Robust Sum-Rate Maximization in Transmissive RMS Transceiver-Enabled SWIPT Networks

In this paper, we propose a state-of-the-art downlink communication transceiver design for transmissive reconfigurable metasurface (RMS)-enabled simultaneous wireless information and power transfer (SWIPT) networks. Specifically, a feed antenna is deployed in the transmissive RMS-based transceiver, which can be used to implement beamforming. According to the relationship between wavelength and propagation distance, the spatial propagation models of plane and spherical waves are built. Then, in the case of imperfect channel state information (CSI), we formulate a robust system sum-rate maximization problem that jointly optimizes RMS transmissive coefficient, transmit power allocation, and power splitting ratio design while taking account of the non-linear energy harvesting model and outage probability criterion. Since the coupling of optimization variables, the whole optimization problem is non-convex and cannot be solved directly. Therefore, the alternating optimization (AO) framework is implemented to decompose the non-convex original problem. In detail, the whole problem is divided into three sub-problems to solve. For the non-convexity of the objective function, successive convex approximation (SCA) is used to transform it, and penalty function method and difference-of-convex (DC) programming are applied to deal with the non-convex constraints. Finally, we alternately solve the three sub-problems until the entire optimization problem converges. Numerical results show that our proposed algorithm has convergence and better performance than other benchmark algorithms

Kindlin-2 inhibits TNF/NF-κB-Caspase 8 pathway in hepatocytes to maintain liver development and function

Inflammatory liver diseases are a major cause of morbidity and mortality worldwide; however, underlying mechanisms are incompletely understood. Here we show that deleting the focal adhesion protein Kindlin-2 expression in hepatocytes using the Alb-Cre transgenic mice causes a severe inflammation, resulting in premature death. Kindlin-2 loss accelerates hepatocyte apoptosis with subsequent compensatory cell proliferation and accumulation of the collagenous extracellular matrix, leading to massive liver fibrosis and dysfunction. Mechanistically, Kindlin-2 loss abnormally activates the tumor necrosis factor (TNF) pathway. Blocking activation of the TNF signaling pathway by deleting TNF receptor or deletion of Caspase 8 expression in hepatocytes essentially restores liver function and prevents premature death caused by Kindlin-2 loss. Finally, of translational significance, adeno-associated virus mediated overexpression of Kindlin-2 in hepatocytes attenuates the D-galactosamine and lipopolysaccharide-induced liver injury and death in mice. Collectively, we establish that Kindlin-2 acts as a novel intrinsic inhibitor of the TNF pathway to maintain liver homeostasis and may define a useful therapeutic target for liver diseases