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Incentive Mechanism based on Game Theory in Kad Network
왕서(Xu Wang),니영청(YongQing Ni),양대헌(DaeHun Nyang) 한국정보보호학회 2010 정보보호학회논문지 Vol.20 No.3
Kad 네트워크는 파일 공유 시스템 중 가장 널리 알려진 네트워크이다. 파일 공유 시스템은 사용자의 일방적 파일 다운로드 받기, 가짜파일 업로드하기, 바이러스 배포하기 등에 사용 되는 등의 문제를 가지고 있고, 이러한 문제점을 극복하기 위하여, 이 논문에서는 게임 이론을 바탕으로 하는 인센티브 메커니즘을 제안한다. 이 메커니즘은 Kad 사용자를 위하여 보다 안정적이고 효율적인 네트워크 환경을 만들어 준다. 즉, 쓸모 없고 위험한 파일 등을 제공하는 다른 사용자들이 처벌받는 것에 반하여, 가치 있는 리소스를 공유한 사용자는 신용이 증가하는 대가를 받는다. Kad 네트워크에서 이 인센티브 메커니즘은 사용자의 악의적인 행동을 찾거나 방지하고 사용자들 사이에서의 정직한 통신을 장려하는데 도움을 준다. The Kad network is a peer-to-peer (P2P) network which implements the Kademlia P2P overlay protocol. Nowadays, the Kad network has attracted wide concern as a popular architecture for file sharing systems. Meanwhile, many problems have been coming out in these file sharing systems such as freeriding of users, uploading fake files, spreading viruses, and so on. In order to overcome these problems, we propose an incentive mechanism based on game theory, it establishes a more stable and efficient network environment for Kad users. Users who share valuable resources receive rewards by increasing their credits, while others who supply useless or harmful files are punished. This incentive mechanism in Kad network can be used to detect and prevent malicious behaviors of users and encourage honest interaction among users.
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Sundong Lin,Lechu Yu,Yongqing Ni,Lulu He,Xiaolu Weng,Xuemian Lu,Chi Zhang 대한당뇨병학회 2020 Diabetes and Metabolism Journal Vol.44 No.1
Background: Epithelial-to-mesenchymal transition (EMT) is required for renal fibrosis, which is a characteristic of diabetic nephropathy (DN). Our previous study demonstrated that fibroblast growth factor 21 (FGF21) prevented DN associated with the suppressing renal connective tissue growth factor expression, a key marker of renal fibrosis. Therefore, the effects of FGF21 on renal fibrosis in a DN mouse model and the underlying mechanisms were investigated in this study. Methods: Type 1 diabetes mellitus was induced in C57BL/6J mice by intraperitoneal injections of multiple low doses of streptozotocin. Then, diabetic and non-diabetic mice were treated with or without FGF21 in the presence of pifithrin-α (p53 inhibitor) or 10-[4´-(N,N-Diethylamino)butyl]-2-chlorophenoxazine hydrochloride (10-DEBC) hydrochloride (Akt inhibitor) for 4 months. Results: DN was diagnosed by renal dysfunction, hypertrophy, tubulointerstitial lesions, and glomerulosclerosis associated with severe fibrosis, all of which were prevented by FGF21. FGF21 also suppressed the diabetes-induced renal EMT in DN mice by negatively regulating transforming growth factor beta (TGF-β)-induced nuclear translocation of Smad2/3, which is required for the transcription of multiple fibrotic genes. The mechanistic studies showed that FGF21 attenuated nuclear translocation of Smad2/3 by inhibiting renal activity of its conjugated protein p53, which carries Smad2/3 into the nucleus. Moreover pifithrin-α inhibited the FGF21-induced preventive effects on the renal EMT and subsequent renal fibrosis in DN mice. In addition, 10-DEBC also blocked FGF21-induced inhibition of renal p53 activity by phosphorylation of mouse double minute-2 homolog (MDM2). Conclusion: FGF21 prevents renal fibrosis via negative regulation of the TGF-β/Smad2/3-mediated EMT process by activation of the Akt/MDM2/p53 signaling pathway.
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