Chaoxiong Wang

This paper considers the minimization of transmit power in Gaussian parallel interference channels, subject to a rate constraint for each user. To derive decentralized solutions that do not require any cooperation among the users, we formulate this power control problem as a (generalized) Nash equilibrium (NE) game. We obtain sufficient conditions that guarantee the existence and nonemptiness of the solution set to our problem. Then, to compute the solutions of the game, we propose two distributed algorithms based on the single user water-filling solution: The <i xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">sequential</i> and the <i xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">simultaneous</i> iterative water-filling algorithms, wherein the users update their own strategies sequentially and simultaneously, respectively. We derive a unified set of sufficient conditions that guarantee the uniqueness of the solution and global convergence of both algorithms. Our results are applicable to all practical distributed multipoint-to-multipoint interference systems, either wired or wireless, where a quality of service in (QoS) terms of information rate must be guaranteed for each link.

These findings implicated Sufu as an important inhibitor of TRAF6 in sepsis and suggest that therapeutics targeting Sufu-TRAF6 may greatly benefit the treatment of sepsis.

Abstract In adults, hepatocytes are mainly replenished from the existing progenitor pools of hepatocytes and cholangiocytes during chronic liver injury. However, it is unclear whether other cell types in addition to classical hepatocytes and cholangiocytes contribute to hepatocyte regeneration after chronic liver injuries. Here, we identified a new biphenotypic cell population that contributes to hepatocyte regeneration during chronic liver injuries. We found that a cell population expressed Gli1 and EpCAM (EpCAM + Gli1 + ), which was further characterized with both epithelial and mesenchymal identities by single-cell RNA sequencing. Genetic lineage tracing using dual recombinases revealed that Gli1 + nonhepatocyte cell population could generate hepatocytes after chronic liver injury. EpCAM + Gli1 + cells exhibited a greater capacity for organoid formation with functional hepatocytes in vitro and liver regeneration upon transplantation in vivo. Collectively, these findings demonstrate that EpCAM + Gli1 + cells can serve as a new source of liver progenitor cells and contribute to liver repair and regeneration.