Environmental Triggering of Type 1 Diabetes Autoimmunity

Type 1 diabetes (T1D) is a chronic autoimmune disease in which pancreatic islet β cells are destroyed by immune cells, ultimately leading to overt diabetes. The progressive increase in T1D incidence over the years points to the role of environmental factors in triggering or accelerating the disease process which develops on a highly multigenic susceptibility background. Evidence that environmental factors induce T1D has mostly been obtained in animal models. In the human, associations between viruses, dietary habits or changes in the microbiota and the development of islet cell autoantibodies or overt diabetes have been reported. So far, prediction of T1D development is mostly based on autoantibody detection. Future work should focus on identifying a causality between the different environmental risk factors and T1D development to improve prediction scores. This should allow developing preventive strategies to limit the T1D burden in the future

Escherichia coli α-Hemolysin Counteracts the Anti-Virulence Innate Immune Response Triggered by the Rho GTPase Activating Toxin CNF1 during Bacteremia

International audienceThe detection of the activities of pathogen-encoded virulence factors by the innate immune system has emerged as a new paradigm of pathogen recognition. Much remains to be determined with regard to the molecular and cellular components contributing to this defense mechanism in mammals and importance during infection. Here, we reveal the central role of the IL-1 beta signaling axis and Gr1+ cells in controlling the Escherichia coli burden in the blood in response to the sensing of the Rho GTPase-activating toxin CNF1. Consistently, this innate immune response is abrogated in caspase-1/11-impaired mice or following the treatment of infected mice with an IL-1 beta antagonist. In vitro experiments further revealed the synergistic effects of CNF1 and LPS in promoting the maturation/secretion of IL-1 beta and establishing the roles of Rac, ASC and caspase-1 in this pathway. Furthermore, we found that the Phi-hemolysin toxin inhibits IL-1 beta secretion without affecting the recruitment of Gr1+ cells. Here, we report the first example of anti-virulence-triggered immunity counteracted by a pore-forming toxin during bacteremia

Death receptor pathways mediate targeted and non-targeted effects of ionizing radiations in breast cancer cells

Delayed cell death by mitotic catastrophe is a frequent mode of solid tumor cell death after γ-irradiation, a widely used treatment of cancer. Whereas the mechanisms that underlie the early γ-irradiation-induced cell death are well documented, those that drive the delayed cell death are largely unknown. Here we show that the Fas, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and tumor necrosis factor (TNF)-α death receptor pathways mediate the delayed cell death observed after γ-irradiation of breast cancer cells. Early after irradiation, we observe the increased expression of Fas, TRAIL-R and TNF-R that first sensitizes cells to apoptosis. Later, the increased expression of FasL, TRAIL and TNF-α permit the apoptosis engagement linked to mitotic catastrophe. Treatments with TNF-α, TRAIL or anti-Fas antibody, early after radiation exposure, induce apoptosis, whereas the neutralization of the three death receptors pathways impairs the delayed cell death. We also show for the first time that irradiated breast cancer cells excrete soluble forms of the three ligands that can induce the death of sensitive bystander cells. Overall, these results define the molecular basis of the delayed cell death of irradiated cancer cells and identify the death receptors pathways as crucial actors in apoptosis induced by targeted as well as non-targeted effects of ionizing radiation

Leading ladies: discursive constructions of women leaders in the UK media

Women continue to be economically disadvantaged and under-represented in positions of power and leadership. A discursive disjunction between cultural and media representations of women and leadership has been implicated in these continuing inequalities. We address this issue through an analysis of the ways in which prominent women leaders were portrayed in a UK radio series, BBC Radio 4’s “Profile” broadcast between July 2011 and July 2013. Verbatim transcripts of 12 broadcasts featuring women were analysed within a critical feminist framework, to explore the ways in which these women leaders were discursively constructed. Our analysis explicates three constructions of “women leaders”: as “traditionally” feminine; as having to balance “masculine” and “feminine” attributes; and as exceptional women who may nevertheless fail. We conclude that the impact of equality legislation continues to be limited while androcentric norms prevail and that we therefore need more gynocentric ways of imagining women leaders

LA PRESCRIPTION MEDICAMENTEUSE A LA MAISON D'ACCUEIL POUR LES PERSONNES AGEES (MAPA) DE LONGUEAU (ETUDE DE QUELQUES CLASSES MEDICAMENTEUSES ET CONSEILS HYGIENO-DIETETIQUES AFIN D'OPTIMISER LA THERAPEUTIQUE)

AMIENS-BU Santé (800212102) / SudocSudocFranceF

Éditer Montaigne | Avancement & poursuites

L’année 2016 aura été largement consacrée à Montaigne. Après la clôture de l’ANR MONLOE (MONtaigne à l’Œuvre) en janvier 2016, l’édition et la mise en ligne du corpus numérique Montaigne se sont poursuivies grâce au projet CORPOREM, financé par BSN5 (la Bibliothèque Scientifique Numérique), consacré à la constitution des deux corpus d’auteurs qui nous sont particulièrement chers : Rabelais et Montaigne ; d’autant que le Livre III des "Essais" est au programme de l’agrégation de lettres en 2017