Structure de bandes expérimentale de TaS2-1 T déterminée par photoémission angulaire

Valence energy bands of 1 T-TaS2 were experimentally determined, at room temperature, along the ΓKMK line in the Brillouin zone using 40 eV photons. The dz2 band is found to be below the Fermi level and this result is explained by the effect of charge density waves.La structure de bandes de valence de TaS2-1 T a été déterminée expérimentalement, à la température ambiante, le long de la ligne ΓKMK de la zone de Brillouin à l'aide de photons de 40 eV. On trouve que la bande dz2 est au-dessous du niveau de Fermi et on explique ce résultat par l'effet d'ondes de densité de charge

REGULATION DE L'EXPRESSION DU PROTO-ONCOGENE C-FOS PAR L'HORMONE SOMATOTROPE AU COURS DE LA DIFFERENCIATION DES PREADIPOCYTES EN CULTURE

International audienc

BK/TD models for analyzing in vitro impedance data on cytotoxicity.

International audienceThe ban of animal testing has enhanced the development of new in vitro technologies for cosmetics safety assessment. Impedance metrics is one such technology which enables monitoring of cell viability in real time. However, analyzing real time data requires moving from static to dynamic toxicity assessment. In the present study, we built mechanistic biokinetic/toxicodynamic (BK/TD) models to analyze the time course of cell viability in cytotoxicity assay using impedance. These models account for the fate of the tested compounds during the assay. BK/TD models were applied to analyze HepaRG cell viability, after single (48h) and repeated (4 weeks) exposures to three hepatotoxic compounds (coumarin, isoeugenol and benzophenone-2). The BK/TD models properly fit the data used for their calibration that was obtained for single or repeated exposure. Only for one out of the three compounds, the models calibrated with a single exposure were able to predict repeated exposure data. We therefore recommend the use of long-term exposure in vitro data in order to adequately account for chronic hepatotoxic effects. The models we propose here are capable of being coupled with human biokinetic models in order to relate dose exposure and human hepatotoxicity

Transcriptome signature of irreversible senescence in human papillomavirus-positive cervical cancer cells

A frequent characteristic of human papillomavirus (HPV)-positive cervical cancers is the loss of viral E2 gene expression in HPV-infected cervical epithelial cells as a consequence of viral DNA integration into the cellular genome. The expression of E2 in HPV-positive cancer cells results in the repression of the viral E6/E7 oncogenes, activation of the p53 and pRB pathways, and a G(1) cell cycle arrest, followed by induction of cellular senescence. The transcriptional consequences of E2-mediated cell cycle arrest that lead to senescence currently are unknown. Using conditional senescence induction in HeLa cells and microarray analysis, we describe here the expression profile of cells irreversibly committed to senescence. Our results provide insight into the molecular anatomy of senescence pathways and its regulation by HPV on-coproteins. These include the induction of the RAB vesicular transport machinery and a general down-regulation of chromatin regulatory molecules. The repression of tumor-specific G antigens during E2 senescence supports a reversal of the tumorigenic phenotype by E2 and the potential approach of tumor-specific G antigen-specific immunotherapy for cervical cancer