29 research outputs found

    Conflit taxis-­‐VTC: À quoi sert la loi ThĂ©venoud ?

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    International audienceContradicting the hopes raised by the thĂ©venoud commission report, the law of the same name is merely a new stone brought to the dike that protects the French taxis against their innovative competitorsContredisant les espoirs suscitĂ©s par le rapport de la commission de ThĂ©venoud, la loi du mĂȘme nom est simplement une nouvelle pierre apportĂ©e Ă  la digue qui protĂšge les taxis français contre leurs concurrents innovant

    Le rapport de la commission Thévenoud : une chance pour faire entrer les taxis dans la modernité

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    The ThĂ©venoud commission report could have given the French taxicabs the tools to strengthen their competitive advantage vis-a-vis the private hire vehicles.Dans les pays oĂč ils ne sont pas dĂ©rĂ©gulĂ©s, les taxis ont le monopole sur le marchĂ© des courses prises en station ou hĂ©lĂ©es dans la rue. En revanche, dans le marchĂ© des courses prĂ©-commandĂ©es, quand il ne leur est pas interdit comme Ă  New York, les taxis sont en concurrence avec les Ă©quivalents des VTC. En France, les taxis ont un Ă©norme avantage dans ce second marchĂ© : ils sont beaucoup plus nombreux que les VTC. Cette densitĂ© de l’offre couplĂ©e avec le droit exclusif d’utiliser les couloirs bus, leur permet d’arriver plus tĂŽt pour prendre la course et d’amener plus vite le client Ă  destination. Il leur revient d’exploiter au mieux cet avantage considĂ©rable, le rapport de la commission ThĂ©venoud leur en montre les moyens. Point n’est besoin d’ajouter des entraves Ă  l’activitĂ© des VTC

    Etude de la ventilation liquide totale hypothermisante sur le syndrome post-arrĂȘt cardiaque chez le lapin

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    Summary not transmittedChaque annĂ©e, l’arrĂȘt cardiaque extra-hospitalier, plus communĂ©ment appelĂ© mort subite, est responsable de plus de 40 000 dĂ©cĂšs en France. Le plus souvent, cela constitue l’ultime complication d’un infarctus du myocarde ou d’autres maladies cardiovasculaires. Le dĂ©veloppement des mĂ©thodes de rĂ©animation cardio-pulmonaire (RCP), leur diffusion publique et l’amĂ©lioration de la prise en charge prĂ©-hospitaliĂšre (« chaĂźne de survie ») ontpermis une forte augmentation du pourcentage de patients rĂ©animĂ©s aprĂšs un arrĂȘt cardiaque depuis une trentaine d’annĂ©es. Malheureusement, la reprise d’une activitĂ© circulatoire spontanĂ©e ne constitue que la premiĂšre Ă©tape de cette prise en charge et la majoritĂ© des patients dĂ©cĂšdent dans les jours suivants de dĂ©faillances multiviscĂ©rales regroupĂ©es sous le nom de « syndrome post-arrĂȘt cardiaque » 2. Seule une minoritĂ© de patients peut i fine survivire et sortirt de l’hĂŽpital aprĂšs une bonne rĂ©cupĂ©ration neurologique. Depuis de nombreuses annĂ©es, les chercheurs tentent donc de dĂ©couvrir des stratĂ©gies cardioprotectrices et neuroprotectrices dont l’application permettrait d’amĂ©liorer le pronostic de ces patients

    DEREGULATION OF URBAN TRANSPORT IN CHILE: WHAT HAVE WE LEARNED IN THE DECADE 1979-1989?

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    Urban bus operation in Chile is totally deregulated. This is the only example in the world where access to the urban bus transport market is totally free, and where the government does not exercise any control over the fares. This policy has been implemented progressively since 1979. Ten years later, it is possible to draw some conclusions from the experience. To summarize these conclusions, one could say that (i) the impact of deregulation has been almost exactly the opposite of what was expected: fares have risen and the diversity of services has been reduced, (ii) the reasons for this discrepancy lie less in the action of a cartel than in the specifics of urban transport supply and (iii) there is probably more to be expected from a refined deregulation policy, taking into account these specifics, than from a drive back to the traditional regulation system

    [Study of the total liquid ventilation hypothermisante on the syndrome cardiac post-cardiac arrest to the rabbit]

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    Chaque annĂ©e, l’arrĂȘt cardiaque extra-hospitalier, plus communĂ©ment appelĂ© mort subite, est responsable de plus de 40 000 dĂ©cĂšs en France. Le plus souvent, cela constitue l’ultime complication d’un infarctus du myocarde ou d’autres maladies cardiovasculaires. Le dĂ©veloppement des mĂ©thodes de rĂ©animation cardio-pulmonaire (RCP), leur diffusion publique et l’amĂ©lioration de la prise en charge prĂ©-hospitaliĂšre (« chaĂźne de survie ») ontpermis une forte augmentation du pourcentage de patients rĂ©animĂ©s aprĂšs un arrĂȘt cardiaque depuis une trentaine d’annĂ©es. Malheureusement, la reprise d’une activitĂ© circulatoire spontanĂ©e ne constitue que la premiĂšre Ă©tape de cette prise en charge et la majoritĂ© des patients dĂ©cĂšdent dans les jours suivants de dĂ©faillances multiviscĂ©rales regroupĂ©es sous le nom de « syndrome post-arrĂȘt cardiaque » 2. Seule une minoritĂ© de patients peut i fine survivire et sortirt de l’hĂŽpital aprĂšs une bonne rĂ©cupĂ©ration neurologique. Depuis de nombreuses annĂ©es, les chercheurs tentent donc de dĂ©couvrir des stratĂ©gies cardioprotectrices et neuroprotectrices dont l’application permettrait d’amĂ©liorer le pronostic de ces patients.Summary not transmitte

    Mild hypothermia reduces per-ischemic reactive oxygen species production and preserves mitochondrial respiratory complexes.: Mild hypothermia, cardioprotection and mitochondria

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    International audienceBACKGROUND: Mitochondrial dysfunction is critical following ischemic disorders. Our goal was to determine whether mild hypothermia could limit this dysfunction through per-ischemic inhibition of reactive oxygen species (ROS) generation. METHODS: First, ROS production was evaluated during simulated ischemia in an vitro model of isolated rat cardiomyocytes at hypothermic (32°C) vs. normothermic (38°C) temperatures. Second, we deciphered the direct effect of hypothermia on mitochondrial respiration and ROS production in oxygenated mitochondria isolated from rabbit hearts. Third, we investigated these parameters in cardiac mitochondria extracted after 30-min of coronary artery occlusion (CAO) under normothermic conditions (CAO-N) or with hypothermia induced by liquid ventilation (CAO-H; target temperature: 32°C). RESULTS: In isolated rat cardiomyocytes, per-ischemic ROS generation was dramatically decreased at 32 vs. 38°C (e.g., -55±8% after 140min of hypoxia). In oxygenated mitochondria isolated from intact rabbit hearts, hypothermia also improved respiratory control ratio (+22±3%) and reduced H2O2 production (-41±1%). Decreased oxidative stress was further observed in rabbit hearts submitted to hypothermic vs. normothermic ischemia (CAO-H vs. CAO-N), using thiobarbituric acid-reactive substances as a marker. This was accompanied by a preservation of the respiratory control ratio as well as the activity of complexes I, II and III in cardiac mitochondria. CONCLUSION: The cardioprotective effect of mild hypothermia involves a direct effect on per-ischemic ROS generation and results in preservation of mitochondrial function. This might explain why the benefit afforded by hypothermia during regional myocardial ischemia depends on how fast it is instituted during the ischemic process

    Comparative effect of hypothermia and adrenaline during cardiopulmonary resuscitation in rabbits.: Intra-arrest hypothermia and cold saline infusion

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    International audienceBACKGROUND: Therapeutic hypothermia was shown to facilitate resumption of spontaneous circulation when instituted during cardiac arrest. Here, we investigated whether it directly improved the chance of successful resuscitation independently of adrenaline administration in rabbits. We further evaluated the direct effect of hypothermia on vascular function in vitro. METHODS: In a first set of experiments, four groups of anesthetized rabbits were submitted to 15 min of cardiac arrest and subsequent cardiopulmonary resuscitation (CPR). The "control" group underwent CPR with only cardiac massage and defibrillation attempts. Two other groups received cold or normothermic saline infusion during CPR (20 mL/kg of NaCl 0.9% at 4°C or 38°C, respectively). In a last group, the animals received adrenaline (15 ”g/kg intravenously) during CPR. In a second set of experiments, we evaluated at 32°C vs. 38°C the vascular function of aortic rings withdrawn from healthy rabbits or after cardiac arrest. RESULTS: In the first set of experiments, cardiac massage efficiency was improved by adrenaline but neither by hypothermic nor normothermic saline administration. Resumption of spontaneous circulation was observed in five of eight animals after adrenaline as compared with none of eight in other groups. Defibrillation rates were conversely similar among groups (7/8 or 8/8). In the second set of experiments, in vitro hypothermia (32°C) was not able to prevent the dramatic alteration of vascular function observed after cardiac arrest. It also did not directly modify vasocontractile or the vasodilating functions in healthy conditions. CONCLUSION: In rabbits, hypothermia did not exert a direct hemodynamic or vascular effect that might explain its beneficial effect during CPR
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