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| 1 | Development of a supercritical and an ultra-supercritical circulating fluidized bed boiler显示文摘The supercritical circulating fluidized bed(CFB)boiler,which combines the advantages of CFB combustion with low cost emission control and supercritical steam cycle with high efficiency of coal energy,is believed to be the future of CFB combustion technology.It is also of greatest importance for low rank coal utilization in China.Different from the supercritical pulverized coal boiler that has been developed more than 50 years,the supercritical CFB boiler is still a new one which requires further investigation.Without any precedentor engineering reference,Chinese researchers have con ducted fundamental research,development,design of the supercritical CFB boilers independently.The design theory and key technology for supercritical CFB boiler were proposed.Key components and novel structures were invented.The first 600 MWe supercritical CFB boiler and its auxiliaries were successfully developed and demonstrated in Baima Power Plant,Shenhua Group as well as the simulator,control technology,installation technology,commissioning technology,system integration and operation technology.Compared with the 460 MWe supercritical CFB in Poland,developed in the same period and the only other supercritical one of commercial running in the word beside Baima,the 600 MWe one in Baima has a better performance.Besides,supercritical CFB boilers of 350 MWe have been developed and widely commercialized in China.In this paper,the updated progress of 660 MWe ultra-supercritical CFB boilers under development is introduced. | Junfu LYU Hairui YANG Wen LING Li NIE Guangxi YUE Ruixin LI Ying CHEN Shilong WANG | 2019 | Frontiers in Energy2019，13，1： | 11 |
| 2 | Built-in piezoelectric field improved photocatalytic performance of nanoflower-like Bi_(2)WO_(6) using low-power white LEDs显示文摘Photocatalysis technology has been proved to be a potential strategy for removal of organic dyes,however high-power light sources are generally necessary to initiate photocatalytic reaction.In this work,we employed an excellent photocatalyst of Bi_(2)WO_(6) with visible light harvest and meanwhile an intrinsic ferroelectricity,which realized the efficient degradation of organic dye via the synergetic photopiezocatalysis.Through coupling the illumination by a low-power(9 W)LED and the ultrasonic vibration(120 W)by an ultrasonic cleaner,the nano flower-like Bi_(2)WO_(6) composed of ultrathin nanosheets showed a much more enhanced photopiezocatalysis performance for purification of organic dye than the individual photocatalysis and piezocatalysis.Furthermore,the high mineralization efficiency and the good durability of the Bi_(2)WO_(6) catalyst were demonstrated.The possible mechanism of photopiezocatalysis was finally proposed,where the ultrasound-induced piezoelectric field in Bi_(2)WO_(6) drove photo-generated electrons and holes to diffuse along opposite directions,consequently promoting the separation efficiency of charge carriers.This work indicates that the synergetic photopiezocatalysis by coupling irradiation and ultrasonic vibration is a promising strategy to purify organic pollutants in wastewater. | Hua Lei Meixuan Wu Ying Liu Fan Mo Jiayao Chen Shilong Ji Yan Zou Xiaoping Dong | 2021 | Chinese Chemical Letters2021，32，7： | 2 |
| 3 | EGFR TKIs impair lysosome-dependent degradation of SQSTM1 to compromise the effectiveness in lung cancer显示文摘Tyrosine kinase inhibitors for epidermal growth factor receptor(EGFR TKIs)greatly improved clinical outcomes of patients with non-small cell lung cancer(NSCLC).Unfortunately,primary and acquired resistance limits their clinical benefits.To overcome such resistance,new generations of EGFR TKIs have been developed by targeting newly identified mutations in EGFR.However,much less effort has been put into alternative strategies,such as targeting the intrinsic protective responses to EGFR TKIs.In this study,we found that EGFR TKIs,including gefitinib and AZD9291,impaired lysosome-dependent degradation of SQSTM1,thus compromising their anti-cancer efficiency.By accumulating in the lysosome lumen,gefitinib and AZD9291 attenuated lysosomal acidification and impaired autolysosomal degradation of SQSTM1 owing to their intrinsic alkalinity.As a result,SQSTM1 protein was stabilized in response to gefitinib and AZD9291 treatment and conferred EGFR TKI resistance.Depleting SQSTM1 significantly increased the sensitivity of NSCLC cells to gefitinib and AZD9291 both in vitro and in vivo.Furthermore,a chemically modified gefitinib analog lacking alkalinity displayed stronger inhibitory effects on NSCLC cells.Therefore,targeting accumulated SQSTM1 or chemically modified EGFR TKIs may represent new strategies to increase the effectiveness of EGFR targeted therapy. | Lixian Yang Shilong Ying Shiman Hu Xiangtong Zhao Muchun Li Miaoqin Chen Yiran Zhu Ping Song Liyuan Zhu Tingting Jiang Huimin An Neelum Aziz Yousafzai Wenxia Xu Zhiguo Zhang Xian Wang Lifeng Feng Hongchuan Jin | 2019 | Signal Transduction and Targeted Therapy2019，4，1： | 2 |
| 4 | α-myosin heavy chain lactylation maintains sarcomeric structure and function and alleviates the development of heart failure显示文摘The sarcomeric interaction ofα-myosin heavy chain(α-MHC)with Titin is vital for cardiac structure and contraction.However,the mechanism regulating this interaction in normal and failing hearts remains unknown.Lactate is a crucial energy substrate of the heart.Here,we identify thatα-MHC undergoes lactylation on lysine 1897 to regulate the interaction ofα-MHC with Titin.We observed a reduction ofα-MHC K1897 lactylation in mice and patients with heart failure.Loss of K1897 lactylation inα-MHC K1897R knock-in mice reducesα-MHC–Titin interaction and leads to impaired cardiac structure and function.Furthermore,we identified that p300 and Sirtuin 1 act as the acyltransferase and delactylase ofα-MHC,respectively.Decreasing lactate production by chemical or genetic manipulation reducesα-MHC lactylation,impairsα-MHC–Titin interaction and worsens heart failure.By contrast,upregulation of the lactate concentration by administering sodium lactate or inhibiting the pivotal lactate transporter in cardiomyocytes can promoteα-MHC K1897 lactylation andα-MHC–Titin interaction,thereby alleviating heart failure.In conclusion,α-MHC lactylation is dynamically regulated and an important determinant of overall cardiac structure and function.Excessive lactate efflux and consumption by cardiomyocytes may decrease the intracellular lactate level,which is the main cause of reducedα-MHC K1897 lactylation during myocardial injury.Our study reveals that cardiac metabolism directly modulates the sarcomeric structure and function through lactate-dependent modification ofα-MHC. | Naijin Zhang Ying Zhang Jiaqi Xu Pengbo Wang Boquan Wu Saien Lu Xinxin Lu Shilong You Xinyue Huang Mohan Li Yuanming Zou Mengke Liu Yuanhui Zhao Guozhe Sun Wenbin Wang Danxi Geng Jingwei Liu Liu Cao Yingxian Sun | 2023 | Cell Research2023，33，9： | 0 |
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