William Leineweber¹, Stephanie I. Fraley^1,2,*

Molecular & Cellular Biomechanics, Vol.16, Suppl.2, pp. 9-9, 2019, DOI:10.32604/mcb.2019.08504

Abstract Cell-extracellular matrix (ECM) interactions are critical modulators of repair and regeneration. However, variability within individual cells of the same cell type and within the ECM microenvironment can lead to heterogeneous outcomes that may limit the reliable application of cell-biomaterial constructs in regenerative medicine. Understanding the origins of heterogeneity is critical to overcoming this challenge and requires measurement of cell-ECM interactions at the single cell level. There are four core biophysical modules that cells employ to interact with their surrounding ECM: protrusion, adhesion, contractility, and matrix remodeling. Conventional approaches measure these interactions in separate experiments on separate cells, resulting in bulk… More >

Qi Zhang¹, Bin Gao¹, Yue Shi¹, Chang Yu^1,*

CMES-Computer Modeling in Engineering & Sciences, Vol.116, No.2, pp. 247-262, 2018, DOI: 10.31614/cmes.2018.04082

Abstract Although pulsatile ECMO, as novel kinds of ECMO, has been attracted more and more attention, the differences of the hemodynamic effects of the pulsatile ECMO on the aorta, the cerebral perfusion, and left ventricular work were still under-investigated. The aim of this study was to clarify the hemodynamic differences of the cardiovascular system between the pulsatile and non-pulsatile VA ECMO. In this study, three ECMO support modes, named as “constant flow mode”, “co-pulse mode” and “counter pulse mode”, were designed. The computational fluid dynamics (CFD) study was carried out. The distribution of the oxygenated blood, the blood velocity vector, the… More >

Donald F. Ward Jr.^*, William A. Williams^*, Nicole E. Schapiro^*, Samuel R. Christy^*, Genevieve L. Weber^*, Megan Salt, Robert F. Klees^*, Adele Boskey^†, George E. Plopper ^∗,‡

Molecular & Cellular Biomechanics, Vol.4, No.4, pp. 177-188, 2007, DOI:10.3970/mcb.2007.004.177

Abstract Focal adhesion kinase (FAK) is a key integrator of integrin-mediated signals from the extracellular matrix to the cytoskeleton and downstream signaling molecules. FAK is activated by phosphorylation at specific tyrosine residues, which then stimulate downstream signaling including the ERK1/2 pathway, leading to a variety of cellular responses. In this study, we examined the effects of FAK point mutations at tyrosine residues (Y397, Y925, Y861, and Y576/7) on osteogenic differentiation of human mesenchymal stem cells exposed to collagen I and cyclic tensile strain. Our results demonstrate that FAK signaling emanating from Y397, Y925, and to a lesser extent Y576/7, but not… More >