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( Youming Sun ),( Hongxiang Shao ),( Xin Liu ),( Jian Zhang ),( Junfei Qiu ),( Yuhua Xu ) 한국인터넷정보학회 2015 KSII Transactions on Internet and Information Syst Vol.9 No.11
This paper investigates the traffic offloading over unlicensed bands for two-tier multi-mode small cell networks. We formulate this problem as a Stackelberg game and apply a hierarchical learning framework to jointly maximize the utilities of both macro base station (MBS) and small base stations (SBSs). During the learning process, the MBS behaves as a leader and the SBSs are followers. A pricing mechanism is adopt by MBS and the price information is broadcasted to all SBSs by MBS firstly, then each SBS competes with other SBSs and takes its best response strategies to appropriately allocate the traffic load in licensed and unlicensed band in the sequel, taking the traffic flow payment charged by MBS into consideration. Then, we present a hierarchical Q-learning algorithm (HQL) to discover the Stackelberg equilibrium. Additionally, if some extra information can be obtained via feedback, we propose an improved hierarchical Q-learning algorithm (IHQL) to speed up the SBSs` learning process. Last but not the least, the convergence performance of the proposed two algorithms is analyzed. Numerical experiments are presented to validate the proposed schemes and show the effectiveness.
Dongwei Yuan,Li Qing,Lu Xing,Lan Jianfeng,Qiu Zhidong,Wang Xuehong,Wang Junnan,Zheng Xiaojiao,Chen Sifan,Zhang Chong,Jin Junfei 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-
Acute liver injury is the basis of the pathogenesis of diverse liver diseases. However, the mechanism underlying liver injury is complex and not completely understood. In our study, we revealed that CERK, which phosphorylates ceramide to produce ceramide-1-phosphate (C1P), was the sphingolipid pathway-related protein that had the most significantly upregulated expression during acute liver injury. A functional study confirmed that CERK and C1P attenuate hepatic injury both in vitro and in vivo through antioxidant effects. Mechanistic studies have shown that CERK and C1P positively regulate the protein expression of NRF2, which is a crucial protein that helps maintain redox homeostasis. Furthermore, our results indicated that C1P disrupted the interaction between NRF2 and KEAP1 by competitively binding to KEAP1, which allowed for the nuclear translocation of NRF2. In addition, pull-down assays and molecular docking analyses revealed that C1P binds to the DGR domain of KEAP1, which allows it to maintain its interaction with NRF2. Importantly, these findings were verified in human primary hepatocytes and a mouse model of hepatic ischemia‒reperfusion injury. Taken together, our findings demonstrated that CERK-mediated C1P metabolism attenuates acute liver injury via the binding of C1P to the DGR domain of KEAP1 and subsequently the release and nuclear translocation of NRF2, which activates the transcription of cytoprotective and antioxidant genes. Our study suggested that the upregulation of CERK and C1P expression may serve as a potential antioxidant strategy to alleviate acute liver injury.