RESUMO
Constructing efficient thermal management system to settle the thermal runaway of energy storage devices via employing phase change microcapsules (MEPCMs) is of great significance. However, it is still a challenge that the conventional MEPCMs go against the electrochemical performance and hardly be homogenously fixed in the electrodes. In order to conquer these long-standing critical issues, we designed a novel electrochemically active double-shell phase change microcapsule by introducing polypyrrole on the surface of dense amine resin shell of the conventional inert MEPCM. The active MEPCMs@PPy are uniformly immobilized on the surface of the electrode material using reduced graphene oxide to ensure the stable and efficient operation of the flexible supercapacitor. The assembled all-solid-state supercapacitor containing MEPCMs@PPy (SCs@MEPCMs@PPy) lagged 103 s to 55 °C than the SCs@00 without the added phase change material. At a high temperature of 55 °C and a scan rate of 50 mV s-1, SCs@MEPCMs@PPy exhibits an areal specific capacitance of 110.6 mA cm-2, which is higher than that of the original SCs@MEPCMs. A capacitance retention of 79.8 % and coulombic efficiency of 98.4 % can be reached after 3000 cycles. This study opens a new avenue for developing applicable microencapsulated phase change materials in temperature-regulated electrode systems for supercapacitors and alkaline-ion batteries.
RESUMO
BACKGROUND: Based on extensive research on cytotoxicity of exogenous compounds in vitro, it is essential to develop a cell model that better mimics environment in vivo to explore cytotoxic mechanisms of exogenous compounds. METHODS: A co-culture system was established using a transwell system with Beas-2B and U937 cells. Cells were treated with fine particulate matter (PM2.5; 25, 50 and 100 µg/mL), nicotine-derived nitrosamine ketone (NNK; 50, 100 and 200 µg/mL) and benzo(a)pyrene diol epoxide (BPDE; 0.5, 2 and 8 µM) for 24 h. Cell proliferation, apoptosis and cell cycle, DNA damage were detected by CCK-8 and EdU, flow cytometry, and comet assay, respectively. Differentially expressed transcript and cytokine concentrations were determined by transcriptome sequencing and Cytokine Array, respectively. RESULTS: Compared with mono-culture, cell proliferation increased, apoptosis decreased, and DNA damage decreased in a dose-response relationship in co-culture. Gene expression profile was significantly different in co-culture, with significantly increased expression levels of 48 cytokines in co-culture. CONCLUSION: Cytotoxic damage to Beas-2B cells induced by exogenous carcinogens, including PM2.5, NNK and BPDE, was significantly reduced in a co-culture system compared with a mono-culture system. The mechanism may be related to changes in expression of cytokines, such as LIF, and activation of related pathways, such as TNF signaling pathway. Cytotoxic damage to Beas-2B induced by PM2.5, NNK and BPDE, was significantly reduced in co-culture. The mechanism may be related to changes in expression of cytokines and activation of related pathways. These findings provide new insights into cytotoxicity and experimental basis for safety evaluations of exogenous carcinogens.