Filter Design for Positive T-S Fuzzy Continuous-Time Systems with Time Delay Using Piecewise-Linear Membership Functions

The file attached to this record is the author's final peer reviewed version. The Publisher's final version can be found by following the DOI link.This work focuses on the filtering problem and stability analysis for positive Takagi-Sugeno (T-S) fuzzy systems with time delay under L1-induced performance. Due to the importance of estimation of system states but the few filter design results on positive nonlinear systems, it is an attractive and meaningful topic well worth studying. In order to fully exploit and take advantage of the positivity of positive T-S fuzzy systems, many commonly used methods, for instance free-weighting matrix approach and similarity transformation are probably not suitable for positive systems. To address the hard-nut-to-crack problem, an auxiliary variable is introduced so that the augmentation approach can be employed to carry out the positivity and stability analysis of filtering error systems. In addition, another obstacle that cannot be ignored is the existence of non-convex terms in the stability and positivity conditions. For getting around this barrier, some iterative linear matrix inequality (ILMI) algorithms have been proposed in the literature. However, considering the weakness that these methods cannot guarantee the convergence to a numerical solution and the iterative process is exhaustive, we present an effective matrix decoupling method to convert the nonconvex conditions into convex ones in this paper. Furthermore, a linear co-positive Lyapunov function which incorporates the positivity of system states and time delay at the same time is chosen so that the positivity characteristic of filtering error systems can be captured further. However, because of plenty of valuable information of membership functions (MFs) being ignored, hence, the obtained results are conservative. For the sake of relaxing the conservativeness, the advanced piecewise-linear membership functions (PLMFs) approximate method is utilized to facilitate the stability and positivity analysis. Therefore, the relaxed stability and positivity conditions which are cast as sum of squares (SOS) are obtained and can be solved numerically. Finally, the effectiveness of the designed fuzzy filtering strategy with satisfying L1-induced performance are demonstrated by a simulation example

Membership-Function-Dependent Design of L1-Gain Output-Feedback Controller for Stabilization of Positive Polynomial Fuzzy Systems

The file attached to this record is the author's final peer reviewed version. The Publisher's final version can be found by following the DOI link.This paper presents the L1-gain polynomial fuzzy output feedback controller design and the stability analysis using sum-of-squares (SOS) approach for positive polynomial fuzzy-model-based (PPFMB) control systems. The polynomials, positivity and optimal L1 performance makes some existing convex methods for general systems inapplicable. To overcome this problem, an augmented system of the positive polynomial fuzzy-model-based control system is first constructed, then by introducing some constrain conditions and mathematical tech niques, the non-convex stability and positivity conditions are skill fully transformed into convex ones simultaneously. In addition, to control the systems flexibly and lower the implementation cost, the imperfect premise matching concept is taken into account for controller design. Besides, the high degree polynomial approximation method is adopted to conduct stability and posi tivity analysis by incorporating the information of membership functions (MFs) and the boundary information of the state variables. On the basis of the Lyapunov stability theory, the relaxed stability and positivity conditions in terms of SOS are obtained. Finally, a simulation example is presented to verify the feasibility of the theoretical result

LncRNA‐CCAT5‐mediated crosstalk between Wnt/β‐Catenin and STAT3 signaling suggests novel therapeutic approaches for metastatic gastric cancer with high Wnt activity

Abstract Background Although the constitutively activated Wnt/β‐catenin signaling pathway plays vital roles in gastric cancer (GC) progression, few Wnt inhibitors are approved for clinical use. Additionally, the clinical significance of long non‐coding RNAs (lncRNAs) in GC intraperitoneal dissemination (IPD) remains elusive. Here, we investigated the function and therapeutic potential of Wnt‐transactivated lncRNA, colon cancer‐associated transcript 5 (CCAT5), in GC metastasis. Methods LncRNA‐sequencing assay was performed to document abundance changes of lncRNAs induced by Wnt family member 3A (Wnt3a) and degradation‐resistant β‐catenin (S33Y mutated) in ascites‐derived GC cells with low Wnt activity. Luciferase reporter, Chromatin immunoprecipitation (ChIP)‐re‐ChIP assays were performed to determine how CCAT5 was transcribed. The clinical significance of CCAT5 was examined in 2 cohorts of GC patients. The biological function of CCAT5 was investigated through gain‐ and loss‐of‐function studies. The molecular mechanism was explored through RNA‐sequencing, mass spectrometry, and CRISPR/Cas9‐knocknout system. The therapeutic potential of CCAT5 was examined through RNAi‐based cell xenograft model and patient‐derived xenograft (PDX) model of IPD. Results We identified a novel Wnt‐regulated lncRNA, CCAT5, which was transactivated by the β‐catenin/transcription factor 3 (TCF3) complex. CCAT5 was significantly upregulated in GC and predicted poor prognosis. Functional studies confirmed the promotive role of CCAT5 in GC growth and metastasis. Mechanistically, CCAT5 bound to the C‐end domain of signal transducer and activator of transcription 3 (STAT3) and blocks Src homology 2 domain‐containing protein tyrosine phosphatase 1 (SHP‐1)‐mediated STAT3Y705 dephosphorylation, leading to STAT3 nuclear entry and transactivation, thus accelerating GC progression. Furthermore, we demonstrated that both Wnt3a and β‐catenin acted as activator of STAT3 signaling pathway, and the interplay between CCAT5 and STAT3 was functionally essential for Wnt‐drived STAT3 signaling and tumor evolution. Finally, we revealed in vivo si‐CCAT5 selectively attenuated growth and metastasis of Wnthigh GC, but not Wntlow GC. The combination of si‐CCAT5 and oxaliplatin displayed obvious synergistic therapeutic effects on Wnthigh PDX mice. Conclusions We identified a novel Wnt‐transactivated lncRNA, CCAT5. Our study revealed a mechanism of STAT3 signaling regulation via canonical Wnt signaling and the functional significance of CCAT5 as critical mediator. We provided conceptual advance that lncRNAs serve as therapeutic targets reversing GC progression