Infinite-dimensional LMI approach to analysis and synthesis for linear time-delay systems

summary:This paper considers an analysis and synthesis problem of controllers for linear time-delay systems in the form of delay-dependent memory state feedback, and develops an Linear Matrix Inequality (LMI) approach. First, we present an existence condition and an explicit formula of controllers, which guarantee a prescribed level of $L^2$ gain of closed loop systems, in terms of infinite-dimensional LMIs. This result is rather general in the sense that it covers, as special cases, some known results for the cases of delay- independent/dependent and memoryless/memory controllers, while the infinity dimensionality of the LMIs makes the result difficult to apply. Second, we introduce a technique to reduce the infinite-dimensional LMIs to a finite number of LMIs, and present a feasible algorithm for synthesis of controllers based on the finite-dimensional LMIs

Downregulation of Plasma miR-215 in Chronic Myeloid Leukemia Patients with Successful Discontinuation of Imatinib

Approximately 40% of chronic myeloid leukemia (CML) patients who discontinue imatinib (IM) therapy maintain undetectable minimal residual disease (UMRD) for more than one year (stopping IM (STOP-IM)). To determine a possible biomarker for STOP-IM CML, we examined plasma miRNA expression in CML patients who were able to discontinue IM. We first screened candidate miRNAs in unselected STOP-IM patients, who had sustained UMRD after discontinuing IM for more than six months, in comparison with healthy volunteers, by using a TaqMan low-density array for plasma or exosomes. Exosomal miR-215 and plasma miR-215 were downregulated in the STOP-IM group compared to the control, indicating that the biological relevance of the plasma miR-215 level is equivalent to that of the exosomal level. Next, we performed real-time quantitative RT-PCR in 20 STOP-IM patients, 32 patients with UMRD on continued IM therapy (IM group) and 28 healthy volunteers. The plasma miRNA-215 level was significantly downregulated in the STOP-IM group (p < 0.0001); we determined the cut-off level and divided the IM group patients into two groups according to whether the plasma miR-215 was downregulated or not. The IM group patients with a low plasma miR-215 level had a significantly higher total IM intake, compared to the patients with elevated miR-215 levels (p = 0.0229). Functional annotation of miR-215 target genes estimated by the Database for Annotation, Visualization and Integrated Discovery (DAVID) bioinformatic tools involved cell cycle, mitosis, DNA repair and cell cycle checkpoint. Our study suggests a possible role of miR-215 in successful IM discontinuation