Polymeric organic battery materials are promising alternatives to the transition-metal-based ones owing to their enriched chemistries. However, the flammability of organic compounds brings in serious concern on batter...Polymeric organic battery materials are promising alternatives to the transition-metal-based ones owing to their enriched chemistries. However, the flammability of organic compounds brings in serious concern on battery safety. In addition to use flame-retarding electrolyte/electrolyte additives or battery separators,flame retardancy can readily be achieved through the integration of flame-retarding unit into the polymer backbone, imparting the flame retardancy permanently. The as-designed polymer based on phenothiazine shows significantly shortened self-extinguished time without deteriorating its intrinsic thermodynamic and electrochemical properties. Moreover, two electron per phenothiazine molecule is realized for the first time in a highly reversible manner with discharge voltages of 3.52 V and 4.16 V versus Li+/Li and an average capacity of ca. 120 mAh g-1 at a current rate of 2 C. The origin of the reversibility is investigated through density functional theory(DFT) calculations. These findings address the importance of molecular design for safer and more stable organic materials for batteries.展开更多
Idiopathic pulmonary fibrosis(IPF)is a progressive disease with unknown etiology and limited therapeutic options.Activation of fibroblasts is a prominent feature of pulmonary fibrosis.Here we report that lncRNA DACH1(...Idiopathic pulmonary fibrosis(IPF)is a progressive disease with unknown etiology and limited therapeutic options.Activation of fibroblasts is a prominent feature of pulmonary fibrosis.Here we report that lncRNA DACH1(dachshund homolog 1)is downregulated in the lungs of IPF patients and in an experimental mouse model of lung fibrosis.LncDACH1 knockout mice develop spontaneous pulmonary fibrosis,whereas overexpression of LncDACH1 attenuated TGF-β1-induced aberrant activation,collagen deposition and differentiation of mouse lung fibroblasts.Similarly,forced expression of LncDACH1 not only prevented bleomycin(BLM)-induced lung fibrosis,but also reversed established lung fibrosis in a BLM model.Mechanistically,LncDACH1 binding to the serine/arginine-rich splicing factor 1(SRSF1)protein decreases its activity and inhibits the accumulation of Ctnnb1.Enhanced expression of SRSF1 blocked the anti-fibrotic effect of LncDACH1 in lung fibroblasts.Furthermore,loss of LncDACH1 promoted proliferation,differentiation,and extracellular matrix(ECM)deposition in mouse lung fibroblasts,whereas such effects were abolished by silencing of Ctnnb1.In addition,a conserved fragment of LncDACH1 alleviated hyperproliferation,ECM deposition and differentiation of MRC-5 cells driven by TGF-β1.Collectively,LncDACH1 inhibits lung fibrosis by interacting with SRSF1 to suppress CTNNB1 accumulation,suggesting that LncDACH1 might be a potential therapeutic target for pulmonary fibrosis.展开更多
基金financial support from the National Natural Science Foundation of China (grant no.51772199)the Natural Science Foundation of Jiangsu Province (Grant no.BK20170329)+2 种基金the Collaborative Innovation Center of Suzhou Nano Science & Technologythe Priority Academic Program Development of Jiangsu Higher Education Institutionsthe 111 Project。
文摘Polymeric organic battery materials are promising alternatives to the transition-metal-based ones owing to their enriched chemistries. However, the flammability of organic compounds brings in serious concern on battery safety. In addition to use flame-retarding electrolyte/electrolyte additives or battery separators,flame retardancy can readily be achieved through the integration of flame-retarding unit into the polymer backbone, imparting the flame retardancy permanently. The as-designed polymer based on phenothiazine shows significantly shortened self-extinguished time without deteriorating its intrinsic thermodynamic and electrochemical properties. Moreover, two electron per phenothiazine molecule is realized for the first time in a highly reversible manner with discharge voltages of 3.52 V and 4.16 V versus Li+/Li and an average capacity of ca. 120 mAh g-1 at a current rate of 2 C. The origin of the reversibility is investigated through density functional theory(DFT) calculations. These findings address the importance of molecular design for safer and more stable organic materials for batteries.
基金supported by the National Natural Science Foundation of China (32171127 and 91949109)the HMU Marshal Initiative Funding (HMUMIF-21023, China)+3 种基金the Major Scientific Fund Project of Heilongjiang Province (ZD2019H001, China)the CAMS Innovation Fund for Medical Sciences (CIFMS, 2019-I2M5-078, China)the Guangdong Province Basic and Applied Basic Research Fund (2021A1515111049, China)Postgraduate Research and Practice Innovation Program of HMU (YJSCX202015HYD, China)
文摘Idiopathic pulmonary fibrosis(IPF)is a progressive disease with unknown etiology and limited therapeutic options.Activation of fibroblasts is a prominent feature of pulmonary fibrosis.Here we report that lncRNA DACH1(dachshund homolog 1)is downregulated in the lungs of IPF patients and in an experimental mouse model of lung fibrosis.LncDACH1 knockout mice develop spontaneous pulmonary fibrosis,whereas overexpression of LncDACH1 attenuated TGF-β1-induced aberrant activation,collagen deposition and differentiation of mouse lung fibroblasts.Similarly,forced expression of LncDACH1 not only prevented bleomycin(BLM)-induced lung fibrosis,but also reversed established lung fibrosis in a BLM model.Mechanistically,LncDACH1 binding to the serine/arginine-rich splicing factor 1(SRSF1)protein decreases its activity and inhibits the accumulation of Ctnnb1.Enhanced expression of SRSF1 blocked the anti-fibrotic effect of LncDACH1 in lung fibroblasts.Furthermore,loss of LncDACH1 promoted proliferation,differentiation,and extracellular matrix(ECM)deposition in mouse lung fibroblasts,whereas such effects were abolished by silencing of Ctnnb1.In addition,a conserved fragment of LncDACH1 alleviated hyperproliferation,ECM deposition and differentiation of MRC-5 cells driven by TGF-β1.Collectively,LncDACH1 inhibits lung fibrosis by interacting with SRSF1 to suppress CTNNB1 accumulation,suggesting that LncDACH1 might be a potential therapeutic target for pulmonary fibrosis.
