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The COVID-19 pandemic has brought a change of priorities, as states buy up masks and ventilators regardless of the cost. Basing economic decisions on human need, not our ability to pay, imposes a principle of equality — allowing us collectively to decide what kinds of production we really need.

_; This proposal adopts a holistic approach to strategic transport investment by discussing the wider economic impacts (WEIs) analysis method in terms of several dominant and emerging methods. The WEIs analysis goes beyond the effects captured in a standard cost-benefit analysis (CBA). A CBA addresses the market for transport services and infrastructure access but neglects the wider impacts on other markets. These wider impacts usually relate to agglomeration, market power, and the behavioral adaptions of firms and households. The high uncertainty in land use changes indicates that WEIs tend to occur in different forms on multiple spatial scales, varying by place and time. Additionally, some activities, such as education, have no direct market value, but may indirectly contribute to the overall economic output and human capital development in cities and regions. Given that the conventional elasticity methods are not goal oriented, it is important to ensure that the WEIs analysis accounts for the stakeholder-specific costs and benefits. Assuming that it is possible to consider all WEIs through theoretical models, major efforts should focus on establishing and maintaining appropriate methodologies and tools. The social and environmental data needed to address biodiversity issues should also be improved and promoted. Complementary to the WEIs, understanding how the behavior of agents changes in response to the new transport options will help clarify the long-term implications of transportation. This will suggest new strategies (territorial appropriation), approaches/ techniques to feasibility, and ?place-based? interrelations, that is, specific interrelations in places. This last aspect is especially important in the current context of the COVID-19 pandemic, which has affected and will likely change transportation behaviors and transport demand in the dynamic future.

International audience; By "We are at war." This was Emmanuel Macron's chosen refrain when he addressed the French nation about the current COVID-19 pandemic. He is certainly not the first to present human/pathogenic microbe relations in this way. Indeed, the history of immunology and epidemiology is littered with the vocabulary of war. But this presidential rhetoric reveals a certain communication strategy based on national unity, a hackneyed but nevertheless effective argument that is perfectly in keeping with a neoliberal ideology, a context in which the life of society is a constant struggle. Who is at war, and against what? For there to be a war, there needs to be an enemy. But while viruses can maintain close relations with humans, and under certain circumstances may even put their lives in danger, the definition of their intentions only commits those who claim to give it. It is important that the perspective of these humans never be reduced to a universal 'us', which would grant them permission to speak on behalf of others, whether that be entire countries, or the whole of humanity.

This text is a report about the "Sex Drugs and the City" Event. // Only the half of the “Sex, Drugs and the City” event could take place. Due to the COVID-19 pandemic, we had to cancel the participative discussion planned for the broader public in the evening. The academic afternoon took place on October 22, 2020, in Bordeaux under the title “Alcohol and drugs in affective or sexual relationships: transactions, consent, grey zones?” A video recording of the event is available in French via the Narcotic City webpage. “Alcohol and Drugs in Affective or Sexual Relationships: Transactions, Consent, Grey Zones?”

Le facteur Willebrand (FW) est une glycoprotéine plasmatique multimérisée, majoritairement d’origine endothéliale, qui au-delà de son rôle classique dans l’hémostase intervient dans l’angiogénèse et l’inflammation. La structure multimérique du FW lui confère une sensibilité élevée aux contraintes hydrodynamiques générées par certaines valvulopathies cardiaques ou dispositifs d’assistance circulatoire qu’ils soient transitoires comme l’ECMO ou prolongés comme les assistances mono-ventriculaires ou les cœurs artificiels. Dans ces circonstances, un excès de protéolyse des formes les plus multimérisées de VWF par l’ADAMTS13 est présent indépendamment de l’interaction entre le FW et son récepteur plaquettaire la GPIbα. Le FW pourrait ainsi constituer un biomarqueur sanguin d’intérêt dans l’évaluation des procédures de cardiologie interventionnelle TAVI sous réserve du développement d’un dispositif « point of care » permettant une évaluation rapide de son degré de multimérisation en salle de cathétérisme. La quantification de la protéolyse du FW fait désormais partie intégrante du benchmark des pompes d’assistances circulatoires et pourrait également constituer une approche d’intérêt pour améliorer la prédiction du risque hémorragique chez les patients implantés. L’inhibition partielle de la protéolyse FW par l’ADAMTS13 par un anticorps monoclonal humanisé dirigé contre le domaine D4 du FW constitue également une piste thérapeutique prometteuse pour la prévention des hémorragies sur angiodysplasies digestives observée aussi bien dans la maladie de Willebrand congénitale que sous assistance circulatoire. La pandémie COVID-19 en cours témoigne d’un rôle probablement sous-estimé du FW dans l’inflammation et l’immuno-thrombose. Nous travaux soulignent que le FW est non seulement un marqueur de sévérité de l’infection à COVID-19 mais pourrait également jouer un rôle direct dans la micro-angiopathie vasculaire impliquée dans la défaillance respiratoire et multi-viscérale. Von Willebrand factor (VWF) is a multimeric glycoprotein mainly synthesized in endothelial cells which beyond its traditional role in hemostasis is also involved in angiogenesis and inflammation. The multimeric structure of VWF confers him a high sensitivity to the abnormal hydrodynamic forces generated by some cardiac valvular diseases and most current circulatory assist devices including ECMO, ventricular assist devices and total artificial hearts. In these clinical conditions, an increased proteolysis of VWF high molecular weight multimers by ADAMTS13 occurs in blood independently from VWF interaction with platelet receptor GPIbα. As both VWF proteolysis induction and reversal are highly dynamics, VWF could be used as an interventional biomarker to assess the efficacy of TAVI procedures indicated for the treatment of severe aortic stenosis, pending the development of a point of care assay allowing a rapid assessment of VWF multimerization in the cathlab. Assessment of VWF proteolysis is now part of the benchmarking of new prototypes of circulatory assist devices and could potentially improve bleeding prediction in patients. A partial inhibition of VWF proteolysis by ADAMTS13 through a humanized monoclonal antibody targeting VWF D4 domain is also a promising therapeutic approach to prevent the occurrence of GI-bleeding from angiodysplasia in Von Willebrand disease and in patients supported with circulatory assist devices. VWF represents also a biomarker of COVID-19 severity. In the context of COVID pandemic, our recent works suggest a role of VWF as potential driver of COVID-19 microvascular thrombosis rather than a mere biomarker of the severity of endotheliopathy.