骨骼肌生物力学特性多尺度建模与仿真

针对肌纤维微观结构模型与显微镜下观察的图像存在一定差异、微观组分生物力学模型无法有效捕获骨骼肌剪切变形时的力学行为、骨骼肌多尺度数值模型计算成本高的问题,本文从实验、多尺度建模和仿真的角度研究骨骼肌被动力学特性,提出以曲边泰森多边形作为肌纤维截面形状,并建立骨骼肌微观尺度代表性体元RVE;提出新的生物力学模型(MMA模型),并将MMA模型作为肌纤维和结缔组织生物力学模型,MMA模型采用完全的应变不变量I₄, I₅, I₆和I₇,使骨骼肌的剪切行为从材料属性层面得以体现;结合骨骼肌力学实验结果、RVE模型、肌纤维和结缔组织的生物力学模型,建立骨骼肌多尺度数值模型.根据实验结果确定生物力学模型参数,通过多尺度均匀化方法实现微观尺度和宏观尺度之间的连接,最终获得骨骼肌宏观力学行为,通过纵向拉伸、横向拉伸、平面外纵向剪切和平面内剪切4种变形形式的仿真结果验证骨骼肌多尺度数值模型的收敛性.研究了生物力学模型中模型参数、肌纤维体积分数和肌纤维结构对骨骼肌宏观力学行为的影响,最后通过实验验证多尺度数值模型的有效性...     

静电雾化锥射流模式下液锥形态的研究

本文分析了静电雾化锥射流模式下液锥表面静电应力、表面张力应力分布特性,基于应力平衡建立了液锥力学模型,并对流量、荷电电压及针形喷嘴的内半径等参数对液锥结构形态的影响进行了预测。首先设计了针形喷嘴静电雾化实验装置,应用高速摄影技术观测了静电雾化的典型雾化模式和液锥形态演化特性。实验结果表明:锥射流雾化模式仅在一定的荷电电压范围内才会出现;针形喷嘴的流量增加,液锥锥角减小,液锥长度增长;随着荷电电压或针形喷嘴内半径的增加,液锥锥角增大,液锥长度缩短。实验结果与液锥力学模型的预测结果一致。     

混凝土三维细观模型的建模方法与力学特性分析

根据混凝土材料的细观组成和结构特点，基于三维Voronoi图形提出了一种简单高效的混凝土细观模型生成方法，利用塑性损伤模型对该细观模型进行了单、多轴应力状态下的准静态分析以及SHPB动态有限元分析。结果表明，数值模拟得到的应力应变曲线和破坏模式与实验结果基本吻合，本文中提出的混凝土三维细观模型可较好地模拟混凝土的静、动态力学特性，为进一步从细观力学角度研究混凝土损伤演化规律和破坏机理提供了模型基础。     

水平井压裂水泥环应力分析

为获取准确的井筒应力分布,根据弹性平面应变力学理论,考虑套管-水泥环-地层系统各部分的应力加载过程和水力裂缝产生的诱导应力场,建立了水平井压裂时套管-水泥环-地层系统应力分布的计算模型。利用该模型,分析了水力裂缝形成前后的系统应力分布,以及裂缝诱导应力场、水泥石杨氏模量、套管壁厚对水泥环内壁应力分布的影响。分析结果表明:随着与裂缝的距离增大,水泥环内壁受到的径向压缩应力逐渐降低,环向应力逐渐由压缩应力变为拉伸应力;优化裂缝间距、降低水泥石杨氏模量、增加套管壁厚可以降低水泥环内壁受力,缓解水泥环内壁的应力集中程度。本文所建模型可为水力压裂水平井的固井设计以及裂缝间距设计提供理论指导。     

基于实验的心肌被动力本构模型

在狗心脏外科手术和心肌力学性能试验的基础上,对心肌力学性能实验数据进行处理和拟合,并应用有限元方法对心肌的单拉实验、松弛实验进行数值模拟和计算. 得到不同心肌位点的本构模型的非线性弹性和黏性参数,从而发展了心肌被动力的非线性黏弹性本构模型,体现了心脏力学行为的非均匀性和黏弹性. 在理论模型和试验数据的基础上,开发了有限元软件ABAQUS的VUMAT材料子程序,应用于数值心脏的仿真研究.      

结构与土接触面的弹黏塑性本构模型

基于Goodman接触面单元,在Clough--Duncan双曲线关系式的基础上改进了三元件宾厄姆体,建立了结构与土接触面的弹黏塑本构模型,使用ABAQUS的FRIC子程序对该模型进行了二次开发.通过改装的应力控制式结构-土接触面剪切试验仪进行了接触面长期剪切试验,验证了该接触面本构模型.研究结果表明:结构与土接触面的弹黏塑本构模型能较好地模拟接触面的力学特性和时间效应;正应力对结构与土接触面的力学行为影响较大,正应力越大,接触面的时间效应越显著.     

高精度石英振梁加速度计挠性支承设计研究

分析了石英振梁加速度计的工作原理和结构设计,确定出挠性支承的结构形式.根据力学原理给出了挠性支承的设计计算公式,并依据挠性支承的结构设计原则,确定了加速度计基本结构参数.利用有限元分析软件对该加速度计建模并进行整体的位移分布、应力特性等有限元力学分析,软件仿真结果与理论计算的摆片端部位移相差小于3%,支承在极限范围内不会断裂,证明了所建立的支承力学模型正确,这为优化结构设计提供了理论依据和方法.     

基于先进生物材料的心肌细胞力——电微环境体外构建

心血管疾病是当前全球范围内导致人类死亡的首要原因, 心肌组织工程的发展为心血管疾病的治疗, 尤其是心肌组织再生修复提供了最有潜力的解决方案.心血管疾病的发生发展与细胞力--电微环境的变化密切相关. 近十几年, 随着先进生物材料和微纳生物制造技术的发展, 越来越多的研究表明, 细胞力--电微环境的调控对工程化心肌组织的成熟和功能化以及心肌组织再生修复具有重要意义. 本文首先阐明了在体心肌细胞所处力学微环境的生物学基础以及电信号的传导过程, 包括正常和疾病状态下心肌细胞所处的力--电微环境.其次调研了用于心肌组织工程的先进生物材料的研究现状.最后总结用于基底硬度与应力应变细胞微环境以及细胞电学微环境的构建和调控, 以及细胞对力--电微环境的生物学响应.%      

不同集流方式下对称双阴极固体氧化物燃料电池的电-化-热-力数值模拟及失效分析

 本文围绕新型对称双阴极固体氧化物燃料电池电堆单元在不同集流位置下热应力分布情况和优化集流方式，建立了一个基于电-化-热-力多场耦合理论的三维SOFC 电堆单元数值模型．引入固体力学热-力学理论，结合Weibull 失效概率分析方法，讨论了不同集流方式对SOFC 内部应力分布及失效的影响．研究结果表明，双侧阴极同时开展电子集流方式下的电解质平均电流密度比单侧单一集流方式下高，改变阳极集流位置会改变电极高温区的分布；SOFC 电堆单元上电极结构处的最大主应力明显大于其他组件上的最大主应力；阳极集流位置设置在阳极气体入口处时电极结构上的最大主应力和失效概率大于集流位置设置在阳极气体出口处的最大主应力和失效概率．     

空间充气薄膜结构的褶皱分析

引入一个表征褶皱在纹理方向收缩特性的参数``收缩系数'来替代泊松比参与计算褶皱形变,并联合褶皱产生时的应力条件和褶皱特性,实现了对空间充气薄膜结构的褶皱分析,得到了褶皱存在时的充气薄膜结构的应力场和变形. 分析中重点讨论了``收缩系数'与泊松比的关系,并讨论了引入``收缩系数'约束变形后的变形协调条件. 将两维的褶皱分析方法拓展应用到三维充气结构的褶皱分析中,分析了充气管的弯皱变形,得到了临界皱曲和极限弯矩随结构及力学参数的变化规律. 通过简单的褶皱试验,定性地分析了褶皱的形变特性并与分析结果进行了比较验证,结果一致.      

In vivo mechanical study of helical cardiac pacing electrode interacting with canine myocardium

Cardiac pacing is a medical device to help human to overcome arrhythmia and to recover the regular beats of heart. A helical configuration of electrode tip is a new type of cardiac pacing lead distal tip. The helical electrode attaches itself to the desired site of heart by screwing its helical tip into the myocardium. In vivo experiments on anesthetized dogs were carried out to measure the acute interactions between helical electrode and myocardium during screw-in and pull-out processes. These data would be helpful for electrode tip design and electrode/myocardium adherence safety evaluation. They also provide reliability data for clinical site choice of human heart to implant and to fix the pacing lead. A special design of the helical tip using strain gauges is instrumented for the measurement of the screw-in and pull-out forces. We obtained the data of screw-in torques and pull-out forces for five different types of helical electrodes at nine designed sites on ten canine hearts. The results indicate that the screw-in torques increased steplike while the torque–time curves presente saw-tooth fashion. The maximum torque has a range of 0.3–1.9 N mm. Obvious differences are observed for different types of helical tips and for different test sites. Large pull-out forces are frequently obtained at epicardium of left ventricle and right ventricle lateral wall, and the forces obtained at right ventricle apex and outflow tract of right ventricle are normally small. The differences in pull-out forces are dictated by the geometrical configuration of helix and regional structures of heart muscle.     

Growth and remodeling of the left ventricle: A case study of myocardial infarction and surgical ventricular restoration

Cardiac growth and remodeling in the form of chamber dilation and wall thinning are typical hallmarks of infarct-induced heart failure. Over time, the infarct region stiffens, the remaining muscle takes over function, and the chamber weakens and dilates. Current therapies seek to attenuate these effects by removing the infarct region or by providing structural support to the ventricular wall. However, the underlying mechanisms of these therapies are unclear, and the results remain suboptimal. Here we show that myocardial infarction induces pronounced regional and transmural variations in cardiac form. We introduce a mechanistic growth model capable of predicting structural alterations in response to mechanical overload. Under a uniform loading, this model predicts non-uniform growth. Using this model, we simulate growth in a patient-specific left ventricle. We compare two cases, growth in an infarcted heart, pre-operative, and growth in the same heart, after the infarct was surgically excluded, post-operative. Our results suggest that removing the infarct and creating a left ventricle with homogeneous mechanical properties does not necessarily reduce the driving forces for growth and remodeling. These preliminary findings agree conceptually with clinical observations.     

A simple model for myocardial changes in a failing heart

In a simplified setting, a multi-network model for remodeling in the left ventricle (LV) is developed that can mimic various pathologies of the heart. The model is an extension of the simple model introduced by Nardinocchi and Teresi [9], Nardinocchi et al. [10], [11] that results in an algebraic relation for LV pressure–volume–contraction. We considered two networks, the original tissue and a new tissue, each of which has its own volume fraction, stress-free reference configuration, elastic properties, and contractility. This is used to explore the consequences of microstructural changes in the muscle tissue on LV function in terms of the pressure–volume loop during a single cardiac cycle. Special attention is paid to the stroke volume, which is directly related to cardiac output, and changes in LV wall stress caused by various disease states, including wall thinning (dilated cardiomyopathy), wall thickening (hypertrophic cardiomyopathy), contractility degradation, and stiffness changes (scarring). Various scenarios are considered that are of clinical relevance, and the extent and nature of remodeling that could lead to heart failure are identified.     

载流圆锥薄壳的磁弹性应力与变形分析

在建立旋转壳体的非线性磁弹性运动方程的基础上,研究了电磁场和机械载荷联合作用下载流圆锥薄壳的磁弹性效应．通过算例,得到了载流圆锥薄壳的位移及应力与通电电流强度之间的关系．解决了圆锥薄壳顶点处的奇异性问题,给出了轴对称条件下的数值解．计算结果表明：改变通电电流强度,可以改变载流圆锥薄壳的应力与变形状态,达到控制圆锥薄壳的受力与变形的目的．     

Theoretical model of piezoelectric fibre pull-out

A theoretical model of a single piezoelectric fibre pull-out is developed to study the interaction between fibre deformation, pull-out stress and corresponding electrical field. Computer simulation of the stress–displacement curve of the fibre pull-out process is presented. Numerical examples show that the piezoelectric fibre pull-out behaviour can be both described and affected by its electrical field. Therefore, the interactions between the mechanical and electric fields of the fibre/matrix system can be employed to monitor and control the fracture behaviour of active fibre composites.     

Effect of trabeculae and papillary muscles on the hemodynamics of the left ventricle

The impact of surface trabeculae and papillary muscles on the hemodynamics of the left ventricle (LV) is investigated using numerical simulations. Simulations of ventricular flow are conducted for two different models of the LV derived from high-resolution cardiac computed tomography (CT) scans using an immersed boundary method-based flow solver. One model comprises a trabeculated left ventricle (TLV) that includes both trabeculae and papillary muscles, while the second model has a smooth left ventricle that is devoid of any of these surface features. Results indicate that the trabeculae and papillary muscles significantly disrupt the vortices that develop during early filling in the TLV model. Large recirculation zones are found to form in the wake of the papillary muscles; these zones enhance the blockage provided by the papillary muscles and create a path for the mitral jet to penetrate deeper into the ventricular apex during diastole. During systole, the trabeculae enhance the apical washout by ‘squeezing’ the flow from the apical region. Finally, the trabeculae enhance viscous dissipation rate of the ventricular flow, but this effect is not significant in the overall power budget.     

Visco-electro-elastic models of fiber-distributed active tissues

We present a constitutive model for stochastically distributed fiber reinforced visco-active tissues, where the behavior of the reinforcement depends on the relative orientation of the electric field. Following our previous works, for the passive behaviors we adopt a second order approximation of the strain energy density associated to the parameters of the fiber distribution. Consistently, we also assume that the active behavior accounts for the stochastic distribution of the fibers. The ensuing mechanical quantities result to be dependent on two average structure tensors. We introduce an extended Helmholtz free energy density characterized by the inclusion of a directional active potential, dependent on a stochastic anisotropic permittivity tensor. The permittivity tensor is expanded in Taylor series up to the second order, allowing to obtain an approximated active potential with the same structure of the passive Helmholtz free energy density. In particular, the explicit expression of active stress and stiffness are dependent on the two average structure tensors that characterize the passive response. Anisotropy follows from the fiber distribution and inherits its stochastic nature through statistics parameters. The active fiber distributed model is extended here to viscous materials by including the contribution of a dual dissipation potential in the variational formulation of the constitutive updates. Additionally, we present a computational example of application of the electro-viscous-mechanical material model by simulating peristaltic contractions on a portion of human intestine.     

Effect of Laminar Orthotropic Myofiber Architecture on Regional Stress and Strain in the Canine Left Ventricle

Recent morphological studies have demonstrated a laminar (sheet) organization of ventricular myofibers. Multiaxial measurements of orthotropic myocardial constitutive properties have not been reported, but regional distributions of three-dimensional diastolic and systolic strains relative to fiber and sheet axes have recently been measured in the dog heart by Takayama et al. [30]. A three-dimensional finite-deformation, finite element model was used to investigate the effects of material orthotropy on regional mechanics in the canine left ventricular wall at end-diastole and end-systole. The prolate spheroidal model incorporated measured transmural distributions of fiber and sheet angles at the base and apex. Compared with transverse isotropy, the orthotropic model of passive myocardial properties yielded improved agreement with measured end-diastolic strains when: (1) normal stiffness transverse to the muscle fibers was increased tangent to the sheets and decreased normal to them; (2) shear coefficients were increased within sheet planes and decreased transverse to them. For end-systole, orthotropic passive properties had little effect, but three-dimensional systolic shear strain distributions were more accurately predicted by a model in which significant active systolic stresses were developed in directions transverse to the mean fiber axis as well as axial to them. Thus the ventricular laminar architecture may give rise to anisotropic material properties transverse to the fibers with greater resting stiffness within than between myocardial laminae. There is also evidence that intact ventricular muscle develops significant transverse stress during systole, though it remains to be seen if active stress is also orthotropic with respect to the laminar architecture. This revised version was published online in July 2006 with corrections to the Cover Date.     

压电薄板板边导电裂纹尖端的力电场分析

采用有限元方法，分析了压电薄板板边不同长度导电裂纹尖端的力电场分布规律，发现导电裂纹尖端的应力场和电场强度存在明显的集中和奇异现象，集中和奇异的程度与裂纹长度有关。而且，在裂纹延长线上分别存在两点，这里的应力和电场对裂纹长度不太敏感，总等于无裂纹时薄板的均匀应力和均匀电场强度；同时，还研究了导电裂纹尖端的应力强度因子和电场强度因子对裂纹长度的依赖关系，发现在线性本构的前提下，导电裂纹尖端的应力强度因子与电场强度因子之间具有近似的线性关系。     

Modeling Heart Development

Mechanics plays a major role in heart development. This paper reviews some of the mechanical aspects involved in theoretical modeling of the embryonic heart as it transforms from a single tube into a four-chambered pump. In particular, large deformations and significant alterations in structure lead to highly nonlinear boundary value problems. First, the biological background for the problem is discussed. Next, a modified elasticity theory is presented that includes active contraction and growth, and the theory is incorporated into a finite element analysis. Finally, models for the heart are presented to illustrate the developmental processes of growth, remodeling, and morphogenesis. Combining such models with appropriate experiments should shed light on the complex mechanisms involved in cardiac development. This revised version was published online in July 2006 with corrections to the Cover Date.