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Detecting LDoS Attacks based on Abnormal Network Traffic
( Kai Chen ),( Huiyu Liu ),( Xiaosu Chen ) 한국인터넷정보학회 2012 KSII Transactions on Internet and Information Syst Vol.6 No.7
By sending periodically short bursts of traffic to reduce legit transmission control protocol (TCP) traffic, the low-rate denial of service (LDoS) attacks are hard to be detected and may endanger covertly a network for a long period. Traditionally, LDoS detecting methods mainly concentrate on the attack stream with feature matching, and only a limited number of attack patterns can be detected off-line with high cost. Recent researches divert focus from the attack stream to the traffic anomalies induced by LDoS attacks, which can detect more kinds of attacks with higher efficiency. However, the limited number of abnormal characteristics and the inadequacy of judgment rules may cause wrong decision in some particular situations. In this paper, we address the problem of detecting LDoS attacks and present a scheme based on the fluctuant features of legit TCP and acknowledgment (ACK) traffic. In the scheme, we define judgment criteria which used to identify LDoS attacks in real time at an optimal detection cost. We evaluate the performance of our strategy in real-world network topologies. Simulations results clearly demonstrate the superiority of the method proposed in detecting LDoS attacks.
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Lei Zhou,Lin Fu,Na Lv,Jing Liu,Yan Li,Xiaosu Chen,Qingyu Xu,Guofeng Chen,Baoxu Pang,Lili Wang,Yonghui Li,Xiaodong Zhang,Li Yu 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
The AML1-ETO fusion protein (A/E), which results from the t(8;21) translocation, is considered to be a leukemiainitiating event. Identifying the mechanisms underlying the oncogenic activity of A/E remains a major challenge. In this study, we identified a specific down-regulation of brain acid-soluble protein 1 (BASP1) in t(8;21) acute myeloid leukemia (AML). A/E recognized AML1-binding sites and recruited DNA methyltransferase 3a (DNMT3a) to the BASP1 promoter sequence, which triggered DNA methylation-mediated silencing of BASP1. Ectopic expression of BASP1 inhibited proliferation and the colony-forming ability of A/E-positive AML cell lines and led to apoptosis and cell cycle arrest. The DNMT inhibitor decitabine up-regulated the expression of BASP1 in A/E-positive AML cell lines. In conclusion, our data suggest that BASP1 silencing via promoter methylation may be involved in A/E-mediated leukemogenesis and that BASP1 targeting may be an actionable therapeutic strategy in t(8;21) AML.
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