基于InSAR的西安地面沉降与地裂缝发育特征研究

哺乳动物细胞胞质分裂过程中伴随着一系列形态学改变,随着分裂沟不断收缩,形成连接两 个子细胞的细胞间桥. 间桥不断拉长、变细,直至断裂、生成两个子细胞. 采用细胞力学 和形态学测量及分析方法,通过施加肌球蛋白II抑制剂,定量研究了NRK细胞间桥变细动力 学; 采用细胞免疫荧光技术, 检测了早期胞质分裂肌动蛋白的分布,揭示肌球蛋白II缺失细 胞胞质分裂可能的机制. 结果表明：施加肌球蛋白II抑制剂的NRK细胞, 其整体形态学和细胞 间桥形态学曲线明显不同于0.3%DMSO组. 根据流体力学特性和所测量的力学参数对曲线 进行模拟发现,表面张力对肌球蛋白II抑制组细胞的间桥动力学曲线轨迹影响很大. 研究结 果提示由细胞力学特性决定的拉普拉斯压力和细胞运动共同参与了肌球蛋白II缺失细胞胞 质分裂的调节.     

肌球蛋白Ⅱ缺失细胞胞质分裂机制研究

哺乳动物细胞胞质分裂过程中伴随着一系列形态学改变,随着分裂沟不断收缩,形成连接两个子细胞的细胞间桥.间桥不断拉长、变细,直至断裂、生成两个子细胞.采用细胞力学和形态学测量及分析方法,通过施加肌球蛋白Ⅱ抑制剂,定量研究了NRK细胞间桥变细动力学;采用细胞免疫荧光技术,检测了早期胞质分裂肌动蛋白的分布,揭示肌球蛋白Ⅱ缺失细胞胞质分裂可能的机制.结果表明:施加肌球蛋白Ⅱ抑制剂的NRK细胞,其整体形态学和细胞间桥形态学曲线明显不同于0.3%DMSO组.根据流体力学特性和所测量的力学参数对曲线进行模拟发现,表面张力对肌球蛋白Ⅱ抑制组细胞的间桥动力学曲线轨迹影响很大.研究结果提示由细胞力学特性决定的拉普拉斯压力和细胞运动共同参与了肌球蛋白Ⅱ缺失细胞胞质分裂的调节.     

基于微丝主动收缩的细胞分裂的力学模型

为了解释动物细胞胞质分裂的力学机理，基于大量的细胞卵裂实验数据，在Zinemanas和 Nir的流体动力学模型基础上，对微丝的分布函数改为随同质膜移动，增加了由于生化刺激 引起主动微丝的影响系数. 数值计算表明：此模型能较好地预测细胞在胞质分裂过程中，细 胞的总体和局部变形，以及卵裂沟处的张力和细胞内压.     

复合材料的宏观性能与参数设计

本文综述了预测复合材料宏观性能──有效刚度的几类方法：自洽模型、单胞模型以及它们的结合──自洽有限元法．阐述了复合材料发生弹塑性变形时的有关力学问题．基于细观力学的定量分析结果，探讨了面向材料宏观刚度的细观结构参数设计的基本原则，以期对建立复合材料细观结构设计的力学和数学模型有所启发．     

部分充液多胞元结构的面内动态力学特性研究

为探究部分充液多胞元结构的抗冲击防护性能,结合充液内凹胞元的落锤冲击试验,建立了充液内凹胞元、部分充液内凹多胞元结构的冲击动态特性二维FEM数值分析,计算得到了部分充液内凹多胞元结构的变形破坏模式,讨论了不同冲击速度下部分充液内凹多胞元结构的动力学响应特性。结果表明:在充液胞元破损后,水介质会流入相邻未充液胞元,形成二次鼓胀吸能效应,从而有效提高结构壁面的变形吸能水平;结构中的充液区域和未充液区域的变形破坏模式分别为鼓胀拉伸和屈曲弯折;随着冲击速度的提高,结构的单位体积应变能以及对初始冲击载荷的削弱作用均得到增强。横向充液方式可以等效为变刚度弹簧的串联布置,该方式仅影响结构的局部刚度,纵向充液方式可以等效为多层变刚度弹簧的并联布置,该方式会影响结构的整体刚度;充液区域与未充液区域的等效刚度呈动态变化,结构变形模式由各区域实时的等效刚度决定。当载荷冲击速度较高时,横向和纵向部分充液内凹多胞元结构对初始冲击载荷的削弱能力均优于未充液内凹多胞元结构。     

微流控通道内细胞及其初级纤毛的力传导行为

细胞处于复杂的生理环境之下,附着在细胞表面的初级纤毛被认为是重要的力学信号传感器,其与细胞的代谢、发育、分裂和增殖等生理活动密切相关.为了研究细胞及其初级纤毛在微流体环境下的力传导行为,本文建立了力-电协同驱动下的矩形微流控通道和含有多孔黏弹性属性的贴壁细胞有限元模型系统.考察了细胞的细胞质和细胞核在振荡层流下的应力、应变、孔隙压力和孔隙流速等力学信号响应,量化研究了初级纤毛作为细胞独特的力学感受器的生物力学行为. 结果表明:细胞在振荡层流下的力学响应表现出和外加力-电驱动载荷相同的震荡规律.渗透率是细胞多孔弹性力学行为的主要影响因素. 初级纤毛是细胞主要的力学感受器,细胞可以通过纤毛长度和直径调节其力学感受敏感性(应力影响区域),随着初级纤毛长度的增大, 其纤毛挠曲刚度减小, 但是敏感性增大.模型的建立为进一步研究微流体剪切作用下的细胞生长、分化等微观机理提供基础,同时也为检测细胞微结构器(纤毛等蛋白链)的力学性能提供了理论技术支持.      

MECHANOTRANSDUCTION OF THE CELL AND ITS PRIMARY CILIUM IN THE MICROFLUIDIC CHANNEL 1)

细胞处于复杂的生理环境之下,附着在细胞表面的初级纤毛被认为是重要的力学信号传感器,其与细胞的代谢、发育、分裂和增殖等生理活动密切相关.为了研究细胞及其初级纤毛在微流体环境下的力传导行为,本文建立了力-电协同驱动下的矩形微流控通道和含有多孔黏弹性属性的贴壁细胞有限元模型系统.考察了细胞的细胞质和细胞核在振荡层流下的应力、应变、孔隙压力和孔隙流速等力学信号响应,量化研究了初级纤毛作为细胞独特的力学感受器的生物力学行为. 结果表明:细胞在振荡层流下的力学响应表现出和外加力-电驱动载荷相同的震荡规律.渗透率是细胞多孔弹性力学行为的主要影响因素. 初级纤毛是细胞主要的力学感受器,细胞可以通过纤毛长度和直径调节其力学感受敏感性(应力影响区域),随着初级纤毛长度的增大, 其纤毛挠曲刚度减小, 但是敏感性增大.模型的建立为进一步研究微流体剪切作用下的细胞生长、分化等微观机理提供基础,同时也为检测细胞微结构器(纤毛等蛋白链)的力学性能提供了理论技术支持.     

动压型分段式圆周密封变形特性及其调控策略研究

在流固耦合作用下，分段式圆周密封的变形特性和密封间隙形状是影响密封运行稳定性和可靠性的关键.通过建立动压型分段式圆周密封的流固耦合模型，研究了密封间隙的流场特性和结构变形规律，采用正交试验设计分析了影响密封变形的主要力学参数，包括密封压差、周向弹簧初始载荷和刚度、轴向弹簧初始载荷和刚度，并探讨了接头形状、接头间隙及辅助密封面槽型对密封环的变形调控效果.结果表明：在流体压力和弹簧力的共同作用下，变形后单段密封环的主密封面径向间隙沿周向呈现中间大两端小、沿轴向泄漏方向呈单调递减的变化趋势；力学参数中密封压差对密封环的变形影响最为显著，其次为周向弹簧初始载荷，最小为周向弹簧刚度；通过合理的接头形状和辅助密封面槽型的设计有望显著改善密封环的变形特性，获得分布更为均匀的主密封面径向间隙.     

车用发动机自动张紧器静态力学特性实测分析

自动张紧器是发动机前端附件驱动系统(front and accessory drive, FEAD)中,用于减小张紧轮两侧带段张力波动和带段横向振动位移的主要零部件之一. 张紧器的静态力学特性的评价参数包括张紧器的静刚度、初始扭矩和阻尼系数. 介绍了张紧器力-位移曲线的实验方法,以及张紧器扭矩-角位移曲线、性能评价参数的求解方法. 张紧器静态力学特性实测数据,为FEAD 系统静态、动态特性计算提供数据基础. 实验方法为类似旋转运动件的扭转静刚度测试提供参考.     

曲壁蜂窝夹层板的振动特性研究

曲壁蜂窝具有负刚度特性,可以在大变形过程中吸收能量、抗冲击,并且在冲击过后可以自我恢复而不像传统蜂窝被压溃。本文将曲梁构成的负刚度蜂窝作为芯层,建立夹层板的动力学模型;推导出了曲壁负刚度蜂窝胞元的等效弹性参数,将其周期性排列为蜂窝芯,应用Reddy高阶剪切变形理论、Von-Karman大变形关系和Hamilton原理推导了负刚度蜂窝夹层板的非线性动力学方程;应用Navier法计算了四边简支边界条件下的固有频率。并利用有限元软件ABAQUS建立模型,计算固有频率,与理论计算结果进行比较,结果显示二者的计算结果具有较好的一致性,验证了芯层等效弹性参数及模型的有效性。探讨了在蜂窝胞元具有较高吸能情形下,夹层板在不同芯层厚度、不同芯厚比以及不同胞元曲壁厚度时的固有频率的变化特性。     

Microstructure and Tensile Mechanical Properties of Anisotropic Rigid Polyurethane Foam

An understanding of the mechanical properties of solid foams facilitates effective use of such materials, which are often deployed in load-bearing applications such as impact absorbers, cushioning and sandwich structures. This study is an experimental investigation that focuses on the deformation response of rigid polyurethane foam to tension. Microstructural features such as the size and geometry of constituent cells and the struts that define the cell edges, as well as their stiffness and tensile strength, are examined. The nature of cell deformation and fracture are identified through microscopy and the associated micromechanics analyzed. Results show that the cells are elongated and thus the foam exhibits anisotropic properties. Flexure of the struts that define the cell edges is the primary mechanism governing deformation and failure. Information on the mechanical, microstructural and deformation characteristics elicited through this investigation will facilitate formulation of idealized cell-based models to account for the mechanical response of rigid polymeric foams.     

Biomechanics of stem cells

干细胞生物力学作为生物力学的重要分支和前沿学科,近年来在力学-生物学、力学-化学耦合等方面取得了重大进展,已成为生物力学乃至生物医学工程最活跃的领域之一,并对发生物学、干细胞生物学、组织修复、再生医学等相关领域产生重要影响.干细胞具有独特的力学性质,可感知、传递、转导和响应生理力学微环境的改变,从而调控干细胞的生长、分化等功能,体现出典型的力学-生物学耦合特征.本文将对干细胞的力学性质与细胞力学模型、在体力学环境对干细胞生长和分化的影响、干细胞对外界力学刺激的响应等方面加以综述.     

Dissecting the Molecular Basis of the Mechanics of Living Cells

Cells establish and modulate their morphology and mechanics through the use of structural networks whose components range in size from a few nanometers to tens of micrometers. Over the past two decades, an exciting suite of sophisticated micro- and nanoscale technologies has emerged that permits investigators to directly probe structural and functional contributions of these components in living cells. Here we review underlying principles and recent applications of four such approaches: atomic force microscopy, subcellular laser ablation, micropatterning, and microfluidics. Together, these new tools are offering valuable insight into the molecular basis of cell structure and mechanics and revealing the remarkably broad influence of the mechanical microenvironment on many aspects of cell biology.     

Mechanopathology of red blood cell diseases — Why mechanics matters

During the onset of a disease a cell may experience alterations in both the composition and organization of its cellular and molecular structures. These alterations may eventually lead to changes in its geometrical and mechanical properties such as cell size and shape, deformability and adhesion. As such, knowing how diseased cells respond to mechanical forces can reveal ways by which they differ from healthy ones. Here, we will present biomechanistic insights into red blood cell related diseases that manifest mechanical property changes and how they directly contribute to the pathophysiology of diseases. By conducting cell and molecular mechanics studies, not only can we elucidate changes in the structure-property-function relationship of diseased cells, we can also exploit the new knowledge gained to develop biomechanics based devices that may better detect and diagnose these diseases as well as help identify important biomechanical targets for possible therapeutic interventions.     

Quantification of the stiffness and strength of cadherin ectodomain binding with different ions

The stiffness and strength of extracellular (EC) region of cadherin are proposed to be two important mechanical properties both for cadherin as a mechanotransductor and for the formation of cell-cell adhesion. In this study, we quantitatively characterized the stiffness and strength of EC structure when it binds with different types of ions by molecular dynamics simulations. Results show that EC structure exhibits a rod-like shape with high stiffness and strength when it binds with the bivalent ions of calcium or magnesium. However, it switches to a soft and collapsed conformation when it binds with the monovalent ions of sodium or potassium. This study sheds light on the important role of the bivalent ions of calcium in the physiological function of EC.     

Some basic questions on mechanosensing in cell–substrate interaction

Cells constantly probe their surrounding microenvironment by pushing and pulling on the extracellular matrix (ECM). While it is widely accepted that cell induced traction forces at the cell–matrix interface play essential roles in cell signaling, cell migration and tissue morphogenesis, a number of puzzling questions remain with respect to mechanosensing in cell–substrate interactions. Here we show that these open questions can be addressed by modeling the cell–substrate system as a pre-strained elastic disk attached to an elastic substrate via molecular bonds at the interface. Based on this model, we establish analytical and numerical solutions for the displacement and stress fields in both cell and substrate, as well as traction forces at the cell–substrate interface. We show that the cell traction generally increases with distance away from the cell center and that the traction-distance relationship changes from linear on soft substrates to exponential on stiff substrates. These results indicate that cell adhesion and migration behaviors can be regulated by cell shape and substrate stiffness. Our analysis also reveals that the cell traction increases linearly with substrate stiffness on soft substrates but then levels off to a constant value on stiff substrates. This biphasic behavior in the dependence of cell traction on substrate stiffness immediately sheds light on an existing debate on whether cells sense mechanical force or deformation when interacting with their surroundings. Finally, it is shown that the cell induced deformation field decays exponentially with distance away from the cell. The characteristic length of this decay is comparable to the cell size and provides a quantitative measure of how far cells feel into the ECM.     

聚合物分子链微结构-力学性能关系的数据驱动模型

聚合物一般由随机分布的大分子链组成,分子链的分布、缠绕、交联等微结构状态显著影响聚合物的力学和物理性能。本文通过数据驱动方法,建立了聚合物分子链微结构-力学性能关系。使用有限元方法建立了两种分子链的随机微结构模型并得到了其力学性能。基于微结构-力学性能关系建立数据集,以聚合物的随机分子链微结构为输入,以聚合物的弹性刚度为响应输出,进行数据驱动模型的训练和验证。得到了精度满意的微结构-力学性能关系的分析结果。结果表明,通过数据驱动方法研究聚合物的弹性刚度问题是可靠的。     

Mechanical Properties of two novel planar lattice structures

Two novel statically indeterminate planar lattice materials are designed: a new Kagome cell (N-Kagome) and a statically indeterminate square cell (SI-square). Their in-plane mechanical properties, such as stiffness, yielding, buckling and collapse mechanisms are investigated by analytical methods. The analytical stiffness is also verified by means of finite element (FE) simulations. In the case of uniaxial loading, effective modulus, yield strength, buckling strength and critical relative density are compared for various lattice structures. At a critical relative density, the collapse mode will change from buckling to yielding. Elastic buckling under macroscopic shear loading is found to have significant influence on failure of lattice structures, especially at low relative densities. Comparison of the analytical bulk and shear moduli with the Hashin–Shtrikman bounds indicates that the mechanical properties of the SI-square honeycomb are relatively close to being optimal. It is found that compared with the other existing stretching-dominated 2D lattice structures, the N-Kagome cell possesses the largest continuous cavities for fixed relative densities and wall thicknesses, which is convenient for oil storage, disposal of heat exchanger, battery deploying and for other functions. And the initial yield strength of the N-Kagome cell is slightly lower than that of the Kagome cell. The SI-square cell has similar high stiffness and strength as the mixed cell while its buckling resistance is about twice than that of the mixed cell.     

MSC折纸结构设计及其双稳态解析与实验

折纸是一门古老艺术,其本质是将平面材料沿着事先设计好的折痕进行折叠,进而形成一个复杂的三维结构．柔性折纸结构是实现三维结构轻量化的重要途径．因此,解析折纸结构几何特性和力学性质十分必要．本文以MSC(Magic Spiral Cube)为研究对象,通过实际折痕和虚拟折痕的方法,建立了该结构的几何模型,确定了实现完全展开和完全折叠对刚性面和可变形面的设计条件,在虚拟折痕上引入了扭转刚度,证明了该扭转刚度与柔性面变形的等效性,从而得到了MSC 折纸结构的弹性势能,得到了使结构变形的力与位移本构．通过力学特性分析,发现了MSC折纸结构具有双稳态特性,这种特性是由面内变形诱发的,与虚拟折痕刚度与弹性折痕刚度的比值有直接的关系．最后,我们对MSC折纸结构进行设计和制备,通过实验,验证了理论 模型的准确性．本文的研究结果不仅进一步加深了我们对于MSC折纸结构力学特性的认识,同时也为其工程应用提供理论基础．     

Effects of polar cortical cytoskeleton and unbalanced cortical surface tension on intercellular bridge thinning during cytokinesis

To probe the contributions of polar cortical cytoskeleton and the surface tension of daughter cells to intercellular bridge thinning dynamics during cytokinesis,we applied cytochalasin D(CD) or colchicine(COLC) in a highly localized manner to polar regions of dividing normal rat kidney(NRK) cells.We observed cellular morphological changes and analyzed the intercellular bridge thinning trajectories of dividing cells with different polar cortical characteristics.Global blebbistatin(BS) application was used to obtain cells losing active contractile force groups.Our results show that locally released CD or colchicine at the polar region caused inhibition of cytokinesis before ingression.Similar treatment at phases after ingression allowed completion of cytokinesis but dramatically influenced the trajectories of intercellular bridge thinning.Disturbing single polar cortical actin induced transformation of the intercellular bridge thinning process,and polar cortical tension controlled deformation time of intercellular bridges.Our study provides a feasible framework to induce and analyze the effects of local changes in mechanical properties of cellular components on single cellular cytokinesis.