Hong Qian^*

Molecular & Cellular Biomechanics, Vol.5, No.2, pp. 107-118, 2008, DOI:10.3970/mcb.2008.005.107

Abstract At the molecular and cellular level, mechanics and chemistry are two aspects of the same macromolecular system. We present a bottom-up approach to such systems based on Kramers' diffusion theory of chemical reactions, the theory of polymer dynamics, and the recently developed models for molecular motors. Using muscle as an example, we develop a viscoelastic theory of muscle in terms of an simple equation for single motor protein movement. Both A.V. Hill's contractile component and A.F. Huxley's equation of sliding-filament motion are shown to be special cases of the general viscoelastic theory of the active material. Some disparity between the… More >

Shaohua Chen^*

Molecular & Cellular Biomechanics, Vol.5, No.2, pp. 97-106, 2008, DOI:10.3970/mcb.2008.005.097

Abstract Recently, contact mechanics has been widely used to get some understanding of the biological adhesion mechanisms, such as cell-cell adhesion, insects' adhesion and locomotion. JKR theory is usually adopted as a basis, in which the interaction of molecules is considered in contrast to the classical Hertz solution. In this paper, two problems are summarized, which may give some insights to cells or bio-molecules sensitivity to environmental signals: (1) cell reorientation on a stretched substrate; (2) spontaneous detachment between cells or bio-molecules under the variation of environmental signals. The intention here is only to illustrate the possibilities that contact mechanics may… More >

Geert W. Schmid-Schönbein^*

Molecular & Cellular Biomechanics, Vol.5, No.2, pp. 83-96, 2008, DOI:10.3970/mcb.2008.005.083

Abstract Increasing evidence suggests that most cardiovascular diseases, tumors and other ailments are associated with an inflammatory cascade. The inflammation is accompanied by activation of cells in the circulation and fundamental changes in the mechanics of the microcirculation, expression of pro-inflammatory genes and downregulation of anti-inflammatory genes, attachment of leukocytes to the endothelium, elevated permeability of the endothelium, and many other events. The evidence has opened great opportunities for medicine to develop new anti-inflammatory interventions. But it also raises a fundamental question: What is the origin of inflammation? I will discuss a basic series of studies that was designed to explore… More >

Hai Ngu^*, Lan Lu^*, Sara J. Oswald^*, Sarah Davis^*, Sumona Nag^*, Frank C-P Yin^†

Molecular & Cellular Biomechanics, Vol.5, No.1, pp. 69-82, 2008, DOI:10.3970/mcb.2008.005.069

Abstract Endothelial cells subjected to cyclic stretching change orientation so as to be aligned perpendicular to the direction of applied strain in a magnitude and time-dependent manner. Although this type of response is not the same as motility, it could be governed by motility-related factors such as substratum adhesiveness and actin-myosin contractile level. To examine this possibility, human aortic endothelial cells (HAEC) were uniaxially, cyclically stretched on silicone rubber membranes coated with various concentrations of fibronectin, collagen type IV and laminin to produce differing amounts of adhesiveness (measured using a radial flow detachment assay). Cells were subjected to 10% pure cyclic… More >

Savio L-Y. Woo^∗,†, Matthew B. Fisher^†, Andrew J. Feola^†

Molecular & Cellular Biomechanics, Vol.5, No.1, pp. 49-68, 2008, DOI:10.3970/mcb.2008.005.049

Abstract The contribution of biomechanics to the advancement of management of ligament and tendon injuries has been significant. Thanks to Professor Y.C. Fung's writing and guidance, our field of research has done fundamental work on anatomy and biology of ligaments and tendons, developed methods to accurately determine mechanical properties, identified various experimental factors which could change the outcome measurements as well as examined biological factors that change tissue properties in-vivo. Professor Fung also gave us his quasi-linear viscoelastic theory for soft tissues so that the time and history dependent properties of ligaments and tendons could be properly described. More >

Yuliya Vengrenyuk^*, Luis Cardoso^*, Sheldon Weinbaum^∗,†

Molecular & Cellular Biomechanics, Vol.5, No.1, pp. 37-48, 2008, DOI:10.3970/mcb.2008.005.037

Abstract In this paper, we further investigate the new paradigm for the rupture of thin cap fibroatheroma (TCFA) proposed in Vengrenyuk et al. (2006 PNAS 103:14678) using a multilevel micro-CT based 3D numerical modeling. The new paradigm proposes that the rupture of TCFA is due to stress-induced interfacial debonding of cellular - level, 10 -- 20 μm microcalcifications in the fibrous cap proper. Such microcalcifications, which lie below the visibility of current in vivo imaging techniques, were detected for the first time using confocal microscopy and high resolution microcomputed tomography (micro-CT) imaging in Vengrenyuk et al. (2006) In the present study,… More >

Patrick H. Campbell^∗,†, Darlene L. Hunt^∗,†, Ying Jones^‡, Fred Harwood^§, David Amiel^§, Jeffrey H. Omens^†,¶, Andrew D. McCulloch^†,||

Molecular & Cellular Biomechanics, Vol.5, No.1, pp. 27-36, 2008, DOI:10.3970/mcb.2008.005.027

Abstract Biglycan, a small leucine-rich proteoglycan, has been shown to interact with extracellular matrix (ECM) collagen and may influence fibrillogenesis. We hypothesized that biglycan contributes to post-myocardial infarction (MI) scar development and that the absence of biglycan would result in altered scar structure and mechanics. Anterior MI was induced in biglycan hemizygous null and wild-type mice by permanent ligation of the left coronary artery. The initial extent of ischemic injury was similar in the two groups, as was the infarct size after 30 days, although there was some tendency toward reduced expansion in the biglycan-null. Electron microscopy revealed that collagen fibrils… More >

Jizeng Wang^*, Jin Qian^*, Huajian Gao^∗,†

Molecular & Cellular Biomechanics, Vol.5, No.1, pp. 19-26, 2008, DOI:10.3970/mcb.2008.005.019

Abstract Experiments have shown that stable adhesion of a variety of animal cells on substrates prepared with precisely controlled ligand distribution can be formed only if the ligand spacing is below 58 nm. To explain this phenomenon, here we propose a confined polymer model to study the stability of molecular adhesion mediated by polymer repellers and ligand-receptor bonds. In this model, both repellers and binders are treated as wormlike chains confined in a nanoslit, and the stability of adhesion is considered as a competition between attractive interactions of ligand-receptor binding and repulsive forces due to the size mismatch between repellers and… More >

Jin Suo^*, John N. Oshinski^∗,†, D.P. Giddens^∗,‡

Molecular & Cellular Biomechanics, Vol.5, No.1, pp. 9-18, 2008, DOI:10.3970/mcb.2008.005.009

Abstract Atherosclerotic plaques in human coronary arteries are focal manifestations of systemic disease, and biomechanical factors have been hypothesized to contribute to plaque genesis and localization. We developed a computational fluid dynamics (CFD) model of the ascending aorta and proximal sections of the right and left coronary arteries of a normal human subject using computed tomography (CT) and magnetic resonance imaging (MRI) and determined the pulsatile flow field. Results demonstrate that flow patterns in the ascending aorta contribute to a pro-atherosclerotic flow environment, specifically through localization of low and oscillatory wall shear stress in the neighborhood of coronary orifices. Furthermore, these… More >

Shu Chien^*

Molecular & Cellular Biomechanics, Vol.5, No.1, pp. 1-8, 2008, DOI:10.3970/mcb.2008.005.001

Abstract Fluid shear stress due to blood flow can modulate functions of endothelial cells (ECs) in blood vessels by activating mechano-sensors, signaling pathways, and gene and protein expressions. Laminar shear stress with a definite forward direction causes transient activations of many genes that are atherogenic, followed by their down-regulation; laminar shear stress also up-regulates genes that inhibit EC growth. In contrast, disturbed flow patterns with little forward direction cause sustained activations of these atherogenic genes and enhancements of EC mitosis and apoptosis. In straight parts of the arterial tree, laminar shear stress with a definite forward direction has anti-atherogenic effects. At… More >