ABSTRACT
Passive daytime radiative cooling (PDRC) is an emerging sustainable technology that can spontaneously radiate heat to outer space through an atmospheric transparency window to achieve self-cooling. PDRC has attracted considerable attention and shows great potential for personal thermal management (PTM). However, PDRC polymers are limited to polyethylene, polyvinylidene fluoride, and their derivatives. In this study, a series of polymer films based on thermoplastic polyurethane (TPU) and their composite films with silica aerogels (aerogel-functionalized TPU (AFTPU)) are prepared using a simple and scalable non-solvent-phase-separation strategy. The TPU and AFTPU films are freestanding, mechanically strong, show high solar reflection up to 94%, and emit strongly in the atmospheric transparency window, thereby achieving subambient cooling of 10.0 and 7.7 °C on a hot summer day for the TPU and AFTPU film (10 wt%), respectively. The AFTPU films can be used as waterproof and moisture permeable coatings for traditional textiles, such as cotton, polyester, and nylon, and the highest temperature drop of 17.6 °C is achieved with respect to pristine nylon fabric, in which both the cooling performance and waterproof properties are highly desirable for the PTM applications. This study opens up a promising route for designing common polymers for highly efficient PDRC.
ABSTRACT
The outbreak of COVID-19 has remained uncontained with urgent need for robust therapeutics. We have previously reported sex difference of COVID-19 for the first time indicating male predisposition. Males are more susceptible than females, and more often to develop into severe cases with higher mortality. This predisposition is potentially linked to higher prevalence of cigarette smoking. Nonetheless, we found for the first time that cigarette smoking extract (CSE) had no effect on angiotensin converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) expression in endothelial cells. The otherwise observed worse outcomes in smokers is likely linked to baseline respiratory diseases associated with chronic smoking. Instead, we hypothesized that estrogen mediated protection might underlie lower morbidity, severity and mortality of COVID-19 in females. Of note, endothelial inflammation and barrier dysfunction are major mediators of disease progression, and development of acute respiratory distress syndrome (ARDS) and multi-organ failure in patients with COVID-19. Therefore, we investigated potential protective effects of estrogen on endothelial cells against oxidative stress induced by interleukin-6 (IL-6) and SARS-CoV-2 spike protein (S protein). Indeed, 17ß-estradiol completely reversed S protein-induced selective activation of NADPH oxidase isoform 2 (NOX2) and reactive oxygen species (ROS) production that are ACE2-dependent, as well as ACE2 upregulation and induction of pro-inflammatory gene monocyte chemoattractant protein-1 (MCP-1) in endothelial cells to effectively attenuate endothelial dysfunction. Effects of IL-6 on activating NOX2-dependent ROS production and upregulation of MCP-1 were also completely attenuated by 17ß-estradiol. Of note, co-treatment with CSE had no additional effects on S protein stimulated endothelial oxidative stress, confirming that current smoking status is likely unrelated to more severe disease in chronic smokers. These data indicate that estrogen can serve as a novel therapy for patients with COVID-19 via inhibition of initial viral responses and attenuation of cytokine storm induced endothelial dysfunction, to substantially alleviate morbidity, severity and mortality of the disease, especially in men and post-menopause women. Short-term administration of estrogen can therefore be readily applied to the clinical management of COVID-19 as a robust therapeutic option.