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Risk Assessment of Computer Network Security in Banks
Tan Juan 보안공학연구지원센터 2016 International Journal of Security and Its Applicat Vol.10 No.4
The importance of computer system security of banks can never be exaggerated. Conducting risk assessment of computer system security of banks can increase safety management and ensure normal operation. This paper firstly figures out risk assessment indexes for computer system security of banks through literature review and survey. Secondly, it uses AHP to confirm the weight of indicators and establishes five security levels. According to the judgment of experts, it finally establishes the risk assessment model for computer system security of banks.
Tan, Xiaobin,Gu, Junfei,Zhao, Bingjie,Wang, Shuyuan,Yuan, Jiarui,Wang, Chunfei,Chen, Juan,Liu, Jiping,Feng, Liang,Jia, Xiaobin The Korean Society of Ginseng 2015 Journal of Ginseng Research Vol.39 No.2
Background: Ginseng, the root of Panax ginseng (PG), is used widely as a herbal medicine to prevent and treat various diseases. Panax ginseng has pharmacological effects on neurodegenerative diseases such as Alzheimer's disease (AD). The present study evaluated the neuroprotective effects of PG and its possible neuroprotective mechanisms in advanced glycation end product (AGE)-induced AD in a rat model. Methods: Advanced glycation end products were injected bilaterally into the CA3 region of the rats' brains. The Morris water maze test and step-down type passive avoidance test were performed to evaluate their memory and cognitive abilities. The oxidation indexes in the hippocampus were detected. Immunohistochemistry was conducted to visualize the receptors for advanced glycation end products (RAGEs) and nuclear factor-kappa-light-chain-enhancer of activated B cell (NF-${\kappa}B$). Results: Behavioral results showed that PG (1 g/kg, 0.5 g/kg, and 0.25 g/kg) significantly shortened the escape latency, remarkably increased the number of crossing times, significantly decreased the number of errors, and prolonged the latency in rats with AGE-induced AD. Panax ginseng also significantly reduced the malondialdehyde level, increased the glutathione content, and increased superoxide dismutase activity in the hippocampus. Panax ginseng significantly decreased the expression of RAGE and NF-${\kappa}B$. The blockade of anti-RAGE antibody could significantly reduce AGE-induced impairments and regulate these expressions. Conclusion: Our results demonstrated that PG significantly inhibits AGE-induced memory impairment and attenuates Alzheimer-like pathophysiological changes. These neuroprotective effects of PG may be associated with the RAGE/NF-${\kappa}B$ pathway. Our results provided the experimental basis for applying PG in preventing and treating AD.
Xiaobin Tan,Junfei Gu,Bingjie Zhao,Shuyuan Wang,Jiarui Yuan,Chunfei Wang,Juan Chen,Jiping Liu,Liang Feng,Xiaobin Jia 고려인삼학회 2015 Journal of Ginseng Research Vol.39 No.2
Background: Ginseng, the root of Panax ginseng (PG), is used widely as a herbal medicine to prevent andtreat various diseases. Panax ginseng has pharmacological effects on neurodegenerative diseases such asAlzheimer’s disease (AD). The present study evaluated the neuroprotective effects of PG and its possibleneuroprotective mechanisms in advanced glycation end product (AGE)-induced AD in a rat model. Methods: Advanced glycation end products were injected bilaterally into the CA3 region of the rats’brains. The Morris water maze test and step-down type passive avoidance test were performed toevaluate their memory and cognitive abilities. The oxidation indexes in the hippocampus were detected. Immunohistochemistry was conducted to visualize the receptors for advanced glycation end products(RAGEs) and nuclear factor-kappa-light-chain-enhancer of activated B cell (NF-kB). Results: Behavioral results showed that PG (1 g/kg, 0.5 g/kg, and 0.25 g/kg) significantly shortened theescape latency, remarkably increased the number of crossing times, significantly decreased the numberof errors, and prolonged the latency in rats with AGE-induced AD. Panax ginseng also significantlyreduced the malondialdehyde level, increased the glutathione content, and increased superoxide dismutaseactivity in the hippocampus. Panax ginseng significantly decreased the expression of RAGE andNF-kB. The blockade of anti-RAGE antibody could significantly reduce AGE-induced impairments andregulate these expressions. Conclusion: Our results demonstrated that PG significantly inhibits AGE-induced memory impairmentand attenuates Alzheimer-like pathophysiological changes. These neuroprotective effects of PG may beassociated with the RAGE/NF-kB pathway. Our results provided the experimental basis for applying PG inpreventing and treating AD.
Genmeng Yang,Juan Li,Yanxia Peng,Baoyu Shen,Yuanyuan Li,Liu Liu,Chan Wang,Yue Xu,Shucheng Lin,Shuwei Zhang,Yi Tan,Huijie Zhang,Xiaofeng Zeng,Qi Li,Gang Lu 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.3
This study investigates the effects of ginsenoside Rb1 (GsRb1) on methamphetamine (METH)-induced toxicity in SH-SY5Y neuroblastoma cells and METH-induced conditioned place preference (CPP)in adult Sprague-Dawley rats. It also examines whether GsRb1 can regulate these effects through theNR2B/ERK/CREB/BDNF signaling pathways. Methods: SH-SY5Y cells were pretreated with GsRb1 (20 mM and 40 mM) for 1 h, followed by METHtreatment (2 mM) for 24 h. Rats were treated with METH (2 mg/kg) or saline on alternating days for 10days to allow CPP to be examined. GsRb1 (5, 10, and 20 mg/kg) was injected intraperitoneally 1 h beforeMETH or saline. Western blot was used to examine the protein expression of NR2B, ERK, P-ERK, CREB, PCREB, and BDNF in the SH-SY5Y cells and the rats' hippocampus, nucleus accumbens (NAc), and prefrontal cortex (PFC). Results: METH dose-dependently reduced the viability of SH-SY5Y cells. Pretreatment of cells with 40mM of GsRb1 increased cell viability and reduced the expression of METH-induced NR2B, p-ERK, p-CREBand BDNF. GsRb1 also attenuated the expression of METH CPP in a dose-dependent manner in rats. Further, GsRb1 dose-dependently reduced the expression of METH-induced NR2B, p-ERK, p-CREB, andBDNF in the PFC, hippocampus, and NAc of rats. Conclusion: GsRb1 regulated METH-induced neurotoxicity in vitro and METH-induced CPP through theNR2B/ERK/CREB/BDNF regulatory pathway. GsRb1 could be a therapeutic target for treating METHinduced neurotoxicity or METH addiction.