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In MMC the matrix is exposed to plastic deformation and damage accumulation in the region close to the reinforcements, following mechanical or thermal stress.
Instead, the collagen I-rich stromal matrix is exposed.
Particularly if the peritoneum is damaged and the etracellular matrix is exposed tumor cell adhesion accumulates [ 5].
During the initial stages of peritoneal metastasis, cancer cells attach to milky spots where the collagen-rich connective tissue matrix is exposed [ 50– 53] (Fig. 1a).
Platelets become activated when the continuity of the endothelial layer is disrupted and the underlying subendothelial matrix is exposed, or if inflammation perturbs the endothelium.
Indeed, during peritoneal metastasis, tumour cells attach preferentially at locations where the mesothelium is disrupted and the underlying collagen I-rich stromal matrix is exposed (Ghosh et al, 2002; Mochizuki et al, 2004).
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In this experimental study, GFRP small specimens and full-scale profiles with polyester matrix were exposed for six months to a constant temperature of 40 °C and relative humidity of 98 100%.
In a subset of experiments the sub-endothelial matrix was exposed and covered with platelets to account for the effects of endothelial injury.
Dinitrophenylation. Three segments of rat bone matrix were exposed before implantation to solutions of l-fluoro-2,4-di-nitrobenzene (FDNB) [ 30] of the following concentrations: 3, 5, 10, 26, 53, and 268 mM/liter.
FDNB reduced the yield of new bone in concentrations higher than 10 mM/liter but did not eliminate all morphogenetic activity until the matrix was exposed to concentrations in excess of 268 mM/liter.
Despite this, when cancer cells were added to a monolayer of mesothelial cells that had been pretreated with TNFα, the cancer cells attached to the intracellular gaps where the sub-mesothelial collagen I matrix was exposed rather than to the mesothelial cells [ 51].
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