterior tissues). Overall, these data give an overview of the gene expression changes resulting from embryonic RA deficiency, and provide new candidate genes and pathways that may help understanding retinoid-dependent molecular events.</p></div

    Details of the gene expression profiles obtained after hierarchical clustering of the experimental samples by relative gene expression level analysis.

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    <p>Eight clusters (panels B–I) have been extracted from the overall clustering analysis (available as additional online information, Figure S1), showing differential gene expression behaviors according to the experimental samples (ANT, RNA from anterior tissues; POST, RNA from posterior tissues; WT, wild-type embryos; KO, <i>Raldh2</i><sup>−/−</sup> embryos). Gene expression profiles are illustrated as a heat map (green: weak expression; red: strong expression – see scale below). The expression profile of the <i>Rarb</i> gene is also shown (panel J), which did not cluster with any other gene. This analysis further validated the experimental samples, as WT and KO samples segregated into fully distinct clusters, both for the ANT and POST tissue samples (panel A above).</p

    Summary diagram of the major molecular pathways emerging from Ingenuity analysis of the <i>Raldh2</i><sup>−/−</sup> transcriptome.

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    <p>The molecular pathways are listed by decreasing order of statistical significance as they appear through analysis of the ANTERIOR (left-side list) and POSTERIOR (right-side list) data sets. The most significant pathways identified for each data set are highlighted in gray. Additional pathways relevant for developmental processes are also listed. A graphic representation of the numbers of genes downregulated (green) or upregulated (red) in anterior (upper bars) or posterior (lower bars) <i>Raldh2</i><sup>−/−</sup> embryonic tissue samples (fold change ±1.2, filtered for FDR <10%) is shown. The total number of genes comprising each pathway (middle line, gray shaded), and the percentages of genes misregulated in each experiment, are also given.</p

    VENN diagrams summarizing a cross-comparison of the genes downregulated in <i>Raldh2</i><sup>−/−</sup> embryos (A, anterior tissues; B, posterior tissues) with those identified as RAR-bound by ChIP-seq analysis of embryonic stem (ES) cells differentiating as embryoid bodies (ref.

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    <p><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0062274#pone.0062274-Moutier1" target="_blank">[<b>72</b>]</a><b>), and those induced after RA treatment of embryoid bodies.</b> This analysis distinguished early RA-responsive genes (2 h after RA exposure: upper numbers; ref. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0062274#pone.0062274-Moutier1" target="_blank">[72]</a>), from those identified at a later stage of differentiation (4 days post-RA treatment: lower numbers; ref. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0062274#pone.0062274-Kim1" target="_blank">[73]</a>). Some selected genes are highlighted in the intersecting data sets.</p

    Overview of the main biological and physiological functions correlating with the affected genes in <b><i>Raldh2</i></b><b><sup>−/−</sup> embryos.</b>

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    <p>The functions are listed by decreasing order of statistical significance [−log(p-values)] of differentially expressed and misregulated genes as calculated by the Ingenuity software. Left side (black bars): ANT microarray data; right side (gray bars): POST microarray data.</p
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