No abstract

The past two decades have witnessed the stagnation of the clock speed of microprocessors followed by the recent faltering of Moore’s law as nanofabrication technology approaches its unavoidable physical limit. Vigorous efforts from various research areas have been made to develop power-efficient and ultrafast computing machines in this post-Moore’s law era. With its unique capacity to integrate complex electro-optic circuits on a single chip, integrated photonics has revolutionized the interconnects and has shown its striking potential in optical computing. Here, we propose an electronic-photonic computing architecture for a wavelength division multiplexing-based electronic-photonic arithmetic logic unit, which disentangles the exponential relationship between power and clock rate, leading to an enhancement in computation speed and power efficiency as compared to the state-of-the-art transistors-based circuits. We experimentally demonstrate its practicality by implementing a 4-bit arithmetic logic unit consisting of 8 high-speed microdisk modulators and operating at 20 GHz. This approach paves the way to future power-saving and high-speed electronic-photonic computing circuits.

In this work, we propose buffer-aided physical-layer network coding (PLNC) techniques for cooperative direct-sequence code-division multiple access systems. In the proposed buffer-aided PLNC schemes, a relay pair selection algorithm is employed to obtain the relay pair and the packets in the buffer entries with the best performance and the associated link combinations used for data transmission. We also devise PLNC schemes based on the design of linear network coding matrices using maximum likelihood and minimum mean-square error criteria to generate the network coded symbols that are sent to the destination. Simulation results show that the proposed techniques significantly outperform prior art.

Lipoxin A 4 (LXA 4 ), as an endogenously produced lipid mediator, promotes the resolution of inflammation. Previously, we demonstrated that LXA 4 stimulated alveolar fluid clearance through alveolar epithelial sodium channel gamma (ENaC-γ). In this study, we sought to investigate the mechanisms of LXA 4 in modulation of ENaC-γ in lipopolysaccharide (LPS)-induced inflammatory lung injury. miR-21 was upregulated during an LPS challenge and downregulated by LXA 4 administration in vivo and in vitro. Serum miR-21 concentration was also elevated in acute respiratory distress syndrome patients as compared with healthy volunteers. LPS increased miR-21 expression by activation of activator protein 1 (AP-1). In A549 cells, miR-21 upregulated phosphorylation of AKT activation via inhibition of phosphatase and tensin homolog (PTEN), and therefore reduced the expression of ENaC-γ. In contrast, LXA 4 reversed LPS-inhibited ENaC-γ expression through inhibition of AP-1 and activation of PTEN. In addition, an miR-21 inhibitor mimicked the effects of LXA 4 ; overexpression of miR-21 abolished the protective effects of LXA 4 . Finally, both AKT and ERK inhibitors (LY294002 and UO126) blocked effects of LPS on the depression of ENaC-γ. However, LXA 4 only inhibited LPS-induced phosphorylation of AKT. In summary, LXA 4 activates ENaC-γ in part via the miR-21/PTEN/AKT signaling pathway.

Inflammation always accompanies infection during sepsis. Mitochondrial dysfunction and the role of reactive oxygen species (ROS) produced by mitochondria have been proposed in the pathogenesis of sepsis. Maresins have protective and resolving effects in experimental models of infection. In the present study, we investigated the effects of maresin 1 (MaR1) on mitochondrial function in cecal ligation and puncture (CLP)-induced sepsis and sepsis patients to identify mechanisms underlying maresin 1-mediated stimulation of ROS in mitochondria. We found that treatment with MaR1 significantly inhibited production of cytokines, decreased bacterial load in the peritoneal lavage fluid, reduced the number of neutrophils, decreased lactic acid level and upregulated cyclic AMP (cAMP) concentration, with the outcome of decreased lung injury in CLP-induced sepsis in mice. The effects of MaR1 on downregulation nitric oxide (NOX) activity, improvement CAT and SOD activity to inhibit ROS production in mitochondria was dependent on lipoxin receptor (ALX) and cAMP. Survival rates were significantly increased after the treatment of mice with MaR1. In BMDM stimulated with LPS, MaR1 inhibited the ROS production, downregulated enzyme activity, reduced mtO2 production, increased mitochondrial membrane potential, improved adenosine triphosphate (ATP) content and mitochondrial DNA (mtDNA) copy number. Finally, the effects of MaR1 on ROS production in the blood of healthy volunteers stimulated with LPS or sepsis patients were associated with ALX and cAMP. Taken together, these data suggest that treatment with MaR1 could attenuate mitochondrial dysfunction during sepsis through regulating ROS production.