D3: Tissue Mechanics


Arthur Mak, Yifei yao, Singwan Wong, Daniel Xiao

The Chinese University of Hong Kong, Hong Kong

Deep tissue injury due to prolonged excessive loadings can lead to clinical pressure ulcers. We assessed the duration-dependent damage thresholds of muscle cells in compression using myoblasts in-vitro, and studied the effects of hydrogen peroxide as extrinsic oxidant and the effects of the biowastes released from other damaged cells on such damage thresholds. We examined the effects of oxidative stress on cytoskeletal actin polymerization and used AFM to monitor the corresponding temporal changes in cell stiffness. We used femtosecond laser to evaluate how oxidative stress affected the pre-tension in the cytoskeletal fibers and the ability of cells to repair submicron-pores on their plasma membranes. Using a confocal image based finite element model, we simulated the effects of the biochemically compromised cytoskeleton on the tensile strain in the cell membrane when the myoblast was subjected to compressive loading. Comparing the in-vitro results with a Weibull-distribution damage model suggested that the damage threshold was roughly equivalent to a 6% critical tensile  strain in the cell membrane. Our findings suggested interesting implications of damage vulnerability when cells were exposed to biowastes released from other damaged cells in their neighbourhood, or when cells are subjected to prolonged oxidative exposures, such as during chronic inflammation. Using a pseudo-3D finite element model of a human buttock on an elastic cushion, we simulated the effects of the biowastes and the effects of the post-ischemic reperfusion oxidative stress on the development of the deep tissue lesions around a loaded bony ischial tuberosity to become fullthickness ulcers.

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