Aging: Facts and Theories - download pdf or read online

By L. Robert, T. Fulop, T. Fulop

ISBN-10: 3318026522

ISBN-13: 9783318026528

Getting older encouraged plenty of theories attempting to rationalize the getting older method universal to all residing beings. during this booklet an important environmental and intrinsic mechanisms focused on the getting older procedure and in its pathological outcomes are reviewed. moreover theoretical and experimental proof of an important theoretical parts in line with Darwinian evolution, mobile getting older, function of telephone membranes, unfastened radicals and oxidative methods, receptor-mediated reactions, the extracellular matrix and immune capabilities in addition to an important environmental and intrinsic mechanisms focused on the getting older strategy and in its pathological effects are mentioned. those shows of theories and comparable experimental proof provide an international evaluate of contemporary ideas of the biology of the getting older method and are of crucial interpreting not just for experts during this box but additionally for practitioners of clinical, clinical, social and experimental sciences.

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It was proposed that dysfunctional telomeres contribute to a DNA damage checkpoint that inhibits the initiation of DNA synthesis. Phase IV fibroblasts display molecular markers characteristic of cells bearing DNA double-strand beaks, which consist in nuclear foci of phosphorylated histone H2AX and their colocalization with DNA repair and DNA damage checkpoint factors. The chromosome ends seem to contribute directly to the DNA damage response. Inactivation of DNA damage checkpoint kinases in senescent cells can restore cell cycle progression into S phase [78].

1159/000358898 29 Experiments performed with cells from Hutchinson-Gilford progeria syndrome showed that telomere length is related to factors other than replication [65]. Telomere length was reduced in fibroblasts and was variable; in contrast, in hematopoietic cells it was within the normal range. These data raise the possibility that lamin A, which is mutated in this syndrome and is expressed in fibroblasts but not in hematopoietic cells, decreases telomere length. In benign leiomyoma tumors, telomere size is unrelated with the proliferation potential [66].

5–1 kb shorter than females in every tissue examined. The data suggested that telomere lengths may decrease due to factors other than the end replication problem during cell division [75]. Chicken telomeres resemble human telomeres in length, but the distribution of telomerase activity is present in the germ line as well as in a wide variety of 30 Macieira-Coelho Robert L, Fulop T (eds): Aging: Facts and Theories. Interdiscipl Top Gerontol. 1159/000358898 somatic tissues as in mice [76]. It is well known that chicken fibroblasts have a finite proliferation span and contrary to mice exhibit extremely low rates of spontaneous immortalization.

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Aging: Facts and Theories by L. Robert, T. Fulop, T. Fulop


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