Wound care
Tor Wo Chiu in Stone’s Plastic Surgery Facts, 2018
Re-epithelialisation begins within hours of wounding with migration of marginal keratinocytes over the matrix due to loss of contact inhibition, staying beneath the eschar. There is a phenotypic conversion of differentiated keratinocytes into non-polarised cells expressing basal cytokeratins similar to cultured cells; increased mobility comes from dissolution of anchoring junctions and reorganisation of the cortical actin cytoskeleton to form lamellipodia. Cells stop migrating when they form a contiguous layer (contact inhibition). As the basement membrane is reconstituted, the cells are induced to adopt their previous morphology and form anchoring junctions with fibronectin. A moist environment increases the rate of (re)-epithelialisation.
Summary and Development of a New Approach to Senescence
Nate F. Cardarelli in The Thymus in Health and Senescence, 2019
Basically, cancer arises from a change in the genome; such a change can be merely an alteration in a single nucleotide.94 A lack of regulation is implied — possibly in the DNA and/or RNA excision and repair mechanism. This defect must also be coupled with a decrease in immune capability. The fact that normal cells in culture die out after so many doublings while transformed cells become an established (i.e., immortal) line points to regulation in one case and a lack thereof in the other. Contact inhibition seen with normal cells in culture, and usually lacking or diminished with cancerous cells, points in the same direction. A common feature of malignant cells is a change in ploidy, usually from diploidy to heteroploidy. Chromosomal changes in themselves, however, do not necessarily cause transformation from normal to neoplastic. Cancer patients do not have an unusual tendency to heteroploidy. The relationship seen is that heteroploidy and cancer incidence increase with senescence.
Tuberous sclerosis complex
J. K. Cowell in Molecular Genetics of Cancer, 2003
The Eker rat was first identified as a model for inherited renal cell carcinoma (Eker and Mossige, 1961). An insertion of an intracisternal A-particle element into the rat tsc2 gene was shown to be the causative mutation (Xiao et al., 1995). Re-introduction of the wild-type TSC2 gene into renal tumor cells derived from Eker rats inhibited proliferation in vitro and reduced their tumorigenicity in vivo (Jin et al., 1996). Both contact inhibition and normal cell morphology were restored. In addition, Eker rats transgenic for the wild-type TSC2 gene did not develop the characteristic renal or associated neoplasms (Kobayashi et al., 1997). Consistent with these findings, over-expression of tuberin reduced the rate of growth of normal rat1 fibroblasts (Jin et al., 1996) and supported the hypothesis that tuberin had a role in the suppression of tumorigenesis.
Numerical modelling of osteocyte growth on different bone tissue scaffolds
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Concepción Paz, Eduardo Suárez, Christian Gil, Oscar Parga
The porosity and permeability of a scaffold can be modified using the proliferation of the cells, which invade and reduce the empty space of the porous scaffold structure. This reduction in the space remaining for the appearance of new cells associated with cell growth causes the contact inhibition phenomenon. The cell metabolism slows down as the cell density increases; hence, the cell proliferation greatly reduces or even ceases entirely when a critical cell density is reached (Huang and Ingber 2004). Typical bioreactor operations are carried out under controlled temperature; therefore, in this work, a constant temperature was assumed, and the possible temperature changes due to metabolic reactions were neglected. The different types of bone cells, the shape and size of the cells, cell detachment, and the cell ageing process, were not considered as hypotheses of the model. The density of the culture medium and the pH were considered to be constant (Coletti et al. 2006).
Peters Anomaly: Novel Non-Invasive Alternatives to Penetrating Keratoplasty
Published in Seminars in Ophthalmology, 2023
Raksheeth Nathan Rajagopal, Merle Fernandes
The posterior stromal and endothelium-DM complex excavation characterizing PA is postulated to occur due to defective centripetal migration of neural crest cells.23,69 The peripheral normal endothelial cells are capable of enlargement and centripetal migration.70,71 Spontaneous migration and differentiation of these cells are prevented by strong contact inhibition. It is the breakage of this contact inhibition that facilitates migration of the peripheral endothelium and restoration of normal endothelial pump function.72–74 This forms the basis of SER, which was reported by Soh et al. to result in an excellent anatomical and visual outcome. Unlike surgical iridectomy, SER addresses the cause of the underlying abnormality in PA, and this resulted in a significant discernible reduction in the density and size of the corneal opacity.75 Though an option only in type I PA (where less extensive corneal involvement ensures at least some normal peripheral endothelium), SER will be a valuable alternative to PK in these cases, once validated by larger studies.
WAM to SeeSaw model for cancer therapy – overcoming LQM difficulties –
Published in International Journal of Radiation Biology, 2021
Masako Bando, Yuichi Tsunoyama, Kazuyo Suzuki, Hiroshi Toki
Indeed, such maximum tumor capacity must be supported by a given environment surrounding the cancer cells which may evolve depending on the oxygen and nutrition supply (Prokopiou et al. 2015; Watanabe et al. 2016). Such necessary energy and resources are needed for cell proliferation. Also contact inhibition may be a regulatory mechanism that functions to keep cells inside the tissue or so depending on the layer profile. The cell-cell contact and onset of proliferation inhibition should also affect the maximum, which determines the capacity of cell number. We here express all those global effects in terms of the maximum number, although detailed assessment of such mechanism should be made clear, which is a future task to be solved. On the other hand, it is a very important point that the radiation sensibility does strongly depend on the cell property (Sobels 1963; Naderi et al. 2002; Dhawan et al. 2014), which we will explain in the following section (see in sub-section 4.2).