Modelling public risk evaluation of natural hazards: a conceptual approach

International audienceIn recent years, the dealing with natural hazards in Switzerland has shifted away from being hazard-oriented towards a risk-based approach. Decreasing societal acceptance of risk, accompanied by increasing marginal costs of protective measures and decreasing financial resources cause an optimization problem. Therefore, the new focus lies on the mitigation of the hazard's risk in accordance with economical, ecological and social considerations. This modern proceeding requires an approach in which not only technological, engineering or scientific aspects of the definition of the hazard or the computation of the risk are considered, but also the public concerns about the acceptance of these risks. These aspects of a modern risk approach enable a comprehensive assessment of the (risk) situation and, thus, sound risk management decisions. In Switzerland, however, the competent authorities suffer from a lack of decision criteria, as they don't know what risk level the public is willing to accept. Consequently, there exists a need for the authorities to know what the society thinks about risks. A formalized model that allows at least a crude simulation of the public risk evaluation could therefore be a useful tool to support effective and efficient risk mitigation measures. This paper presents a conceptual approach of such an evaluation model using perception affecting factors PAF, evaluation criteria EC and several factors without any immediate relation to the risk itself, but to the evaluating person. Finally, the decision about the acceptance Acc of a certain risk i is made by a comparison of the perceived risk Ri,perc with the acceptable risk Ri,acc

Reggies/flotillins regulate E-cadherin-mediated cell contact formation by affecting EGFR trafficking.

The reggie/flotillin proteins are implicated in membrane trafficking and, together with the cellular prion protein (PrP), in the recruitment of E-cadherin to cell contact sites. Here, we demonstrate that reggies, as well as PrP down-regulation, in epithelial A431 cells cause overlapping processes and abnormal formation of adherens junctions (AJs). This defect in cell adhesion results from reggie effects on Src tyrosine kinases and epidermal growth factor receptor (EGFR): loss of reggies reduces Src activation and EGFR phosphorylation at residues targeted by Src and c-cbl and leads to increased surface exposure of EGFR by blocking its internalization. The prolonged EGFR signaling at the plasma membrane enhances cell motility and macropinocytosis, by which junction-associated E-cadherin is internalized and recycled back to AJs. Accordingly, blockage of EGFR signaling or macropinocytosis in reggie-deficient cells restores normal AJ formation. Thus, by promoting EGFR internalization, reggies restrict the EGFR signaling involved in E-cadherin macropinocytosis and recycling and regulate AJ formation and dynamics and thereby cell adhesion