Channel power equalization based on joint optimization of EDFA and ROADM configuration in open optical network.

Deterioration of the signal-to-noise ratio (SNR) is an important challenge in ultra-long multi optical line system (OLS) optical transmission systems. The non-uniform gain and cascading of the Erbium-doped fiber amplifier (EDFA) lead to SNR deterioration in transmission systems. In this paper, we propose two channel power equalization methods based on joint optimization of EDFA and Reconfigurable optical add-drop multiplexer (ROADM) configurations: 1) reinforcement learning (RL)-based channel power equalization (RL-PE) and 2) covariance matrix adaptive evolution strategy (CMA-ES) channel power equalization (CMA-PE). The simulation results indicate that the power equalization effect was improved by 1.9 dB through the CMA-PE method, while the RL-PE method led to a 1.5 dB improvement in an ultra-long 80-channel 7-OLS transmission system.

Synergistic apoptosis induction in leukemic cells by miR-15a/16-1 and arsenic trioxide.

MicroRNAs (miRNAs) are small noncoding RNAs that regulate target gene expression through translation repression or messenger RNA degradation. MiR-15a and 16-1 form a cluster at the chromosomal region 13q14, which is frequently deleted or down-regulated in chronic lymphocytic leukemia. Arsenic trioxide (As(2)O(3), ATO) has been successfully applied to treat acute promyelocytic leukemia (APL). Its combination with other drugs presented therapeutic activities in hematologic and solid tumors. Here we investigated the potential synergy between miR-15a/16-1 and ATO on Bcr-Abl positive leukemic K562 cells. In this study, we found that combination of miR-15a/16-1 and ATO synergistically induced growth inhibition and apoptosis in K562 cells. The apoptosis, at least in part, through regulating mitochondrial function including the release of cytochrome c and loss of mitochondrial transmembrane potential, also activation of caspase-3 and degradation of poly-adenosine diphosphate-ribose polymerase. However, the expression of Bcr-Abl was not affected by ATO and/or miR-15a/16-1. Moreover, apoptotic synergy between miR-15a/16-1 and ATO was observed in Bcr-Abl negative leukemic cell lines and primary leukemic cells. Taken together, these findings suggested that the combined regiment of miR-15a/16-1 and ATO might be a potential therapeutic remedy for the treatment of leukemia.