Synergetic learning structure-based neuro-optimal fault tolerant control for unknown nonlinear systems.

In this paper, a synergetic learning structure-based neuro-optimal fault tolerant control (SLSNOFTC) method is proposed for unknown nonlinear continuous-time systems with actuator failures. Under the framework of the synergetic learning structure (SLS), the optimal control input and the actuator failure are viewed as two subsystems. Then, the fault tolerant control (FTC) problem can be regarded as a two-player zero-sum differential game according to the game theory. A radial basis function neural network-based identifier, which uses the measured input/output data, is constructed to identify the completely unknown system dynamics. To develop the SLSNOFTC method, the Hamilton-Jacobi-Isaacs equation is solved by an asymptotically stable critic neural network (ASCNN) which is composed of cooperative adaptive tuning laws. Besides, with the help of the Lyapunov stability analysis, the identification error, the weight error of ASCNN, and all signals of closed-loop system are guaranteed to be converged to zero asymptotically, rather than uniformly ultimately bounded. Numerical simulation examples further verify the effectiveness and reliability of the proposed method.

Circ-ZNF609 promotes migration of colorectal cancer by inhibiting Gli1 expression via microRNA-150.

PURPOSE: To investigate the effect of circular (circ)-ZNF609 on the pathogenesis of colorectal cancer and its underlying mechanism. METHODS: 24 cases of postoperative colorectal cancer tissues and 36 cases of mucosa tissues were selected as experimental group and control group, respectively. Circ-ZNF609 expression in colorectal cancer tissues and mucosa tissues were detected by quantitative real-time PCR (qRT-PCR). For in vitro experiments, subcellular localization of Circ-ZNF609 in nuclear and cytoplasmic HCT116 cells was assessed. MicroRNA-150 was found to bind to Circ-ZNF609 by dual luciferase reporter assay. Furthermore, migration ability of transfected HCT116 cells was assessed by Transwell assay. Additionally, mRNA and protein levels of glioma-associated oncogene 1 (Gli1) in HCT116 cells were detected by qRT-PCR and Western blot, respectively. RESULTS: Higher expressions of Circ-ZNF609 and Gli1 were found in colorectal cancer tissues compared to paracancerous tissues. MicroRNA-150 was downregulated in colorectal cancer tissues. Pearson correlation analysis showed that Circ-ZNF609 was positively correlated with Gli1, and microRNA-150 was negatively correlated with Circ-ZNF609 and Gli1. Dual luciferase reporter assay confirmed that microRNA-150 was bound with cytoplasmic Circ-ZNF609. Furthermore, downregulated Circ-ZNF609 inhibited migration of HCT116 cells. In addition, knockdown of Circ-ZNF609 or overexpression of microRNA-150 inhibited cell migration, which was reversed by co-transfection with microRNA-150 inhibitor and Circ-ZNF609 siRNA. CONCLUSIONS: Circ-ZNF609 regulates Gli1 expression via microRNA-150, thus affecting the migration of colorectal cancer.