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- 저자 : Guoyong Han (검색결과 3 건)
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An Upper Bound of the Longest Impossible Differentials of Several Block Ciphers
( Guoyong Han ),( Wenying Zhang ),( Hongluan Zhao ) 한국인터넷정보학회 2019 KSII Transactions on Internet and Information Syst Vol.13 No.1
Impossible differential cryptanalysis is an essential cryptanalytic technique and its key point is whether there is an impossible differential path. The main factor of influencing impossible differential cryptanalysis is the length of the rounds of the impossible differential trail because the attack will be more close to the real encryption algorithm with the number becoming longer. We provide the upper bound of the longest impossible differential trails of several important block ciphers. We first analyse the national standard of the Russian Federation in 2015, Kuznyechik, which utilizes the 16-byte LFSR to achieve the linear transformation. We conclude that there is no any 3-round impossible differential trail of the Kuznyechik without the consideration of the specific S-boxes. Then we ascertain the longest impossible differential paths of several other important block ciphers by using the matrix method which can be extended to many other block ciphers. As a result, we show that, unless considering the details of the S-boxes, there is no any more than or equal to 5-round, 7-round and 9-round impossible differential paths for KLEIN, Midori64 and MIBS respectively.
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Revisited Security Evaluation on Midori-64 against Differential Cryptanalysis
Guoyong Han,Hongluan Zhao 한국인터넷정보학회 2024 KSII Transactions on Internet and Information Syst Vol.18 No.2
In this paper, the Mixed Integer Linear Programming (MILP) model is improved for searching differential characteristics of block cipher Midori-64, and 4 search strategies of differential path are given. By using strategy IV, set 1 S-box on the top of the distinguisher to be active, and set 3 S-boxes at the bottom to be active and the difference to be the same, then we obtain a 5-round differential characteristics. Based on the distinguisher, we attack 12-round Midori-64 with data and time complexities of 263 and 2103.83, respectively. To our best knowledge, these results are superior to current ones.
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Honglin Xu,Haifeng Miao,Guanghong Chen,Guoyong Zhang,Yue Hua,Yuting Wu,Tong Xu,Changlei Hu,Mingjie Pang,Leyi Tan,Xin Han,Bin Liu,Yingchun Zhou 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.6
Background: Myocardial fibrosis post-myocardial infarction (MI) can induce maladaptive cardiacremodeling as well as heart failure. Although 20(S)-ginsenoside Rg3 (Rg3) has been applied to cardiovasculardiseases, its efficacy and specific molecular mechanism in myocardial fibrosis are largely unknown. Herein, we aimed to explore whether TGFBR1 signaling was involved in Rg3's anti-fibrotic effectpost-MI. Methods: Left anterior descending (LAD) coronary artery ligation-induced MI mice and TGF-b1-stimulated primary cardiac fibroblasts (CFs) were adopted. Echocardiography, hematoxlin-eosin andMasson staining, Western-blot and immunohistochemistry, CCK8 and Edu were used to study the effectsof Rg3 on myocardial fibrosis and TGFBR1 signaling. The combination mechanism of Rg3 and TGFBR1 wasexplored by surface plasmon resonance imaging (SPRi). Moreover, myocardial Tgfbr1-deficient mice andTGFBR1 adenovirus were adopted to confirm the pharmacological mechanism of Rg3. Results: In vivo experiments, Rg3 ameliorated myocardial fibrosis and hypertrophy and enhanced cardiacfunction. Rg3-TGFBR1 had the 1.78 10 7 M equilibrium dissociation constant based on SPRi analysis,and Rg3 inhibited the activation of TGFBR1/Smads signaling dose-dependently. Cardiac-specific Tgfbr1knockdown abolished Rg3's protection against myocardial fibrosis post-MI. In addition, Rg3 downregulatedthe TGF-b1-mediated CFs growth together with collagen production in vitro through TGFBR1signaling. Moreover, TGFBR1 adenovirus partially blocked the inhibitory effect of Rg3. Conclusion: Rg3 improves myocardial fibrosis and cardiac function through suppressing CFs proliferationalong with collagen deposition by inactivation of TGFBR1 pathway.
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