20 research outputs found
Lâappropriation du changement de politiques universitaires par les Ă©tudiants en Afrique subsaharienne : le cas de la rĂ©forme Licence-Master-Doctorat au Burkina Faso
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 âBachelor-Master-Doctorate (BMD) reform.â 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 dâAfrique subsaharienne francophone ont dĂ» sâadapter Ă un environnement marquĂ© par lâinternationalisation de lâenseignement supĂ©rieur et les transferts des politiques Ă©ducatives en sâalignant sur le processus de Bologne par une nouvelle politique dite « rĂ©forme Licence-Master-Doctorat (LMD) ». Cette Ă©tude a pour objectif dâanalyser et de comprendre lâappropriation de la rĂ©forme LMD par les Ă©tudiants au Burkina Faso. Ă partir dâune dĂ©finition de lâappropriation cohĂ©rente avec la sociologie de lâaction 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 lâappropriation chez les Ă©tudiants sont reliĂ©s Ă leurs caractĂ©ristiques sociodĂ©mographiques
Transcriptomic Analysis of Murine Embryos Lacking Endogenous Retinoic Acid Signaling
<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>â/â</sup>) embryos â unable to synthesize RA from maternally-derived retinol â 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.
<p>Eight clusters (panels BâI) 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>â/â</sup> embryos). Gene expression profiles are illustrated as a heat map (green: weak expression; red: strong expression â 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>â/â</sup> transcriptome.
<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>â/â</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
Volcano plots representing corrected p-values (ordinates, âlog10 scale) from Student t-test of the mRNA levels compared in wild-type and <i>Raldh2</i><sup>â/â</sup> samples anterior (A) and posterior (B) embryonic tissue samples.
<p>Genes with a fold change (abscissae) higher than 1.5 and a false discovery rate lower than 0.1 are shown in red.</p
VENN diagrams summarizing a cross-comparison of the genes downregulated in <i>Raldh2</i><sup>â/â</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.
<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
Genes acting in selected signaling pathways and misregulated in <i>Raldh2</i><sup>â/â</sup> tissue samples (ANT: anterior samples; POST: posterior samples).
<p>Key: <b>Bold</b> indicates a fold change exceeding ±1.5.</p><p><i>Italics</i> indicate a p-value >0.05 (ANT) or >0.03 (POST).</p
Overview of the main biological and physiological functions correlating with the affected genes in <b><i>Raldh2</i></b><b><sup>â/â</sup> embryos.</b>
<p>The functions are listed by decreasing order of statistical significance [âlog(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