Talk:Hayflick limit

Latest comment: 1 year ago by Boud in topic Say what?

does hayflick effectr vary with liquid or plate tissue culture

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Id appreciate it noting the kind of tissue culture, right now im thinking about the difference between the hayflick effect at a liquid culture compared with a plate culture. At a liquid culture neighbor cyte surface receptors as well as chemokines would apparently be much less directive of longevity than a plate tissue culture where each cyte has actual neighbors that it shares receptors as well as microchemoenvironment with. thus if liquid culture cytes have the same hayflick number as neighbored plate culture cytes, then surface receptor communication or spacing would be nonrelevant to cytosenescence.

a long way of saying, I urge someone to note whether the hayflick effect is liquid or plate culture at the article. — Preceding unsigned comment added by 63.224.196.40 (talk) 19:35, 25 January 2012 (UTC)Reply

Repetition repetition

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holy immortal cells, batman (four times in one sentence, geez)

{{sofixit}}, robin. JFW | T@lk 01:50, 29 January 2006 (UTC)Reply

PS Moorhead deserves mention in this aricle as it was "their" seminal paper in 1961. Research in tissue culture biology basically. They are a number of good history of tissue culture books.GetAgrippa 14:30, 20 November 2006 (UTC)Reply

Reference?

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Where can one find more information pertaining to the sentence about long-lived marine birds? 64.106.37.180 (talk) 16:25, 23 October 2008 (UTC)Reply

Telomeres and Aging

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I added a citation needed tag next to the statement that telomere shortening in humans is correlated with aging. While I think it's pretty well explained - perhaps, anyway - how telomere shortening in individual cells is related (or even causes) the "aging" of those individual cells. What is far less clear is how this applies to the human body as a whole. I think this article deserves a section dedicated to aging - not of cells, but of the whole body. It is an extremely interesting catalyst for discussion and investigation of the aging process (I've participated in some very interesting dinner conversations on exactly this topic). Anyone who has material that addresses the macroscopic aging process's relationship with telomeres (and telomerase) would be very appreciated for contributing it! Spiral5800 (talk) 12:24, 4 January 2010 (UTC)Reply

I have since removed that citation needed tag - but I believe the statement that "Telomere shortening in humans eventually blocks cell division and correlates with aging" needs clarification. I've therefore replaced my citation needed tag with a clarify tag. The discussion about the details of what role telomeres play in aging, however, would probably be best located in the article on telomeres and in the article on aging. Spiral5800 (talk) 20:59, 5 January 2010 (UTC)Reply

Direct quotation without attribution

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A large part of the Discovery section of this article is a direct quotation from [1] without attribution. Not sure of the proper way to fix this -- clearly it needs to be cited; should it be highlighted as a quotation? What's the general policy on such copying once it's properly cited? OrbitSoldier (talk) 17:05, 19 January 2011 (UTC)Reply

References

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  1. ^ Shay, J. W. and Wright, W. E. (2000). "Hayflick, his limit, and cellular ageing". Nat. Rev. Molec. Cell Biol. 1 (1): 72–76. doi:10.1038/35036093.{{cite journal}}: CS1 maint: multiple names: authors list (link)

This article needs a rewritting

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Huge confusion between senescence and cell crisis. Cells grows in vitro, then stops because of physiologic stress (for exemple, the proliferative capacity of cell population is greater when you cultivate them under 3% of Oxygen instead of 20%) When they reach senescence they remain viable but don't duplicates anymore. If you trick the cell past this hayflick limit (inhibition of CDK inhibitors like P16, P21, pRb, p53..) they will duplicates another 10 or 20 times, then reach "crisis" and enter apoptosis. Crisis is due to shortening telomeres. Senescence isn't —Preceding unsigned comment added by 87.88.187.66 (talk) 10:50, 9 March 2011 (UTC)Reply

I agree with 87.88.187.66 that this article needs rewriting. Here are some relevant excerpts from a scientific book, which may help to those who will do such rewriting: http://longevity-science.org/pdf/Biology-of-Lifespan-5.6.pdf Good luck! Gavrilov (talk) 23:45, 20 August 2011 (UTC)Reply


Please see below an insertion to the article suggested by MoJohn47 (talk) 17:07, 25 August 2010 (UTC)MoJohn and initially posted at Talk:Leonard Hayflick: http://en.wiki.x.io/wiki/Talk:Leonard_Hayflick
======= August 25, 2010 ====== COMMENT ================

"Weismann-Swim-Hayflick Limit The antiquated idea that lifespan might be determined by the limited capacity of somatic cells to divide was originated by the famous German biologist August Weismann in 1892 (1). Mechnikov, who coined the term “gerontology,” discussed Weismann’s theory of cell division limit in his book “Essais optimistes” published in 1907 (2). In the 1950s the first convincing experimental evidence that animal cells in culture cannot be propagated indefinitely was presented by Swim, Parker, and Haff from Western Reserve University School of Medicine (3 – 5), and their results were reproduced by Hayflick and Moorhead in 1961 (6). The popular press has persisted in using the term “The Hayflick Limit” to promote the scientifically naïve idea that the human lifespan is determined by a limited number of cell divisions, although the relevance of finite divisions by fibroblasts in culture to lifespan in an organism, e.g. a person, is highly questionable (7, 8, 9). The observation that many types of cells derived from normal tissue have a finite capacity to divide in culture might be more accurately termed the Weismann-Swim-Hayflick Limit (10). 1. Weismann, A. (1892). Uber Leben und Tod. Verlag von Gustav Fisher, Jena. 2. Mechnikov, I.I. (1907). Essais optimistes. Paris, 438 p. Author: Mechnikov, I. I. (Ilíà Ilich), 1845-1916 Subject: Longévité Publisher: Paris: A. Maloine Language: French; Russian Call number: b1650679 Digitizing sponsor: University of Ottawa Written in French. Titre original: Etiudy optimizma. 3. Haff, R.F. and Swim, H.E. (1956). Serial propagation of 3 strains of rabbit fibroblasts; their susceptibility to infection with Vaccinia virus. Proc.Soc.Exp.Biol.Med., 93, 200-204. 4. Swim, H.E. and Parker, R.F. (1957). Culture characteristics of human fibroblasts propagated serially. Am.J.Hygiene, 66, 235-243. 5. Swim, H.E. (1959). Microbiological aspects of tissue culture. Ann.Rev.Microbiol. 13, 141-176. 6. Hayflick, L., Moorhead, P.S. The serial cultivation of human diploid cell strains. Exp Cell Res. 1961;25:585-621. 7. Rubin H. The disparity between human cell senescence in vitro and lifelong replication in vivo. Nat Biotechnol. 2002 Jul;20(7):675-81. Review. PMID: 12089551 8. Macieira-Coelho A. The implications of the 'hayflick limit' for aging of the organism have been misunderstood by many gerontologists. Gerontology. 1995;41(2):94-7. Review. 1995;41(4):241. PMID: 7744273 9. de Magalhães JP. From cells to ageing: a review of models and mechanisms of cellular senescence and their impact on human ageing. Exp Cell Res. 2004 Oct 15;300(1):1-10. Review.PMID: 15383309 10. Gavrilov, L.A. and Gavrilova, N.S. (1991). The Biology of Life Span: a Quantitative Approach. Harwood Academic Publishers GMBH, Chur, etc. ISBN: 3-7186-4983-7. MoJohn47 (talk) 17:07, 25 August 2010 (UTC)MoJohn"Reply

End of citation — Preceding unsigned comment added by Gavrilov (talkcontribs) 01:40, 24 August 2011 (UTC)Reply

Man masturbation and active sexual life

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Just read the article and sitting in a bad mood. Just curious. If this theory is true... than every coitus will led to ill kids for a man. Man forcing the DNA splits on every coitus. And this will damage DNA in germ cells. Can any biologist comment this? 91.77.231.247 (talk) 15:06, 16 July 2012 (UTC)Reply

Germ cells have telomerase on, so limit does not apply. 2A00:1370:8184:164:44D3:B894:4A84:3BFC (talk) 22:27, 15 April 2022 (UTC)Reply

Carnosine is now mentioned, any other beneficial compounds for humans?

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https://examine.com/supplements/astragalus-membranaceus/ "The HDTIC isomers from Astragalus have been shown to shorten the rate of telomere shortening in vitro" "There may be more than one bioactive in Astragalus Membranceus contributing to telomere length".


https://examine.com/supplements/beta-alanine/ "Beta-alanine is the building block of carnosine" "This anti-aging effect may be due to carnosine’s ability to reduce the rate of telomere shortening, as was noted at 20 mM in cultured human fibroblasts".

ee1518 (talk) 18:18, 3 October 2016 (UTC)Reply

Say what?

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The article goes to pretty long lengths to tell and demonstrate the effect, and point out the exceptions. At the end of the section about experimentation, this is anomalously stuck onto the end:

"However, L. Franks and others (Loo et al. 1987; Nooden and Tompson 1995; Frolkis 1988a), have shown that the number of cell divisions can be considerably greater than that stipulated by the "Hayflick Limit", having practically no limit at all."

That would seem to be a pretty important point that would need to be amplified upon in view of the rest of the article, probably its own section. The references given are 27 years old or greater and not linked, they appear to have been copied from some other paper. Is it real or a prank? SkoreKeep (talk) 18:33, 3 January 2022 (UTC)Reply

I put a chunk of this sentence into a search engine, and it has indeed been copied wholesale from a paper - https://www.researchgate.net/publication/236227809_Three_layer_functional_model_and_energy_exchange_concept_of_aging_process . It looks like a one-horse paper in a one-horse journal, speculating about the ageing process by way of discussing energy inputs and outputs and drawing parallels between the structure of cells, the structure of human bodies and the structure of planets, but the other papers referenced in that sentence seem to be quite genuine. This rather more mainstream-looking review seems to cite at least one of them and give some more information about the context https://www.researchgate.net/profile/Graham-Pawelec/publication/11378277_T_cells_and_aging_January_2002_update/links/0912f50c08782afdf2000000/T-cells-and-aging-January-2002-update.pdf (page 32, for instance).
Rather than a prank, it seems to be a symptom of the Wikipedia article being in a bit of a muddle. It seems to equate the Hayflick limit (aka replicative senescence) with running out of telomere (aka cell crisis), but apparently they're not the same thing. Apparently in cultures of human cells they happen at roughly the same time, but in cultures of rodent cells, which have very long telomeres (possibly because rodents wear through cells faster so they have to divide more often), the Hayflick limit is usually reached long before the telomeres run out, and using a different culture medium (something to do with using growth factors instead of serum) can overcome this so that the cells go on dividing until, after many more divisions, the telomeres run out and cell crisis occurs. (I think, though I'm not sure - I'm not a specialist in biology and this is just based on a quick look at some of the papers). It seems to be a bit of a mess and maybe somebody who knows about cell biology can rewrite the article. Wombat140 (talk) 04:39, 19 December 2022 (UTC)Reply
Boud (talk · contribs) Possibly, this, and also the "This article needs a rewritting" section, explain what's going on with those citations. Wombat140 (talk) 07:16, 5 August 2023 (UTC)Reply
@Wombat140: I suspect that it was neither real nor a prank - it seems like an accident, since this seems to be the first time that the user was alerted for copyvios, and the edit description doesn't match the edit.
My impression is that someone with the patience to find good reviews and proper references shouldn't need too much work to update and tidy the article. A lot of the content seems good (to me with no specialist knowledge of the topic). Boud (talk) 20:55, 6 August 2023 (UTC)Reply