The long range objective of this work is to develop a cartilage growth finite element model (CGFEM), based on the theories of growing mixtures that has the capability to depict the evolution of the anisotropic and inhomogeneous mechanical properties, residual stresses, and nonhomogeneities that are attained by native adult cartilage. The CGFEM developed here simulates isotropic in vitro growth of cartilage with and without mechanical stimulation. To accomplish this analysis a commercial finite element code (ABAQUS) is combined with an external program (MAT-LAB) to solve an incremental equilibrium boundary value problem representing one increment of growth. This procedure is repeated for as many increments as needed to simulate the desired growth protocol. A case study is presented utilizing a growth law dependent on the magnitude of the diffusive fluid velocity to simulate an in vitro dynamic confined compression loading protocol run for 2 weeks. The results include changes in tissue size and shape, nonhomogeneities that develop in the tissue, as well as the variation that occurs in the tissue constitutive behavior from growth.
Exposure of skin tissue to UV radiation has been shown to cause DNA photodamage. If this damaged DNA is allowed to replicate, carcinogenesis may occur. DNA damage is prevented from being passed on to daughter cells by upregulation of the protein p21. p21 halts the cells cycle allowing the cell to undergo apoptosis, or repair its DNA before replication. Previous work suggested that milk phospholipids may possess protective properties against UV damage. In this study, we observed cell morphology, cell apoptosis, and p21 expression in tissue engineered epidermis through the use of Hematoxylin and Eosin staining, confocal microscopy, and western blot respectively. Tissues were divided into four treatment groups including: a control group with no UV and no milk phospholipid treatment, a group exposed to UV alone, a group incubated with milk phospholipids alone, and a group treated with milk phospholipids and UV. All groups were incubated for twenty-four hours after treatment. Tissues were then fixed, processed, and embedded in paraffin. Performing western blots resulted in visible p21 bands for the UV group only, implying that in every other group, p21 expression was lesser. Numbers of apoptotic cells were determined by observing the tissues treated with Hoechst dye under a confocal microscope, and counting the number of apoptotic and total cells to obtain a percentage of apoptotic cells. We found a decrease in apoptotic cells in tissues treated with milk phospholipids and UV compared to tissues exposed to UV alone. Collectively, these results suggest that milk phospholipids protect cell DNA from damage incurred from UV light.
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