Unified traction and battery charging systems for electric vehicles: a sustainability perspective

This paper presents an analysis of unified traction and battery charging systems for electric vehicles (EVs), both in terms of operation modes and in terms of implementation cost, when compared to dedicated solutions that perform the same operation modes. Regarding the connection of the EV battery charging system with the power grid, four operation modes are analyzed: (1) Grid–to–Vehicle (G2V); (2) Vehicle–to–Grid (V2G); (3) Vehicle–to–Home (V2H); and (4) Vehicle–for–Grid (V4G). With an EV unified system, each of these operation modes can be used in single–phase and three–phase power grids. Furthermore, a cost estimation is performed for an EV unified system and for dedicated systems that can perform the same functionalities, in order to prove the benefits of the EV unified approach. The cost estimation comprises two power levels, namely 6 kW, single–phase, related to domestic installations, and 50 kW, three–phase, related to industrial installations. The relevance of unified traction and battery charging systems for EVs is proven for single–phase and three–phase power grids.This work has been supported by FCT – Fundação para a Ciência e Tecnologia within the Project Scope: UID/CEC/00319/2019. This work has been supported by the FCT Project DAIPESEV PTDC/EEI-EEE/30382/2017, and by the FCT Project new ERA4GRIDs PTDC/EEI-EEE/30283/2017

p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours.

p73 (ref. 1) has high homology with the tumour suppressor p53 (refs 2-4), as well as with p63, a gene implicated in the maintenance of epithelial stem cells. Despite the localization of the p73 gene to chromosome 1p36.3 a region of frequent aberration in a wide range of human cancers, and the ability of p73 to transactivate p53 target genes, it is unclear whether p73 functions as a tumour suppressor. Here we show that mice functionally deficient for all p73 isoforms exhibit profound defects, including hippocampal dysgenesis, hydrocephalus, chronic infections and inflammation, as well as abnormalities in pheromone sensory pathways. In contrast to p53-deficient mice, however, those lacking p73 show no increased susceptibility to spontaneous tumorigenesis. We report the mechanistic basis of the hippocampal dysgenesis and the loss of pheromone responses, and show that new, potentially dominant-negative, p73 variants are the predominant expression products of this gene in developing and adult tissues. Our data suggest that there is a marked divergence in the physiological functions of the p53 family members, and reveal unique roles for p73 in neurogenesis, sensory pathways and homeostatic control