Accompagnement virtuel personnalisé: motivation et réussite scolaire

Titre de l'écran-titre (visionné le 21 juin 2007)Également disponible en format papierMédiagraphi

Accompagnement virtuel personnalisé motivation et réussite scolaire : rapport de recherche PREP /

Titre de l'écran-titre (visionné le 21 juin 2007)Également disponible en format papierMédiagraphi

PI3K-Dependent GSK3？(Ser9)-Phosphorylation Is Implicated in the Intestinal Epithelial Cell Wound-Healing Response

Introduction The ability of the intestinal epithelial barrier to respond to various injurious insults is an essential component of intestinal homeostasis. However, the molecular mechanisms responsible for wound-healing and repair in the intestine are poorly understood. The glycogen synthase kinase 3？ (GSK3？) has been implicated in various biological processes such as cellular motility, cell spreading and recently inflammation. Aim To investigate the role of GSK3？ in intestinal epithelial cell restitution. Methods Rat intestinal epithelial IEC18 cells were serum-starved for 16 to 24h and wounded by multiple scraping. Akt(Ser473)-, GSK3？(Ser9)- and RelA(Ser536)-phosphorylation were determined by Western blot using specific phospho-antibodies. The inhibitors AG1478 (1 μM) and Ly294002 (25 μM) were used to block EGF-R autophosphorylation and PI3K-activation, respectively. ？-catenin/LEF/TCF dependent transcription was determined by reporter gene assay (TOP/FOP system). C-myc gene expression was evaluated by real-time RT-PCR. GSK3？？/？ mouse embryonic fibroblasts were used to characterize the role of GSK3？ in wounding-induced cell migration. Results Wounding induced GSK3？(Ser9) phosphorylation in IEC-18 cells, which led to ？-catenin accumulation as well as nuclear translocation of ？-catenin. ？-catenin stabilization/nuclear translocation led to enhanced LEF-TCF transcriptional activity and subsequent c-myc mRNA accumulation in wounded cell monolayers. Blocking PI3K/Akt signaling with Ly294002 prevented wound-induced GSK3？(Ser9) phosphorylation as well as ？-catenin nuclear translocation and significantly attenuated restitution. Additionally, wounding induced rapid NF-kB(Ser536) phosphorylation, which was inhibited by AG1478, but not by Ly294002. GSK3？？/？ cells demonstrated significantly attenuated wound-induced restitution compared to wild-type cells. Conclusion We conclude that PI3K-mediated GSK3？ phosphorylation is involved in the intestinal epithelial wound-healing response. Phosphorylation of GSK3？ may be important for intestinal restitution by promoting cell motility in response to wounding

Interval dosing with the HDAC inhibitor vorinostat effectively reverses HIV latency

BACKGROUND. The histone deacetylase (HDAC) inhibitor vorinostat (VOR) can increase HIV RNA expression in vivo within resting CD4+ T cells of aviremic HIV+ individuals. However, while studies of VOR or other HDAC inhibitors have reported reversal of latency, none has demonstrated clearance of latent infection. We sought to identify the optimal dosing of VOR for effective serial reversal of HIV latency

Gnotobiotic IL-10−/−; NF-κBEGFP Mice Develop Rapid and Severe Colitis Following Campylobacter jejuni Infection

Limited information is available on the molecular mechanisms associated with Campylobacter jejuni (C. jejuni) induced food-borne diarrheal illnesses. In this study, we investigated the function of TLR/NF-κB signaling in C. jejuni induced pathogenesis using gnotobiotic IL-10−/−; NF-κBEGFP mice. In vitro analysis showed that C. jejuni induced IκB phosphorylation, followed by enhanced NF-κB transcriptional activity and increased IL-6, MIP-2α and NOD2 mRNA accumulation in infected-mouse colonic epithelial cells CMT93. Importantly, these events were blocked by molecular delivery of an IκB inhibitor (Ad5IκBAA). NF-κB signalling was also important for C.jejuni-induced cytokine gene expression in bone marrow-derived dendritic cells. Importantly, C. jejuni associated IL-10−/−; NF-κBEGFP mice developed mild (day 5) and severe (day 14) ulcerating colonic inflammation and bloody diarrhea as assessed by colonoscopy and histological analysis. Macroscopic analysis showed elevated EGFP expression indicating NF-κB activation throughout the colon of C. jejuni associated IL-10−/−; NF-κBEGFP mice, while fluorescence microscopy revealed EGFP positive cells to be exclusively located in lamina propria mononuclear cells. Pharmacological NF-κB inhibition using Bay 11-7085 did not ameliorate C. jejuni induced colonic inflammation. Our findings indicate that C. jejuni induces rapid and severe intestinal inflammation in a susceptible host that correlates with enhanced NF-κB activity from lamina propria immune cells

FlowVR (calculs interactifs et visualisation sur grappe)

Cette thèse combine le calcul haute performance à la réalité virtuelle pour permettre la conception de méthodes de couplage de composants parallèles à l'intérieur d'applications distribuées et interactives. Un nouveau modèle de couplage est présenté, conçu selon des critères de modularité, simplicité, efficacité et extensibilité. La construction des applications repose sur une séparation entre la programmation de modules parallèles réutilisables et la définition de l'application sous forme de graphe de flux de données contenant des mécanismes de filtrage et de synchronisations, permettant d'exprimer des schémas de communication collective et des politiques de couplage avancées. Ce travail sur le couplage interactif est complété par une extension haut niveau concernant le rendu distribué. En exploitant une description modulaire de la scène 3D en primitives indépendantes basées sur l'utilisation de shaders, des réseaux de filtrage permettent de combiner plusieurs flux pour acheminer efficacement les informations aux machines de rendu. Ce système est très extensible et permet la création de nouvelles applications exploitant la puissance des cartes graphiques pour décharger certains calculs des processeurs et réduire les transferts réseau. De nombreuses applications nouvelles sont ainsi développées, combinant des algorithmes de vision parallélisés immergeant l'utilisateur dans l'environnement virtuel, et des interactions avec des objets contrôlés par des simulations physiques distribuées (poterie, collisions, fluides).GRENOBLE1-BU Sciences (384212103) / SudocSudocFranceF