Enhanced Near-cloak by FSH Lining

We consider regularized approximate cloaking for the Helmholtz equation. Various cloaking schemes have been recently proposed and extensively investigated. The existing cloaking schemes in literature are (optimally) within $|\ln\rho|^{-1}$ in 2D and $\rho$ in 3D of the perfect cloaking, where $\rho$ denotes the regularization parameter. In this work, we develop a cloaking scheme with a well-designed lossy layer right outside the cloaked region that can produce significantly enhanced near-cloaking performance. In fact, it is proved that the proposed cloaking scheme could (optimally) achieve $\rho^N$ in $\mathbb{R}^N$, $N\geq 2$, within the perfect cloaking. It is also shown that the limit of the proposed lossy layer corresponds to a sound-hard layer. We work with general geometry and arbitrary cloaked contents of the proposed cloaking device

CK1α protects cardiomyocytes in sepsis-induced myocardial depression by repressing the interaction of ATG5 with myD88/NF-kappaB signaling

Purpose: To explore the effects of casein kinase 1α (CK1α) on cardiomyocytes in sepsis-induced myocardial depression.Methods: Colorectal ligation puncture (CLP) surgery was performed for the establishment of the mouse model. Total RNAs of the lungs, kidneys, liver tissues and alveolar macrophages were extracted using TRIzol™ reagent, while gene expression analysis was performed by quantitative polymerase chain reaction (qPCR) following reverse transcription. Western blot was employed to evaluate protein expression, and echocardiography was conducted to assess cardiac function. Immunofluorescent assay was performed to determine the expression of p-FOXO3a in primary cardiomyocytes.Results: Inhibition of CK1α impaired autophagy influx, and significantly increased inflammatory cytokines in H9C2 cells after lipopolysaccharide (LPS) treatment (p < 0.05). Moreover, aberrant activation of the Toll-like receptor 4(TLR4)/myD88/NF-kappaB pathway was observed in the H9C2 cell line after LPS treatment (p < 0.05). Immunoprecipitation analysis revealed an interaction between MyD88 and autophagy-related gene 5 (Atg5), and cardiac dysfunction in mice intravenously injectedwith an adenoviral vector containing shRNA (casein kinase 1 α) CSNK1A1 was suppressed (p < 0.05). In contrast, overexpression of CK1α remarkably improved cardiac systolic function (p < 0.05), the expression of inflammatory cytokines was repressed, and autophagy was enhanced in the hearts of mice with the specific overexpression of CSNK1A1 in cardiomyocytes (p < 0.05). In Atg5-deficient mice pretreated with DC661, the protective effect of adenoviral vector containing CK1α overexpression was eliminated.Conclusion: CK1α protects cardiomyocytes during sepsis after the inhibition of TLR/MyD88/NF-kappaBpathway via interaction of Atg5 with MyD88. The results of the current study may provide new insights into the treatment of sepsis-induced myocardial depression

A stochastic preconditioned Douglas-Rachford splitting method for saddle-point problems

In this article, we propose and study a stochastic preconditioned Douglas-Rachford splitting method to solve saddle-point problems which have separable dual variables. We prove the almost sure convergence of the iteration sequences in Hilbert spaces for a class of convexconcave and nonsmooth saddle-point problems. We also provide the sublinear convergence rate for the ergodic sequence with respect to the expectation of the restricted primal-dual gap functions. Numerical experiments show the high efficiency of the proposed stochastic preconditioned Douglas-Rachford splitting methods