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| 1 | 一种可滑移式铅芯橡胶支座的显式数值模拟与试验验证(英文)显示文摘目的:随着隔震技术在工程结构中的逐步推广应用,橡胶隔震支座的试验与数值模拟都得到国内外工程研究人员的重视。其中后者因支座大变形时计算较难收敛、铅芯与周边橡胶以及钢板的复杂接触关系较难模拟、采用隐式积分算法时计算规模较难控制等问题,目前仍是这一方向的研究热点。本文旨在探讨基于显式积分算法对一种新型可滑移式铅芯橡胶支座进行准确可行的数值模拟的方法。创新点:1.探究基于显式积分算法的隔震支座数值模拟方法;2.采取多种方法有效地控制了数值模拟计算规模,同时实现了较高的数值模拟精度;3.采用程序中提供的3种接触方式较好地模拟了支座中存在的复杂接触关系。方法:本文主要采用4种方法减小数值模拟计算规模:1.激活程序内置的质量缩放功能;2.合理增大支座中对支座竖向刚度与水平剪切性能影响较小的非关键部件——叠层钢板的厚度;3.合理减小叠层钢板的弹性模量;4.考虑到支座中所有材料均未考虑材料的率变效应,即加载速率对支座的力学性能没有影响,本文数值模拟中所用加载频率为实际加载频率的10倍。此外,本文采用了一般接触、绑定接触与单边接触模拟支座中不同的接触关系。结论:1.显式积分的计算时间步长由2.4×10-7 s增大到3.5×10-6 s;2.与试验结果对比验证了本文提出的基于显式积分算法对该新型可滑移式铅芯橡胶支座进行数值模拟的方法的准确实用性;3.该支座在纯压作用下,部分铅芯发生塑性变形,而在最大剪切位移时,铅芯发生了很大的塑性流动变形;4.与采用隐式算法对该支座进行数值模拟研究所用时间相比,显式算法所用时间少很多。 | Yi-feng WU Hao WANG Ai-qun LI Dong-ming FENG Ben SHA Yu-ping ZHANG | 2017 | Journal of Zhejiang University-Science A(Applied Physics & Engineering)2017，18，5： | 2 |
| 2 | Caveolae-dependent Endocytosis Is Required for Class A Macrophage Scavenger Receptor-mediated Apoptosis in Macrophages显示文摘 | Zhu, Xu-Dong Zhuang, Yan Ben, Jing-Jing Qian, Ling-Ling Huang, Han-Peng Bai, Hui Sha, Jia-Hao He, Zhi-Gang Chen, Qi | 2011 | 南京医科大学学报(自然科学版)2011，31，6： | 1 |
| 3 | Analysis of flavonoids from lotus (Nelumbo nucifera) leaves using high performance liquid chromatography/ photodiode array detector tandem electrospray ionization mass spectrometry and an extraction method optimized by orthogonal design显示文摘 | Sha C N Ben H Wub | 2012 | Journal of Chromatography A2012，1227，： | 1 |
| 4 | Glucose-regulated protein 78 inhibits scavenger receptor A-mediated internalization of acetylated low density lipoprotein显示文摘Class A scavenger receptor(SR-A) plays an important role in foam cell formation.However, the mechanism underlying the internalization of the receptor-ligand complexes remains unclear.The aim of the present study was to investigate the molecular mechanism to regulate SR-A-mediated intracellular lipid accumulation in macrophages A pull-clown assay was performed and glucoseregulated protein 78(GRP78) was identified to bind with the cytoplasmic domain of SR-A(CSR-A).Immunoprecipitation and artificially expressed protein binding assay demonstrated the direct specific binding of GRP78 with SR-A in cells.Indirect immunofluorescence assay and western blot analysis showed their co-localization in membrane and cytoplasm.Over-expression of GRP78 specifically inhibited SR-A-mediated uptake of fluorescent acetylated low-density lipoprotein, a specific ligand for SR-A, without altering cellular SR-A expression and binding ability, and significantly inhibited cholesterol ester accumulation in cells, which can be partly attributed to the suppression of c-Jun-NH2-terminal kinase signaling pathway.These results suggest that GRP78 may act as an inhibitor of SR-A-mediated internalization of modified low-density lipoprotein into macrophages(C) 2009 Elsevier Inc.All rights reserved. | Ben, Jingjing Gao, Song Zhu, Xudong Zheng, Yuan Zhuang, Yan Bai, Hui Xu, Yong Ji, Yong Sha, Jiahao He, Zhigang Chen, Qi | 2010 | 南京医科大学学报(自然科学版)2010，30，1： | 0 |
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