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The mechanism of cell death induced by mechanical compression was studied using bio-artificial skeletal muscle tissues.
Subsequently, the mechanical compression was performed on the film.
The porous RGO film after mechanical compression was patterned to give interdigitated electrodes by irradiation with a picosecond laser.
The results of this study have demonstrated that fluid perfusion can result in a higher cell density in the scaffold region closed to the outlet, while cell density distribution under mechanical compression was similar with static condition.
Mechanical compression was applied on costal cartilage, as previously described [ 24].
Usually, compression stimulus was extensively used for bone and cartilage tissue engineering [ 71– 73]; however the favourable effect of mechanical compression was successfully certified in a cardiac tissue engineering protocol.
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Therefore, cell death in bio-artificial muscle tissue caused by mechanical compression is primarily caused by a physiological mechanism, rather than through a physical mechanism which kills the cell directly.
Proteomic studies of mechanical compression are applied to understand how different proteins are orchestrated to respond.
Differential gene expression under mechanical compression is one of key issues in chondrocyte mechanotransduction.
Previously we have shown that mechanical compression is an important ALK5/Smad2/3P activator in cartilage explants.
Shear flow, tensile stretch, and mechanical compression are most typical in vivo mechanical stimuli, which are in action alone or synergistically with other mechanical and even biochemical factors (Wang, 2006; Cohen and Chen, 2008).
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