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        Decomposable polynomial response surface method and its adaptive order revision around most probable point

        Wentong Zhang,Yiqing Xiao 국제구조공학회 2020 Structural Engineering and Mechanics, An Int'l Jou Vol.76 No.6

        As the classical response surface method (RSM), the polynomial RSM is so easy-to-apply that it is widely used in reliability analysis. However, the trade-off of accuracy and efficiency is still a challenge and the “curse of dimension” usually confines RSM to low dimension systems. In this paper, based on the univariate decomposition, the polynomial RSM is executed in a new mode, called as DPRSM. The general form of DPRSM is given and its implementation is designed referring to the classical RSM firstly. Then, in order to balance the accuracy and efficiency of DPRSM, its adaptive order revision around the most probable point (MPP) is proposed by introducing the univariate polynomial order analysis, noted as RDPRSM, which can analyze the exact nonlinearity of the limit state surface in the region around MPP. For testing the proposed techniques, several numerical examples are studied in detail, and the results indicate that DPRSM with low order can obtain similar results to the classical RSM, DPRSM with high order can obtain more precision with a large efficiency loss; RDPRSM can perform a good balance between accuracy and efficiency and preserve the good robustness property meanwhile, especially for those problems with high nonlinearity and complex problems; the proposed methods can also give a good performance in the high-dimensional cases.

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        Modulatory Potential of LncRNA Zfas1 for Inflammation and Neuronal Apoptosis in Temporal Lobe Epilepsy

        Chuan He,Caixia Su,Wentong Zhang,Qin Zhou,Xu Shen,Junjie Yang,Naixian Shi 연세대학교의과대학 2021 Yonsei medical journal Vol.62 No.3

        Purpose: This study aimed to elucidate whether lncRNA ZFAS1 is involved in neuronal apoptosis and inflammation in temporal lobe epilepsy (TLE). Materials and Methods: Ninety-six TLE patients were recruited, and their peripheral venous blood was gathered to determine Zfas1 expression with polymerase chain reaction. Neurons were separated from hippocampal tissue of newborn SD rats, and siZfas1 or pcDNA3.1-Zfas1 was transfected into the neurons. Inflammatory cytokines released by neurons were determined, and neuronal activities were evaluated through MTT assay, colony formation assay, and flow cytometry. Results: Serum levels of Zfas1 were higher in TLE patients than in healthy controls (p<0.05). Furthermore, Zfas1 expression in neurons was raised by pcDNA3.1-Zfas1 and declined after silencing of Zfas1 (p<0.05). Transfection of pcDNA-Zfas1 weakened the viability and proliferation of neurons and increased neuronal apoptosis (p<0.05). Meanwhile, pcDNA3.1-Zfas1 transfection promoted lipopolysaccharide-induced release of cytokines, including tumor necrosis factor-α, interleukin (IL)-1, IL-6, and intercellular adhesion molecule-1 (p<0.05), and boosted NF-κB activation by elevating the expression of NF-κB p65, pIκBα, and IKKβ in neurons (p<0.05). Conclusion: Our results indicated that lncRNA ZFAS1 exacerbates epilepsy development by promoting neuronal apoptosis and inflammation, implying ZFAS1 as a promising treatment target for epilepsy.

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