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Xiajun Ding,Hongbo Bi,Xiaodan Jiang,Lu zhang 보안공학연구지원센터 2016 International Journal of Future Generation Communi Vol.9 No.3
With the development of sensor technology, network technology, embedded control technology and wireless communication technology, the application of wireless sensor networks (WSN) has become more and more widely. Wireless sensor networks have been named the most influential and important technology of the world in twenty-first Century. In wireless sensor networks, data fusion is an important research branch. In this paper, a data prediction model of wireless sensor network based on weight improved particle swarm optimization neural network algorithm is proposed. In view of the deficiency of the traditional BP neural network model, this paper combines with the characteristics of the data prediction model, and the BP neural network model is improved and integrated. After that, we train the neural network's sample set, and add the momentum item to correct the weight, so that the neural network can be predicted more quickly and accurately. The main idea of this paper is to predict the future data based on the historical data which are collected by sensor nodes, so as to achieve the purpose of reducing the amount of data transmission in the network and saving the energy of nodes. Finally, the experimental results show that the improved particle swarm optimization algorithm based on weight improved particle swarm optimization neural network algorithm has higher accuracy than the multiple regression method and the grey prediction method. In addition, the method can be used to effectively save energy in wireless sensor data transmission.
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Xin YANG,Huiyin ZHENG,Xiajun YI 한국유통과학회 2018 KODISA ICBE (International Conference on Business Vol.2018 No.-
In recent years, FinTech has become a new force in the financial industry. The development of FinTech is undoubtedly an improvement in both financial product and services. New technologies such as P2P finance, blockchain and mobile payment are gradually approaching daily life, and the increasing demand of users also test the innovation and competitiveness of FinTech companies. Innovation efficiency directly affects the development of finance and also affects economic development. Therefore, from the perspective of innovation efficiency and government supervision of China s FinTech, this paper analyzes the strategic choices among financial technology enterprises and governments by means of game theory model, and discusses the interaction between innovation efficiency of Chinese FinTech and government supervision. In summary, to improve the innovation efficiency of China s FinTech enterprises, we need to start from two aspects, one is the financial technology enterprise itself, and the other is the government. As the financial market is in a constantly changing environment, financial technology companies and governments should also change from time to time and make corresponding adjustments in a timely manner. Therefore, the level of China s financial technology innovation efficiency and regulatory issues are the core issues of China s financial technology development.
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miRNA-183 Suppresses Apoptosis and Promotes Proliferation in Esophageal Cancer by Targeting PDCD4
Miao Yang,Ran Liu,Xiajun Li,Juan Liao,Yuepu Pu,Enchun Pan,Lihong Yin,Yi Wang 한국분자세포생물학회 2014 Molecules and cells Vol.37 No.12
In our previous study, miRNA-183, a miRNA in the miR-96-182-183 cluster, was significantly over-expressed in esophageal squamous cell carcinoma (ESCC). In the present study, we explored the oncogenic roles of miR-183 in ESCC by gain and loss of function analysis in an esophageal cancer cell line (EC9706). Genome-wide mRNA microarray was applied to determine the genes that were regulated directly or indirectly by miR-183. 3UTR luciferase reporter assay, RT-PCR, and Western blot were conducted to verify the target gene of miR-183. Cell culture results showed that miR-183 inhibited apoptosis (p < 0.05), enhanced cell proliferation (p < 0.05), and accelerated G1/S transition (p < 0.05). Moreo-ver, the inhibitory effect of miR-183 on apoptosis was rescued when miR-183 was suppressed via miR-183 inhibitor (p < 0.05). Western blot analysis showed that the expression of programmed cell death 4 (PDCD4), which was predicted as the target gene of miR-183 by microarray profiling and bioinformatics predictions, decreased when miR-183 was over-expressed. The 3'UTR luciferase reporter assay confirmed that miR-183 directly regulated PDCD4 by binding to sequences in the 3'UTR of PDCD4. Pearson correlation analysis fur-ther confirmed the significant negative correlation between miR-183 and PDCD4 in both cell lines and in ESCC patients. Our data suggest that miR-183 might play an oncogenic role in ESCC by regulating PDCD4 expression.
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miRNA-183 Suppresses Apoptosis and Promotes Proliferation in Esophageal Cancer by Targeting PDCD4
Yang, Miao,Liu, Ran,Li, Xiajun,Liao, Juan,Pu, Yuepu,Pan, Enchun,Yin, Lihong,Wang, Yi Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.12
In our previous study, miRNA-183, a miRNA in the miR-96-182-183 cluster, was significantly over-expressed in esophageal squamous cell carcinoma (ESCC). In the present study, we explored the oncogenic roles of miR-183 in ESCC by gain and loss of function analysis in an esophageal cancer cell line (EC9706). Genome-wide mRNA micro-array was applied to determine the genes that were regulated directly or indirectly by miR-183. 3'UTR luciferase reporter assay, RT-PCR, and Western blot were conducted to verify the target gene of miR-183. Cell culture results showed that miR-183 inhibited apoptosis (p < 0.05), enhanced cell proliferation (p < 0.05), and accelerated G1/S transition (p < 0.05). Moreover, the inhibitory effect of miR-183 on apoptosis was rescued when miR-183 was suppressed via miR-183 inhibitor (p < 0.05). Western blot analysis showed that the expression of programmed cell death 4 (PDCD4), which was predicted as the target gene of miR-183 by microarray profiling and bioinformatics predictions, decreased when miR-183 was over-expressed. The 3'UTR luciferase reporter assay confirmed that miR-183 directly regulated PDCD4 by binding to sequences in the 3'UTR of PDCD4. Pearson correlation analysis further confirmed the significant negative correlation between miR-183 and PDCD4 in both cell lines and in ESCC patients. Our data suggest that miR-183 might play an oncogenic role in ESCC by regulating PDCD4 expression.
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