By Michael B. Fossel
Cells, getting older, and Human Disease is the 1st booklet to discover getting older the entire manner from genes to scientific software, reading the basic mobile alterations which underlie human age-related illness. With over 4,000 references, this article explores either the elemental procedures of human getting older and the tissue-by-tissue pathology, detailing either breaking examine and present state of the art medical interventions in getting older and age-related sickness. faraway from basically sharing a standard onset overdue within the lifespan, age-related illnesses are associated by means of basic universal features on the genetic and mobile degrees. Emphasizing human telephone mechanisms, the 1st part offers and analyzes our present knowledege of telomere biology and cellphone senescence. In incredible educational element, the textual content brings the reader modern on telomere upkeep, telomerase dynamics, and present examine on cellphone senescence--and the final model--cell senescence because the imperative part in human senescence and melanoma. for every human malignancy, the bankruptcy reports and analyzes all to be had information on telomeres and telomerase, in addition to summarizing present paintings on their scientific software in either prognosis and melanoma remedy. the second one version, orientated via organs and tissues, explores the particular physiological effect of cellphone senescence and getting older on scientific ailment. After a precis of the literature on early getting older syndromes--the progerias--the textual content stories getting older illnesses (Alzheimer's dementia, osteoarthritis, atherosclerosis, immune getting older, presbyopia, sarcopenia, etc.) within the context of the tissues during which they take place. all the ten scientific chapters--skin, cardiovascular procedure, bone and joints, hematopoetic and immune platforms, endocrine, CNS, renal, muscle, GI, and eyes--examines what we all know in their pathology, the function of phone sensescence, and clinical interventions, either present and strength.
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Extra info for Cells, Aging, and Human Disease
1980). In the 1980s, cell senescence theories (Kirkwood, 1984, 1987) attempted to incorporate earlier aging theories, including error catastrophe (Gallant and Prothero, 1980) and free radical theory (Harman, 1956). In the early 1990s, attempts were made to revive these theories (Kowald and Kirkwood, 1994). , 1994b). For two decades, the insights of Olovnikov and Watson lay fallow, with little credence paid to telomere mechanisms. The focus remained on somatic cells and the distinction between somatic and germ cell mortality, largely ignoring cancer cell immortality (Crocker, 2001), despite clinical implications.
2001). , 2002), ensuring simultaneous activity on both chromosomal strands, obviating long, unmatched strands. , 2001). , 1997; Lowell and Pillus, 1998). , 2000). Telomerase activity, hence length and stability, may be controlled through access to the telomere (Shay, 1999a). , 2001). , 2000). , 1998), even if their regulation remains unclear (Kipling, 1995b, pp 111–113; Greider, 1996; Shore, 1997a). , 1997), with the lessons of one species likely relevant to another. Crossbreeding Mus musculus (telomeres >25 kb) and M.
Chromosomes replicate in another fashion and telomere shortening does not occur, or 3. an unknown mechanism relengthens telomeres (at least in germ cells) and maintains species survival. Readers may dismiss the first mechanism, while the second has a modicum of truth. We do not fully understand replication nor the gamut of mechanisms responsible for telomere maintenance. The third mechanism proved accurate. Early theory (Blackburn and Szostak, 1984; Zakian, 1989) has yielded to data on telomere-extending mechanisms (Greider and Blackburn, 1985; Greider, 1995), especially telomerase.