By Michael B. Fossel
Cells, getting older, and Human Disease is the 1st ebook to discover getting older all of the manner from genes to scientific program, studying the basic mobile adjustments which underlie human age-related illness. With over 4,000 references, this article explores either the basic tactics of human getting older and the tissue-by-tissue pathology, detailing either breaking study and present state of the art medical interventions in getting older and age-related affliction. faraway from only sharing a typical onset overdue within the lifespan, age-related illnesses are associated by way of basic universal features on the genetic and mobile degrees. Emphasizing human cellphone mechanisms, the 1st part provides and analyzes our present knowledege of telomere biology and mobilephone senescence. In outstanding educational aspect, the textual content brings the reader brand new on telomere upkeep, telomerase dynamics, and present examine on phone senescence--and the overall model--cell senescence because the significant part in human senescence and melanoma. for every human malignancy, the bankruptcy studies and analyzes all on hand facts on telomeres and telomerase, in addition to summarizing present paintings on their scientific software in either analysis and melanoma treatment. the second one variation, orientated through organs and tissues, explores the particular physiological impression of cellphone senescence and getting older on medical disorder. After a precis of the literature on early getting older syndromes--the progerias--the textual content studies getting older ailments (Alzheimer's dementia, osteoarthritis, atherosclerosis, immune getting older, presbyopia, sarcopenia, etc.) within the context of the tissues within which they ensue. all of the ten medical chapters--skin, cardiovascular approach, bone and joints, hematopoetic and immune structures, endocrine, CNS, renal, muscle, GI, and eyes--examines what we all know in their pathology, the function of telephone sensescence, and scientific interventions, either present and strength.
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Sample text
In four decades, telomerase has changed from Watson’s theoretical “loose end” to a method of immortalizing human somatic cells with enormous clinical potential. In answer to our first question: telomeres and telomerase control cell senescence. , 1994; Hayflick, 1998a), has occupied many researchers over four decades (Hayflick, 1989, 1991) and is the foundation for this book. The potential relevance for aging provided a strong impetus for research (Cristofalo, 1996), but little was initially known (Hayflick, 1984a).
2000; Shay and Wright, 2000b). , 1998). Exceptions include germ and stem cells, and likely a few potentially proliferative cells in otherwise telomerase-negative tissues. , 1998). , 2002). , 1993). The regulation of hTERT expression may be the norm for human cells, but with exceptions. Human lymphocytes may express hTR and hTERT, while telomerase activity remains undetectable. , 2000). , 2002). , 2000) and might conceivably regulate hTERT in normal cells. , 1997a), hStau, and L22. These apparently independent proteins may play roles in hTR processing, telomerase assembly, or localization within the cell.
1996), much remained unclear and without a unifying theoretical framework. , 1977). , 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.