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RISS 인기검색어
- 검색키워드
- 저자 : Gaofeng Lu (검색결과 3 건)
- 무료
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- 유료
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A Novel Safe File Sharing Method Based on Cloud Storage Structure in DHT Networks
Zhongning Lu,Gaofeng Shen 보안공학연구지원센터 2015 International Journal of Security and Its Applicat Vol.9 No.7
Safe file sharing mechanism in cloud storage is one of the most significant elements that affects the development of security technology. With application of homomorphic key agreement mechanism、Shamir secret sharing algorithm. Bloom Filter and B-tree search algorithm and Rsync data updating algorithm, a safe file sharing scheme in cloud storage is established based on cloud storage infrastructure of DHT networks. Under the circumstance of cloud storage, the scheme can make full use of the sharing mechanism and achieve the confidentiality and integrity of the file. Based on DHT networks, the analysis and test of data sharing are conducted in the paper. Together with file upload and download, the test of data encryption and decryption is done on the basis of Dropbox. As the result shows, the scheme puts forward a safe and effective solution to safe file sharing in cloud storage.
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Guo, Qi,Shen, Zhiyang,Yu, Hongxia,Lu, Gaofeng,Yu, Yong,Liu, Xia,Zheng, Pengyuan The Korean Society of Pharmacology 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.1
Acetaminophen (APAP) overdose is one of the most common causes of acute liver failure. The study aimed to investigate the protective effect of carnosic acid (CA) on APAP-induced acute hepatotoxicity and its underlying mechanism in mice. To induce hepatotoxicity, APAP solution (400 mg/kg) was administered into mice by intraperitoneal injection. Histological analysis revealed that CA treatment significantly ameliorated APAP-induced hepatic necrosis. The levels of both alanine aminotransferase (ALT) and aspartate transaminase (AST) in serum were reduced by CA treatment. Moreover, CA treatment significantly inhibited APAP-induced hepatocytes necrosis and lactate dehydrogenase (LDH) releasing. Western blot analysis showed that CA abrogated APAP-induced cleaved caspase-3, Bax and phosphorylated JNK protein expression. Further results showed that CA treatment markedly inhibited APAP-induced pro-inflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$, IL-6 and MCP-1 mRNA expression and the levels of phosphorylated $I{\kappa}B{\alpha}$ and p65 protein in the liver. In addition, CA treatment reduced APAP- induced hepatic malondialdehyde (MDA) contents and reactive oxygen species (ROS) accumulation. Conversely, hepatic glutathione (GSH) level was increased by administration of CA in APAP-treated mice. Mechanistically, CA facilitated Nrf2 translocation into nuclear through blocking the interaction between Nrf2 and Keap1, which, in turn, upregulated anti-oxidant genes mRNA expression. Taken together, our results indicate that CA facilitates Nrf2 nuclear translocation, causing induction of Nrf2-dependent genes, which contributes to protection from acetaminophen hepatotoxicity.
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Qi Guo,Zhiyang Shen,Hongxia Yu,Gaofeng Lu,Yong Yu,Xia Liu,Pengyuan Zheng 대한생리학회-대한약리학회 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.1
Acetaminophen (APAP) overdose is one of the most common causes of acute liver failure. The study aimed to investigate the protective effect of carnosic acid (CA) on APAP-induced acute hepatotoxicity and its underlying mechanism in mice. To induce hepatotoxicity, APAP solution (400 mg/kg) was administered into mice by intraperitoneal injection. Histological analysis revealed that CA treatment significantly ameliorated APAP-induced hepatic necrosis. The levels of both alanine aminotransferase (ALT) and aspartate transaminase (AST) in serum were reduced by CA treatment. Moreover, CA treatment significantly inhibited APAP-induced hepatocytes necrosis and lactate dehydrogenase (LDH) releasing. Western blot analysis showed that CA abrogated APAP-induced cleaved caspase-3, Bax and phosphorylated JNK protein expression. Further results showed that CA treatment markedly inhibited APAP-induced pro-inflammatory cytokines TNF-a, IL-1b, IL-6 and MCP-1 mRNA expression and the levels of phosphorylated IkBa and p65 protein in the liver. In addition, CA treatment reduced APAP- induced hepatic malondialdehyde (MDA) contents and reactive oxygen species (ROS) accumulation. Conversely, hepatic glutathione (GSH) level was increased by administration of CA in APAP-treated mice. Mechanistically, CA facilitated Nrf2 translocation into nuclear through blocking the interaction between Nrf2 and Keap1, which, in turn, upregulated anti-oxidant genes mRNA expression. Taken together, our results indicate that CA facilitates Nrf2 nuclear translocation, causing induction of Nrf2-dependent genes, which contributes to protection from acetaminophen hepatotoxicity.
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