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| 1 | Adaptive Pseudo Inverse Control for a Class of Nonlinear Asymmetric and Saturated Nonlinear Hysteretic Systems显示文摘This paper aims at eliminating the asymmetric and saturated hysteresis nonlinearities by designing hysteresis pseudo inverse compensator and robust adaptive dynamic surface control(DSC)scheme.The'pseudo inverse'means that an on-line calculation mechanism of approximate control signal is developed by applying a searching method to the designed temporary control signal where the true control signal is included.The main contributions are summarized as:1)to our best knowledge,it is the first time to compensate the asymmetric and saturated hysteresis by using hysteresis pseudo inverse compensator because the construction of the true saturated-type hysteresis inverse model is very difficult;2)by designing the saturated-type hysteresis pseudo inverse compensator,the construction of true explicit hysteresis inverse and the identifications of its corresponding unknown parameters are not required when dealing with the saturated-type hysteresis;3)by combining DSC technique with the tracking error transformed function,the'explosion of complexity'problem in backstepping method is overcome and the prespecified tracking performance is achieved.Analysis of stability and experimental results on the hardware-inloop platform illustrate the effectiveness of the proposed adaptive pseudo inverse control scheme. | Xiuyu Zhang Ruijing Jing Zhiwei Li Zhi Li Xinkai Chen Chun-Yi Su | 2021 | IEEE/CAA Journal of Automatica Sinica2021，8，4： | 4 |
| 2 | FLNa negatively regulated proliferation and metastasis in lung adenocarcinoma A549 cells via suppression of EGFR显示文摘Filamin A (FLNa ) 是无所不在地表示的细胞质的蛋白质,它 24 次象 Ig 一样重复跟随的一个 N 终端肌动朊绑定领域(ABD ) 创作。FLNa 作为连接 transmembrane 受体的细胞骨架蛋白质工作,包括 integrins,到 F 肌动朊并且用作发信号的中介。最近的研究作为与超过 90 蛋白质交往并且在细胞的发信号的 transduction 起重要作用的支架蛋白质识别了 FLNa。在人的 FLNa 基因的变化或缺点被显示了引起众多的发展缺点。而且, FLNa 的异常表示在许多癌症被观察了例如甲状旁腺的肿瘤,颈的癌症,和乳癌。然而,它在肺腺癌的角色很少被讨论了。在现在的学习,我们的在里面 vitro 并且在 vivo,研究证明在肺癌症房间线 A549 房间的那 silencing FLNa 表情由提高表皮的生长因素受体和英皇家空军之阶级最低之兵发信号小径的激活支持了 A549 房间的增长,移植,和侵略。这些结果在肺癌症和揭开的新奇机制使 FLNa 的新奇功能清楚些,这些结果为肺腺癌为预言和治疗提供了可能的目标。 | Yuna Zhang Tienian Zhu Jingpu Liu Jiankun Liu Dongmei Gao Tongyi Su Ruijing Zhao | 2018 | Acta Biochimica et Biophysica Sinica2018，50，2： | 2 |
| 3 | Intermedin/adrenomedullin 2 protects against tubular cell hypoxia‐reoxygenation injury in vitro by promoting cell proliferation and upregulating cyclin D 1 expression显示文摘 | Yanhong Wang Rongshan Li Xi Qiao Jihua Tian Xiaole Su Ruiping Wu Ruijing Zhang Xiaoshuang Zhou Jiaming Li Shan Shao | 2013 | Nephrology2013，，9： | 1 |
| 4 | Supported cobalt oxide on graphene oxide: Highly efficient catalysts for the removal of Orange II from water显示文摘 | Penghui Shi Ruijing Su Shaobo Zhu Mincong Zhu Dengxin Li Shihong Xu | 2012 | Journal of Hazardous Materials2012，，： | 1 |
| 5 | Leaching effects of metal from electroplating sludge under phosphate participation in hydrochloric acid medium显示文摘 | Su Ruijing Liang Bo Guan Jie | 2016 | Procedia Environmental Sciences2016，31，： | 1 |
| 6 | Hepatic retinaldehyde deficiency is involved in diabetes deterioration by enhancing PCK1-and G6PC-mediated gluconeogenesis显示文摘Type 2 diabetes(T2D) is often accompanied with an induction of retinaldehyde dehydrogenase 1(RALDH1 or ALDH1A1) expression and a consequent decrease in hepatic retinaldehyde(Rald)levels. However, the role of hepatic Rald deficiency in T2D progression remains unclear. In this study, we demonstrated that reversing T2D-mediated hepatic Rald deficiency by Rald or citral treatments, or liverspecific Raldh1 silencing substantially lowered fasting glycemia levels, inhibited hepatic glucogenesis,and downregulated phosphoenolpyruvate carboxykinase 1(PCK1) and glucose-6-phosphatase(G6PC)expression in diabetic db/db mice. Fasting glycemia and Pck1/G6pc mRNA expression levels were strongly negatively correlated with hepatic Rald levels, indicating the involvement of hepatic Rald depletion in T2D deterioration. A similar result that liver-specific Raldh1 silencing improved glucose metabolism was also observed in high-fat diet-fed mice. In primary human hepatocytes and oleic acidtreated HepG2 cells, Rald or Rald + RALDH1 silencing resulted in decreased glucose production and downregulated PCK1/G6PC mRNA and protein expression. Mechanistically, Rald downregulated direct repeat 1-mediated PCK1 and G6PC expression by antagonizing retinoid X receptor a, as confirmed by luciferase reporter assays and molecular docking. These results highlight the link between hepatic Rald deficiency, glucose dyshomeostasis, and the progression of T2D, whilst also suggesting RALDH1 as a potential therapeutic target for T2D. | Hanyu Yang Mengxiang Su Ming Liu Yun Sheng Liang Zhu Lu Yang Ruijing Mu Jianjun Zou Xiaodong Liu Li Liu | 2023 | Acta Pharmaceutica Sinica B2023，13，9： | 0 |
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