The duration of this repair phase is the same in ascites and bone marrow cells (Fig. 6).
The inflammatory phase is characterized by the presence of polymorphonuclear leukocytes (PMNLs), while the repair phase is characterised by fibroblast migration and proliferation, new blood vessel formation, protein synthesis, collagen deposition, epithelialisation, and wound contraction [ 7].
Typically, increased expression of arginase 1, secretion of immune-modulatory cytokines (such as IL-10, TGF- β), and involvement in tissue repair phase are considered as indicators of M2 differentiation.
These two repair phases are exponentially distributed with the expectation coefficient of ( raisebox{1ex}{$1$} left/ raisebox{-1ex raisebox{-1ex}{ight. ) and ( raisebox{1ex}{$1$}!left/ !raisebox{mu}x}{${mu}_{sc}$}right. ), respectively.
A similar pattern indicating injury and repair phases was displayed by 5-HETE, but with the maximum occurring at 6 hr.
Therefore, examination of endometrial repair factors during the menstrual phase is essential when examining the process of repair in the context of menstruation.
Tensile strength decrease of the repair, during the initial inflammatory phase, is expected, derived from oedema and tendon degradation.
Thus, in tumors arising in tissues with circadian rhythmicity, provided the tumor maintains rhythmicity in phase with the normal tissue, administration of cisplatin when excision repair is in the descending phase is expected to improve the therapeutic index by administering a less toxic dose.
The first phase primarily consists of clot formation and inflammation from days 1 to 5. The second major phase is that of repair from day 3 to 14, and involves neovascularization, perivascular maturation, mesenchymal stem cell migration, proliferation and condensation, osteoblastic differentiation, and woven bone formation.
In this period, the structural characteristics of the repair tissue indicate that the reorganization phase is already established in this period.
This phase is followed by repair and remodelling phases, in which undifferentiated satellite cells, in response to various growth factors, proliferate and differentiate into mature myoblasts in an effort to replace the injured muscle fibers [ 1].
