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- 저자 : Jing Quanmin (검색결과 2 건)
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Shaoxue Jing,Tianhong Pan,Quanmin Zhu 제어·로봇·시스템학회 2022 International Journal of Control, Automation, and Vol.20 No.10
In this paper, a novel stochastic gradient algorithm based on the minimum Renyi entropy is proposed to identify a nonlinear rational model contaminated by the impulse noise. Firstly, the minimum error entropy using the Epanechnikov kernel is taken to suppress the impulse noise. Secondly, the stochastic gradient of the Renyi entropy rather than the Shannon entropy is adopted to decrease the computational cost. Finally, an adaptive step size considering the energy of the errors is used to accelerate the algorithm. The proposed algorithm is validated by numerical examples and case study. Results show that the algorithm can give accurate estimates with a fast convergence rate for the nonlinear rational model with the impulse noise.
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Liu Dan,Xing Ruinan,Zhang Quanyu,Tian Xiaoxiang,Qi Yanping,Song Haixu,Liu Yanxia,Yu Haibo,Zhang Xiaolin,Jing Quanmin,Yan Chenghui,Han Yaling 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Autophagy plays an important role in the development of diabetic cardiomyopathy. Cellular repressor of E1A-stimulated genes 1 (CREG1) is an important myocardial protective factor. The aim of this study was to investigate the effects and mechanisms of CREG1 in diabetic cardiomyopathy. Male C57BL/6 J mice, Creg1 transgenic mice and cardiac-specific knockout mice were used to establish a type 2 diabetes model. Small animal ultrasound, Masson’s staining and western blotting were used to evaluate cardiac function, myocardial fibrosis and autophagy. Neonatal mouse cardiomyocytes (NMCMs) were stimulated with palmitate, and the effects of CREG1 on NMCMs autophagy were examined. CREG1 deficiency exacerbated cardiac dysfunction, cardiac hypertrophy and fibrosis in mice with diabetic cardiomyopathy, which was accompanied by exacerbated autophagy dysfunction. CREG1 overexpression improved cardiac function and ameliorated cardiac hypertrophy and fibrosis in diabetic cardiomyopathy by improving autophagy. CREG1 protein expression was decreased in palmitate-induced NMCMs. CREG1 knockdown exacerbated cardiomyocyte hypertrophy and inhibited autophagy. CREG1 overexpression inhibited cardiomyocyte hypertrophy and improved autophagy. LAMP2 overexpression reversed the effect of CREG1 knockdown on palmitate-induced inhibition of cardiomyocyte autophagy. CREG1 inhibited LAMP2 protein degradation by inhibiting the protein expression of F-box protein 27 (FBXO27). Our findings indicate new roles of CREG1 in the development of diabetic cardiomyopathy.
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