RESUMEN
This study focuses on improving human thermal comfort in a high-temperature outdoor environment using vests with a radiative cooling coating. The effects of coating thickness on the radiative cooling performance were first evaluated, and an optimal thickness of 160 µm was achieved. Then, six subjects were recruited to evaluate the thermal comfort in two scenarios: wearing the vest with radiative cooling coatings, and wearing the standard vest. Compared with the standard vest, the coated vest decreases the maximum temperature at the vest inner surface and the outer surface by 5.54 °C and 4.37 °C, respectively. The results show that thermal comfort is improved by wearing radiative cooling vests. With an increase of wet bulb globe temperature (WBGT), the improving effects tend to decline. A significant improvement in human thermal comfort is observed at a WBGT of 26 °C. Specifically, the percentage of thermal sensation vote (TSV) wearing the cooling vest in the range of 0 to 1 increases from 29.2% to 66.7% compared with that of the untreated vest. At the same time, the average value of thermal comfort vote (TCV) increases from -0.5 to 0.2.
RESUMEN
BACKGROUND: p66Shc, as a redox enzyme, regulates reactive oxygen species (ROS) production in mitochondria and autophagy. However, the mechanisms by which p66Shc affects autophagosome formation are not fully understood. METHODS: p66Shc expression and its location in the trophoblast cells were detected in vivo and in vitro. Small hairpin RNAs or CRISPR/Cas9, RNA sequencing, and confocal laser scanning microscope were used to clarify p66Shc's role in regulating autophagic flux and STING activation. In addition, p66Shc affects mitochondrial-associated endoplasmic reticulum membranes (MAMs) formation were observed by transmission electron microscopy (TEM). Mitochondrial function was evaluated by detected cytoplastic mitochondrial DNA (mtDNA) and mitochondrial membrane potential (MMP). RESULTS: High glucose induces the expression and mitochondrial translocation of p66Shc, which promotes MAMs formation and stimulates PINK1-PRKN-mediated mitophagy. Moreover, mitochondrial localized p66Shc reduces MMP and triggers cytosolic mtDNA release, thus activates cGAS/STING signaling and ultimately leads to enhanced autophagy and cellular senescence. Specially, we found p66Shc is required for the interaction between STING and LC3II, as well as between STING and ATG5, thereby regulates cGAS/STING-mediated autophagy. We also identified hundreds of genes associated several biological processes including aging are co-regulated by p66Shc and ATG5, deletion either of which results in diminished cellular senescence. CONCLUSION: p66Shc is not only implicated in the initiation of autophagy by promoting MAMs formation, but also helps stabilizing active autophagic flux by activating cGAS/STING pathway in trophoblast.
