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RISS 인기검색어
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- 저자 : Hesheng Shi (검색결과 2 건)
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Dynamic Behavior Analysis of a Class of Neurons Network Model
Kaijun Wu,Hesheng Shi,Huaiwei Lu,Yazhou Shan 보안공학연구지원센터 2015 International Journal of Signal Processing, Image Vol.8 No.2
A mathematical model of neurons network cells was studied. Firstly the study conducted numerical calculation by the C language program, and then simulated drawings with the grapher to analyze the model's complex dynamic conduct under different control parameters in the change interval of bifurcation parameter. Period-adding bifurcation and period doubling bifurcation must exist in the graph of ISI for different control parameters. As the external electric fields join in, the dynamic conduct of neuron model will change under corresponding parameters. The research results indicate external electric fields can change the discharge range of the model, which is helpful to explore the influence of external electric field on the excitability of biological neural system and pathogenic mechanism of neural system disease.
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Fan Wang,Renliang Yu,Shengnan Wen,Jie Yin,Yugen Shi,Hesheng Hu,Suhua Yan 대한약학회 2021 Archives of Pharmacal Research Vol.44 No.5
Myocardial infarction (MI) is one of the leadingcauses of high mortality worldwide. Long non-codingRNA myocardial infarction associated transcript (MIAT)and mitochondrial coupling factor 6 (CF6) aggravate MI. This study aimed to elucidate whether miR-203 interactedwith MIAT and CF6 in MI. Results revealed that MIAT andCF6 expressions were upregulated and that miR-203 wasdownregulated in mouse myocardial tissues after MI, as wellas in hypoxic mouse cardiomyocytes. The overexpressionof MIAT in mouse cardiomyocytes raised CF6 expression,whereas the knockdown of MIAT had the opposite eff ect. Mechanistically, the luciferase reporter and RNA pull-downassays corroborated the binding between miR-203 and CF63′UTR and between miR-203 and MIAT. The simultaneousoverexpression of miR-203 and MIAT restored the reductionof CF6 caused by miR-203 overexpression alone, andthe overexpression of miR-203 diminished the percentage ofinfarct area and the apoptosis of cardiomyocytes in vivo. Our fi ndings corroborate that overexpressing miR-203 alleviatesMI via interacting with MIAT and CF6.
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