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Optimization Model of Reliable Data Storage in Cloud Environment Using Genetic Algorithm
Feng Liu,Haitao Wu,Xiaochun Lu,Xiyang Liu 보안공학연구지원센터 2014 International Journal of Grid and Distributed Comp Vol.7 No.6
Massive data storage is one of the great challenges for cloud computing service, and reliable storage of sensitive data directly affects quality of storage service. In this paper, based on analysis of data storage process in cloud environment, the cost of massive data storage is considered to be comprised of data storage price, data migration and communication; and the storage reliability consists of data transmission reliability and hardware dependability. A multi-objective optimization model for reliable massive storage is proposed, in which storage cost and reliability are the objectives. Then, a genetic algorithm for solving the model is designed. Finally, experimental results indicate that the proposed model is positive and effective.
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Parallel Distributed Acceleration Based on MPI and OpenMP Technology
Feng Liu,Haitao Wu,Xiaochun Lu,Xiyang Liu 보안공학연구지원센터 2015 International Journal of Grid and Distributed Comp Vol.8 No.6
In order to speed up data processing in a signal monitoring and evaluation system, we need to use a parallel method. It is obvious that the traditional stand-alone store has no ability to satisfy the performance requirements, and the use of single core CPU is unable to content the severe requirement of speed. Consequently, multi-machine parallel acceleration technique based on MPI (cooperated with multi-core parallel acceleration technique based on OpenMP) can effectively solve all above problems. In this paper, a parallel distributed acceleration framework based on MPI and Open MP technology was given. Experimental tests were carried to verify our proposal. Finally, some suggestions to speed up the data processing was given.
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Huang Guangwei,Bao Hailong,Zhan Peng,Lu Xiyang,Duan Zonggang,Xiong Xinlin,Lin Muzhi,Wang Bing,An Hongxin,Xiahou Luanda,Zhou Haiyan,Luo Zhenhua,Li Wei 대한독성 유전단백체 학회 2024 Molecular & cellular toxicology Vol.20 No.2
Objectives This study aimed at investigating the role of the proprotein convertase subtilisin/Kexin type 9 (PCSK9)-mediated autophagy on myocardial ischemia/reperfusion injury (MIRI). To determine the relationship between autophagy, apoptosis, fibrosis, and inflammation in the myocardium, to provide experience in preventing and treating the myocardial ischemia/reperfusion (I/R) injury. Methods An AC16 hypoxia-reoxygenation model and a rat myocardial ischemia–reperfusion model were established. The concentrations of cardiac troponin T (cTnT) and creatine kinase-MB (CKMB) in plasma were measured by ELISA. To determine the size of the myocardial infarction, TTC/EB staining was performed. In addition to identifying pathological changes in myocardial tissue, Masson’s trichrome stains and H&E stains were used to identify pathological changes. Echocardiography was employed to detect cardiac function. Western blot analysis was then performed to detect the protein expression of Parkin, Pink1, and markers associated with autophagy (Beclin-1, p62, LC3). Results A significant increase in PCSK9 was observed in the myocardium during H/R. In the cardiac-specific PCSK9 knockdown model, cardiac autophagy was significantly inhibited, whereas cardiac-specific PCSK9 overexpression promoted cardiac autophagy. In vivo studies have demonstrated a significant decrease in cardiac autophagy when the PCSK9 inhibitor was administered. Apoptosis induced by I/R was greatly decreased, and myocardial infarction size and function were both improved by PCSK9 inhibitors. Mechanistically, the PCSK9 inhibitor improved the degree of myocardial fibrosis and inhibited the development of inflammation. Conclusions Our results demonstrated that increased PCSK9 via the parkin/pink1 signaling pathway contributes to I/R and H/R by exaggerating excessive autophagy during reperfusion/reoxygenation. In addition, the PCSK9 inhibitor blocked the development of inflammation and improved Infarct size, myocardial function, and myocardial fibrosis.
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