Vehicle electrification presents a great opportunity to reduce transportation greenhouse gas emissions. The greater use of plug-in electric vehicles (PEVs), however, puts stress on local distribution networks. This paper presents an optimal PEV charging control method integrated with utility demand response (DR) signals to mitigate the impact of PEV charging to several aspects of a grid, including load surge, distribution accumulative voltage deviation, and transformer aging. To build a realistic PEV charging load model, the results of National Household Travel Survey (NHTS) have been analyzed and a stochastic PEV charging model has been defined based on survey results. The residential distribution grid contains 120 houses and is modeled in GridLAB-D. Co-simulation is performed using Matlab and GridLAB-D to enable the optimal control algorithm in Matlab to control PEV charging loads in the residential grid modeled in GridLAB-D. Simulation results demonstrate the effectiveness of the proposed optimal charging control method in mitigating the negative impacts of PEV charging on the residential grid.
Inflammatory bowel disease (IBD) is an incurable disease of the gastrointestinal tract with a lack of effective therapeutic strategies. The proinflammatory microenvironment plays a significant role in both amplifying and sustaining inflammation during IBD progression. Herein, biocompatible drug-free ceria nanoparticles (CeNP-PEG) with regenerable scavenging activities against multiple reactive oxygen species (ROS) were developed. CeNP-PEG exerted therapeutic effect in dextran sulfate sodium (DSS)-induced colitis murine model, evidenced by corrected the disease activity index, restrained colon length shortening, improved intestinal permeability and restored the colonic epithelium disruption. CeNP-PEG ameliorated the proinflammatory microenvironment by persistently scavenging ROS, down-regulating the levels of multiple proinflammatory cytokines, restraining the proinflammatory profile of macrophages and Th1/Th17 response. The underlying mechanism may involve restraining the co-activation of NF-κB and JAK2/STAT3 pathways. In summary, this work demonstrates an effective strategy for IBD treatment by ameliorating the self-perpetuating proinflammatory microenvironment, which offers a new avenue in the treatment of inflammation-related diseases.
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