19 research outputs found

    Microstructural analysis of deformation-induced hypoxic damage in skeletal muscle

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    Deep pressure ulcers are caused by sustained mechanical loading and involve skeletal muscle tissue injury. The exact underlying mechanisms are unclear, and the prevalence is high. Our hypothesis is that the aetiology is dominated by cellular deformation (Bouten et al. in Ann Biomed Eng 29:153–63, 2001; Breuls et al. in Ann Biomed Eng 31:1357–364, 2003; Stekelenburg et al. in J App Physiol 100(6):1946–954, 2006) and deformation-induced ischaemia. The experimental observation that mechanical compression induced a pattern of interspersed healthy and dead cells in skeletal muscle (Stekelenburg et al. in J App Physiol 100(6):1946–954, 2006) strongly suggests to take into account the muscle microstructure in studying damage development. The present paper describes a computational model for deformation-induced hypoxic damage in skeletal muscle tissue. Dead cells stop consuming oxygen and are assumed to decrease in stiffness due to loss of structure. The questions addressed are if these two consequences of cell death influence the development of cell injury in the remaining cells. The results show that weakening of dead cells indeed affects the damage accumulation in other cells. Further, the fact that cells stop consuming oxygen after they have died, delays cell death of other cells

    Improving prediction of heart attacks and strokes : anisotropic mechanical behaviour of plaques

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    Biomechanical models allow stress analysis and can predict stress peaks in atherosclerotic plaques. Studies have shown that these models might be capable to predict failure locations and improve the risk assessment of plaque rupture. However, biomechanical models depend strongly on the applied material model. Current models assume isotropic behaviour, but biological tissue, including plaque tissue, behave highly anisotropic. Therefore, current biomechanical models rely on general over-simplifications. Material parameters describing the anisotropic mechanical behaviour of plaque tissue are scarce. Therefore, the aim of this study is to characterise the local anisotropic mechanical behaviour of human atherosclerotic plaque tissue
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