Social innovation as a way to reduce vulnerability to flash flood: How social innovation can be an innovative approach to prevent and to reduce flash flood risk in rural areas

International audienceFloods’ impacts nowadays cause important damages in more densified territories within interwoven networks. We highlight the relevance of a cross-disciplinary approach focused on interactions between humans and their environment at a local scale

Conquérir la Nature pour nourrir le Monde ? Une controverse géographique sur les usages de la technique en agriculture

National audienceRésumé disponible sur le lien suivant : http://www.groupe-dupont.org/ColloqueGeopoint/Geopoint14/Documents/GP14_PropositionsDebat_Web/GP14-A3-1-Gisclard-Benos.pd

Endothelial dysfunction and vascular disease

The endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO). The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDHF-mediated responses). Endothelium-dependent relaxations involve both pertussis toxin-sensitive G i (e.g. responses to serotonin and thrombin) and pertussis toxin-insensitive G q (e.g. adenosine diphosphate and bradykinin) coupling proteins. The release of NO by the endothelial cell can be up-regulated (e.g. by oestrogens, exercise and dietary factors) and down-regulated (e.g. oxidative stress, smoking and oxidized low-density lipoproteins). It is reduced in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively loose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and causing endothelium-dependent hyperpolarizations), endothelial cells also can evoke contraction (constriction) of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factor (EDCF). Most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells. EDCF-mediated responses are exacerbated when the production of NO is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive patients. © 2008 Scandinavian Physiological Society.postprin

Isoflavones and endothelial function

Dietary isoflavones are thought to be cardioprotective due to their structural similarity to oestrogen. Oestrogen is believed to have beneficial effects on endothelial function and may be one of the mechanisms by which premenopausal women are protected against CVD. Decreased NO production and endothelial NO synthase activity, and increased endothelin-1 concentrations, impaired lipoprotein metabolism and increased circulating inflammatory factors result from oestrogen deficiency. Oestrogen acts by binding to oestrogen receptors alpha and beta. Isoflavones have been shown to bind with greater affinity to the latter. Oestrogen replacement therapy is no longer thought to be a safe treatment for prevention of CVD; isoflavones are a possible alternative. Limited evidence from human intervention studies suggests that isoflavones may improve endothelial function, but the available data are not conclusive. Animal studies provide stronger support for a role of isoflavones in the vasculature, with increased vasodilation and endothelial NO synthase activity demonstrated. Cellular mechanisms underlying the effects of isoflavones on endothelial cell function are not yet clear. Possible oestrogen receptor-mediated pathways include modulation of gene transcription, and also non-genomic oestrogen receptor-mediated signalling pathways. Putative non-oestrogenic pathways include inhibition of reactive oxygen species production and up regulation of the protein kinase A pathway (increasing NO bioavailability). Further research is needed to unravel effects of isoflavones on intracellular regulation of the endothelial function. Moreover, there is an urgent need for adequately powered, robustly designed human intervention studies in order to clarify the present equivocal finding

Étude et mise en place d’un outil de suivi de la biodiversité rupestre sur la vallée du Célé (Lot)

Sur le territoire du Parc naturel régional des Causses du Quercy, des mesures pour la cohabitation entre pratique de l’escalade et biodiversité rupestre se sont traduites en 2010 par la signature d’une Charte des bonnes pratiques de l’escalade. Malheureusement, celle-ci semble aujourd’hui au point mort et des tensions sont apparues entre pratiquants et institutions de gestion du territoire. Ce stage veut poser les bases de la réouverture du dialogue par la mise en place d’un outil partagé de suivi de la biodiversité rupestre. L’outil de suivi se veut le plus précis possible afin de permettre l’auto-diagnostic des falaises par les grimpeurs. Il présente une localisation des espèces et équipements sur photographies intégrées dans un SIG. Partagé via une plateforme informatique, il est proposé d’instaurer des niveaux d’accès aux données sensibles. Une campagne d’entretiens avec les acteurs en lien avec le milieu rupestre a permis de mettre en lumière les représentations et connaissances des acteurs ainsi que d’identifier les attentes de chacun

Quelles contributions passées, actuelles et futures des savoirs spatiaux à citoyenneté et à l’élaboration des projets politiques

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