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NO AGING GENES. “Many confuse aging with longevity determination, which is indirectly driven by genes. There are no genes for aging. There are genes to maintain the biological functionality of an organism up to and including reproductive success. There is no mechanism that immediately causes death after reproductive maturation; it’s too costly. Longevity determination asks ‘Why do we live as long as we do?’ Aging research asks ‘Why does everything ultimately fail?’ and that is a huge difference.” https://lnkd.in/dQMB4k7 View in LinkedIn

ENTROPY AND PATHOLOGY. “When molecular disorder occurs in dividing cells in vivo, post mitotics may also be affected and both may then reveal increasing vulnerability to pathology and subsequent death of the individual well before species maximum longevity is reached.” https://lnkd.in/esfPTAR View in LinkedIn

YOUTH YIELDS TO AGE. “The number of population doublings that a cell strain is capable of undergoing and that is determined by telomere length, may be the in vitro expression of maximum potential longevity. The hundreds of molecular disorders that herald the approaching loss of replicative capacity, and diminution of telomere length, are age changes.” https://lnkd.in/esfPTAR View in LinkedIn

CELLULAR ENTROPY. “Hundreds of biological changes occur in normal cells as they replicate in vitro resulting in increasing molecular disorder and loss of cell function.” https://lnkd.in/esfPTAR View in LinkedIn

THE REMNANT. “After reproductive maturity in animals that age, the level of remaining physiological reserve determines longevity. The reserve does not renew at the same rate that it incurs losses because mole- cular disorder increases at a rate greater than does capacity for repair. This increase in molecular disorder is aging which increases vulnerability to predation, accidents or disease.” https://lnkd.in/esfPTAR View in LinkedIn

ACROSS KINGDOMS. “In normal mammalian somatic tissues, the stem or progenitor cells with high proliferation capacity have telomerase competence or the ability to express telomerase. In addition, increasing evidence has linked telomerase expression to cell proliferation rates. This model was extended by findings in the plant kingdom. Cells with high proliferation capacity and high mitotic activity reside in meristematic tissue. Telomerase activities were detected in these tissues as well as in cultured cells, whereas non-dividing cells from leaves and axillary buds were telomerase negative.” http://onlinelibrary.wiley.com/doi/10.1016/S0014-5793(98)01020-5/full View in LinkedIn

TELOMERASE LEVELS. “While normal human cells have little or no telomerase, stem cells were found to have high levels. Cancer cells, which have very high telomerase activity, are thought to achieve immortality in this way. It has since been established that telomerase defects are behind some inherited diseases, such as congenital aplastic anaemia, where stem cells in the bone marrow do not replicate sufficiently." http://www.bionews.org.uk/page_367898.asp View in LinkedIn

TETRAHYMENA THERMOPHILA “contains telomerase, that could replenish telomeres. Dr Blackburn established this unequivocally by mutating the telomerase gene in the tetrahymena and showing that this caused cell malfunction.” https://lnkd.in/d-EtCGX View in LinkedIn

VERY VARIED SYSTEM. "Some plants have only one type of sporophyte, but two types of gametophytes (essentially male and female gametophytes; the male only produces sperm, the female only produces eggs). Other plants have male and female sporophytes as well (male sporophyte only produces spores that create male gametophytes, and so on). Some plants can have just one type of sporophyte and just one type of gametophyte (in this case the single gametophyte produces both eggs and sperm)." https://lnkd.in/dDq6NXv View in LinkedIn

“TELOMERASE ACTIVATION may be possible, to help reverse natural senescence in cells. Humans lack sufficient telomerase enzyme to stop telomeres from shortening and causing aging. Telomerase activation is an area of research aimed to try and slow cellular aging.” https://lnkd.in/deXSTEu View in LinkedIn