How Do Shared Dockless E-Scooter Services Affect Mobility Practices in Paris? A Survey-Based Estimation of Modal Shift

Shared dockless e-scooters were first launched in Paris in the summer of 2018. These services were met with mixed reception: although some praised them for offering a new mobility solution to urban dwellers, others soon questioned their environmental impact. An emerging body of literature using lifecycle analysis shows that shared e-scooters are more pollutant than walking, cycling, and public transportation, but remain preferable to cars. To better grasp the impacts of dockless e-scooters, it is therefore necessary to identify which modes of transportation they replace. As mobility highly depends on local context, city-specific data are needed. Although modal change data from cities in North America and New Zealand are available, there is no similar information from dense European cities. Using quantitative survey data collected from shared e-scooter users in Paris, the present research offers novel data on modal shift toward dockless e-scooters in the French capital. Results show that for their last trip riding a shared e-scooter, most users would have walked or used public transportation had e-scooters not been an option, and only a limited share of them would have used a car. However, the overall impact of e-scooters on walking and public transportation use remains limited and they display a significant complementarity with public transportation. Such city-specific data on e-scooter use and impacts provide valuable inputs for local public authorities to implement efficient and tailored regulatory measures, so as to include these services in sustainable mobility policies

Ethanol induces oxidative stress in primary rat hepatocytes through the early involvement of lipid raft clustering.

International audienceThe role of the hepatocyte plasma membrane structure in the development of oxidative stress during alcoholic liver diseases is not yet fully understood. Previously, we have established the pivotal role of membrane fluidity in ethanol-induced oxidative stress, but no study has so far tested the involvement of lipid rafts. In this study, methyl-beta-cyclodextrin or cholesterol oxidase, which were found to disrupt lipid rafts in hepatocytes, inhibited both reactive oxygen species production and lipid peroxidation, and this suggested a role for these microstructures in oxidative stress. By immunostaining of lipid raft components, a raft clustering was detected in ethanol-treated hepatocytes. In addition, we found that rafts were modified by formation of malondialdehyde adducts and disulfide bridges. Interestingly, pretreatment of cells by 4-methyl-pyrazole (to inhibit ethanol metabolism) and various antioxidants prevented the ethanol-induced raft aggregation. In addition, treatment of hepatocytes by a stabilizing agent (ursodeoxycholic acid) or a fluidizing compound [2-(2-methoxyethoxy)ethyl 8-(cis-2-n-octylcyclopropyl)octanoate] led to inhibition or enhancement of raft clustering, respectively, which pointed to a relationship between membrane fluidity and lipid rafts during ethanol-induced oxidative stress. We finally investigated the involvement of phospholipase C in raft-induced oxidative stress upon ethanol exposure. Phospholipase C was shown to be translocated into rafts and to participate in oxidative stress by controlling hepatocyte iron content. Conclusion: Membrane structure, depicted as membrane fluidity and lipid rafts, plays a key role in ethanol-induced oxidative stress of the liver, and its modulation may be of therapeutic relevance