By Richard G. A. Faragher (auth.), Richard Aspinall (eds.)
During the final forty years, the research of the organic foundation of getting older has advanced significantly, and it has now develop into an self sustaining and decent box of analysis and research.
This quantity on "Aging of Organs and Systems", is an try to deliver knowing to either the getting older technique and the illness approaches of outdated age. Bringing jointly contributions from a global crew of authors, will probably be of curiosity to graduates and postgraduates within the fields of drugs and nursing, researchers of other points of biogerontology and people within the pharmaceutical, cosmeceutical, nutriceutical and health-care undefined.
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Additional resources for Aging of the Organs and Systems
25 E¡ros RB, Pawelec G (1997). Replicative senescence of T cells: does the Hay£ick Limit lead to immune exhaustion? Immunol Today 18(9): 450^4. Kirkwood TBL, Holliday R (1975). Commitment to senescence: a model for the ¢nite and in¢nite growth of diploid and transformed human ¢broblasts in culture J Therot Biol. 53: 481^96. Shall S, Stein WD (1979). A mortalisation theory for the control of cell proliferation and for the origin of immortal cell lines J Theoret Biol. 76: 219^31. Protero J, Gallant JA (1981).
Prog Cell Cycle Res. 3: 211^20. Shelton DN, Chang E, Whittier PS, Choi D, Funk WD (1999). Microarray analysis of replicative senescence. Curr Biol. 9(17): 939^45. Doggett DL, Rotenburg MO, Pignolo RJ, Phillips PD, Cristofallo VJ (1992). Di¡erential gene expression between young and quiescent, senescent WI-38 cells. Mech Age Dev. 65: 239^55. Lecka-Czernik B, Moerman EJ, Jones RA, Goldstein S (1996). Identi¢cation of gene sequences overexpressed in senescent and Werner syndrome human ¢broblasts. Exp Gerontol.
One of the main contributory features of the chronic environment is the formation of the ¢brin cu¡s which are thought to trap not only growth factors but also neutrophils (see above). This leads to the persistence of these cells with a resulting increase in proteolytic enzyme and ROS release which in turn leads to increased ECM breakdown. What is also typical of the chronic wound environment is the imbalance between pro-in£ammatory cytokines/growth factors and their inhibitors. For example, it has been demonstrated by comparing chronic and acute wounds that overall levels of tumor necrosis factor (TNF)-a and IL-1b are increased in chronic wounds due to decreased levels of their respective inhibitors; namely p55 (the soluble TNF Aging of the Skin 45 receptor protein) and the IL-1 receptor antagonist [139^141].