From owner-ageing@net.bio.net Fri Jul 01 23:00:00 1994 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!munnari.oz.au!sol.ccs.deakin.edu.au!pc19-slip.ccs-stub.deakin.edu.au!drierac From: drierac@deakin.edu.au (Chris Driver) Newsgroups: bionet.molbio.ageing Subject: menopause Date: Sat, 2 Jul 1994 11:23:30 Organization: Deakin University Lines: 22 Message-ID: NNTP-Posting-Host: pc19-slip.ccs-stub.deakin.edu.au Keywords: Drosophila X-Newsreader: Trumpet for Windows [Version 1.0 Rev A] It might be worth pointing out that some experimental animals also enter a sort of menpause. I have found with Drosophila (Canton-S) that I can maintain them for 60-80 days (sometimes less, sometimes more) and the females stop producing offspring by about 40-50 days. There is a also a decline in mating ability-old males lose their ability to make young females pregnant, because they can't get the mating dance right. There is the occasional old male who can suucessfully mount but is unable to dismount and dies on the females back. Old females by contrast seem to accept the old males because they are less choosy. Draw your own conclusions about the application of these studies to humans. There is also some other behavioral changes such as the loss of alarm responsiveness and failure of "memory" which is also virtually complete by late middle age. It looks to me like asynchronous loss of separate organ systems, and I cannot find any positive survival advantage for this. Chris Driver Deakin University Australia From owner-ageing@net.bio.net Mon Jul 04 23:00:00 1994 Path: biosci!galaxy.ucr.edu!library.ucla.edu!europa.eng.gtefsd.com!howland.reston.ans.net!gatech!concert!bigblue.oit.unc.edu!samba.oit.unc.edu!not-for-mail From: Mitchell.Porter@launchpad.unc.edu (Mitchell Porter) Newsgroups: bionet.molbio.ageing,sci.life-extension,sci.cryonics Subject: Net resources on ageing and life extension Date: 5 Jul 1994 05:58:23 GMT Organization: University of North Carolina Extended Bulletin Board Service Lines: 11 Distribution: world Message-ID: <2vaspv$qrs@samba.oit.unc.edu> NNTP-Posting-Host: lambada.oit.unc.edu Xref: biosci bionet.molbio.ageing:891 sci.life-extension:1598 sci.cryonics:992 I intend to assemble a guide containing pointers to all known _net_ resources regarding research on ageing and the concept of life extension. E-mail or post references please. I will post Version 1.0 to these newsgroups, and hope to get it linked into the WorldWideWeb eventually. (If such a guide already exists, of course, outside Usenet FAQs, please lte me know.) -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- Launchpad is an experimental internet BBS. The views of its users do not necessarily represent those of UNC-Chapel Hill, OIT, or the SysOps. -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- From owner-ageing@net.bio.net Tue Jul 05 23:00:00 1994 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!munnari.oz.au!sol.ccs.deakin.edu.au!pc20-slip.ccs-stub.deakin.edu.au!drierac From: drierac@deakin.edu.au (Chris Driver) Newsgroups: bionet.molbio.ageing Subject: Transposable elements cause ageing? Date: Wed, 6 Jul 1994 10:09:54 Organization: Deakin University Lines: 65 Message-ID: NNTP-Posting-Host: pc20-slip.ccs-stub.deakin.edu.au X-Newsreader: Trumpet for Windows [Version 1.0 Rev A] I would like networkers opinions on an idea we have been discussing in Australia. This is that transposable elements are the principal cause of ageing. If you consider all methods of mutation accumulation,most mutations that are deleterious would be removed from a population by selection. Transposable elements, particularly retro-transposons are different. They can replicate within a cell, accumulating for some time without conferring any disadvantage. However the exponential growth within the cell means that at some time the rate of damage accumulation is sufficient to stop all cells in their tracks. I suggest that the type of damage that is critical to cessation of growth is ss DNa breaks. These would lead to aneuploidy and worse if replication proceeded. The cell contains a set of guardians including p53 and p21 which are responsible for preventing entry into S phase until the damage is repaired. Senesecence is characterised by sufficient ss DNA breaks to slow and ultimately stop cell cycling. The same reaction is responsible for the alterations in protein synthesis. Notice that this process would be independent of ploidy number. Immortalisation: the first step- loss of functional guardian genes. This would result in chromosomal instability and ultimately death for most cells. However if a cell is able to lose sufficient of the active transposable elements when it loses chromosomal pieces, it can continue to replicate and has progressed through to a immortality In non dividing cells. other modes of DNA damage may not be so readily removed. At the same time many of the DNA alterations may not be so deleterious. However TEs have to be able to replicate in non dividing cells as described above, and because they can exponentially increase, may pose the single biggest threat to non dividing cells as well. Steve McKechnie and I have published a paper in Ann NY Acad Sci , 673, 83-91, 1993 in which we indicate that TEs are important in the ageing of Drosophila. A paper follows in which Inhibitors of reverse transcriptase, which would be expected to inhibit replication of TEs, slows ageing. This is Driver and Vogrig, Ann NY Acad Sci, in press. TEs are faced with the survival logic of a parasite. To replicate they msut do some damage, but if they replicate too much they will kill the host and die with it. There is a double problem. Germ line mutations cannot be too high. In addition most transposable elements are active in somatic tissue, in many cases more so than in the germ line. As far as the somatic activity goes, there will be no selection if the activity is sufficiently that the host would be expected to die of something else first, such as predation or starvation. Thus one would expect that in general ageing would not set in until after most animals would die in the wild. A rapid change in environmental conditions such as has happened with some human populations, would change this and ageing could be a major factor in adult viability. See also Murrey, V (1990) Mut Res 237:59-63 Brown, AR, Tso POP and Cutler RG (1991). Arch Gerontol and Geriatrics 13:15-30 I would particularly like to hear from someone from the RG Cutler group. Chris Driver Deakin University Australia 15-30 From owner-ageing@net.bio.net Tue Jul 05 23:00:00 1994 Path: biosci!DRUID.HSC.COLORADO.EDU!mandy From: mandy@DRUID.HSC.COLORADO.EDU (Mandy Caird PhD) Newsgroups: bionet.molbio.ageing Subject: Experimental drug E09? Date: 6 Jul 1994 08:24:08 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 8 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Does anyone know of any database/place I could look to find information on an experimental cancer drug called E09? ^^^ I think is has been tested in Amsterdam and I have heard that patients lose protein from their kidneys. Does anyone have other information on mechanism, etc? Thanks, Mandy From owner-ageing@net.bio.net Thu Jul 07 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!cs.utexas.edu!convex!news.duke.edu!news-feed-1.peachnet.edu!ukma!seqanal.mi.uky.edu!mpm From: mpm@seqanal.mi.uky.edu (Mark Mattson) Newsgroups: bionet.molbio.ageing Subject: Re: Transposable elements cause ageing? Date: 8 Jul 1994 14:40:02 GMT Organization: University of Kentucky, Dept. of Math Sciences Lines: 91 Message-ID: <2vjog2$3cs@s.ms.uky.edu> References: NNTP-Posting-Host: seqanal.mi.uky.edu X-Newsreader: TIN [version 1.1 PL9] Chris Driver (drierac@deakin.edu.au) wrote: : I would like networkers opinions on an idea we have been discussing in : Australia. This is that transposable elements are the principal cause of : ageing. : If you consider all methods of mutation accumulation,most mutations that are : deleterious would be removed from a population by selection. Transposable : elements, particularly retro-transposons are different. They can replicate : within a cell, accumulating for some time without conferring any disadvantage. : However the exponential growth within the cell means that at some time the : rate of damage accumulation is sufficient to stop all cells in their tracks. : I suggest that the type of damage that is critical to cessation of growth is : ss DNa breaks. These would lead to aneuploidy and worse if replication : proceeded. The cell contains a set of guardians including p53 and p21 which : are responsible for preventing entry into S phase until the damage is : repaired. Senesecence is characterised by sufficient ss DNA breaks to slow and : ultimately stop cell cycling. The same reaction is responsible for the : alterations in protein synthesis. : Notice that this process would be independent of ploidy number. : Immortalisation: the first step- loss of functional guardian genes. This would : result in chromosomal instability and ultimately death for most cells. However : if a cell is able to lose sufficient of the active transposable elements when : it loses chromosomal pieces, it can continue to replicate and has progressed : through to a immortality : In non dividing cells. other modes of DNA damage may not be so readily : removed. At the same time many of the DNA alterations may not be so : deleterious. However TEs have to be able to replicate in non dividing cells as : described above, and because they can exponentially increase, may pose the : single biggest threat to non dividing cells as well. Steve McKechnie and I : have published a paper in Ann NY Acad Sci , 673, 83-91, 1993 in which we : indicate that TEs are important in the ageing of Drosophila. A paper follows : in which Inhibitors of reverse transcriptase, which would be expected to : inhibit replication of TEs, slows ageing. This is Driver and Vogrig, Ann NY : Acad Sci, in press. : TEs are faced with the survival logic of a parasite. To replicate they msut do : some damage, but if they replicate too much they will kill the host and die : with it. There is a double problem. Germ line mutations cannot be too high. In : addition most transposable elements are active in somatic tissue, in many : cases more so than in the germ line. As far as the somatic activity goes, : there will be no selection if the activity is sufficiently that the host would : be expected to die of something else first, such as predation or starvation. : Thus one would expect that in general ageing would not set in until after most : animals would die in the wild. A rapid change in environmental conditions such : as has happened with some human populations, would change this and ageing : could be a major factor in adult viability. : See also : Murrey, V (1990) Mut Res 237:59-63 : Brown, AR, Tso POP and Cutler RG (1991). Arch Gerontol and Geriatrics 13:15-30 : I would particularly like to hear from someone from the RG Cutler group. : Chris Driver : Deakin University : Australia : : 15-30 As is often the case, I think it is important here to distinguish the umbrella of "aging" from senesence. Clearly there are components of aging which are completely independent of the genome. Loss of elasticity in fibrous, acellular tissue and accumulation of calcium-phosphate precipitates in the mitochondrial matrix come to mind. In this regard, I applaud you for separately discussing senesence and non-dividing cells. The immortalization problem is sticky. Although I don't have the references handy, others have shown correlation of immortalization with oncogenes (e.g., v-myc) or loss of tumor suppressor genes. It is difficult to believe intuitively that -- given the number of TE's you propose to be flopping around in our genomes -- that all of the senesence-invoking ones could be lost simultaneously often enough to generate immortalization at the rate one sees it occur in cultured cells. The odds just seem against it. I look forward to reading your Ann. NY Acad. Sci. paper(s). Best regards, Steven W. Barger, Ph.D. Sanders-Brown Center on Aging University of Kentucky USA From owner-ageing@net.bio.net Thu Jul 07 23:00:00 1994 Path: biosci!DRUID.HSC.COLORADO.EDU!mandy From: mandy@DRUID.HSC.COLORADO.EDU (Mandy Caird PhD) Newsgroups: bionet.molbio.ageing Subject: Non-radio-isotope-detection???? Date: 8 Jul 1994 14:13:02 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 17 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net I am starting to screen some expression and non-expression libraries and I would like to try to do this by using non-radioactive probes. On reading the bumph from:- Amersham ECL system BM Genius system Promega Lightsmith systems I am completely bamboozled as to which systems are best for what! Does any one have any preferences regarding different company's systems with antibodies or oligos? Or should I stick with P-32? Thanks Mandy From owner-ageing@net.bio.net Fri Jul 08 23:00:00 1994 Path: biosci!agate!ihnp4.ucsd.edu!sdd.hp.com!portal.com!stf From: stf@shell.portal.com (Samuel T Fivian) Newsgroups: bionet.molbio.ageing,sci.life-extension,sci.cryonics Subject: Re: Net resources on ageing and life extension Date: 9 Jul 1994 14:05:06 GMT Organization: Portal Communications Company -- 408/973-9111 (voice) 408/973-8091 (data) Lines: 34 Message-ID: <2vmaqi$i7s@news1.svc.portal.com> References: <2vaspv$qrs@samba.oit.unc.edu> NNTP-Posting-Host: jobe.shell.portal.com Xref: biosci bionet.molbio.ageing:896 sci.life-extension:1613 sci.cryonics:995 In article <2vaspv$qrs@samba.oit.unc.edu>, Mitchell Porter wrote: >I intend to assemble a guide containing pointers to all known _net_ >resources regarding research on ageing and the concept of life extension. >E-mail or post references please. I will post Version 1.0 to these >newsgroups, and hope to get it linked into the WorldWideWeb eventually. > (If such a guide already exists, of course, outside Usenet FAQs, please >lte me know.) >-- >-- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- >Launchpad is an experimental internet BBS. The views of its users do not >necessarily represent those of UNC-Chapel Hill, OIT, or the SysOps. >-- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- Excellent idea. Obtain "The Directory of Life Extension Nutrients and Drugs" 1994, Published by The Life Extension Foundation, P.O.Box 229120, Hollywood, Florida 33022-9120. If you want to join, call 1-800-841-LIFE. It will cost you $50 until July 31st, $75 thereafter ... but, you may be able to obtain the directory by just indicating your interest in, say, Melatonin, or, "Brain-Boosting" Nutrients, such as, DMAE-Ginkgo, Hydergine, etc. etc. Good luck! -- _/stf * Samuel T. Fivian * E-mail : stf@fivian.com * * S.T. FIVIAN, CPA * Internet : stf@shell.portal.com * * si Deus nobiscum est * 156.151.1.104 : nova.unix.portal.com * * quis contra nos erit * Phone : +1 716 271-7470 * From owner-ageing@net.bio.net Mon Jul 18 23:00:00 1994 Path: biosci!agate!doc.ic.ac.uk!daresbury!not-for-mail From: Newsgroups: bionet.molbio.ageing Subject: Smile Date: 19 Jul 1994 13:11:38 +0100 Lines: 8 Sender: daemon@mserv1.dl.ac.uk Distribution: bionet Message-ID: <30gftq$red@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk Secret of long life: A young researcher enquiring from a 100yr man: What is the secret of your long life? Man: Laughing everyday. Researcher: But many people laugh everyday, they all don't live as long! Man: They die early, because they don't keep laughing for long enough...... Aarhus/Denmark From owner-ageing@net.bio.net Tue Jul 19 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!uknet!daresbury!not-for-mail From: Newsgroups: bionet.molbio.ageing Subject: Wise words Date: 20 Jul 1994 11:55:16 +0100 Lines: 4 Sender: daemon@mserv1.dl.ac.uk Distribution: bionet Message-ID: <30ivqk$p8d@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk I thought I have found the key to success, but when I tried it, I found that they had changed the lock!!!!!! Rattan/Aarhus/Denmark From owner-ageing@net.bio.net Tue Jul 19 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!uknet!daresbury!not-for-mail From: Newsgroups: bionet.molbio.ageing Subject: Anti-ageing news Date: 20 Jul 1994 12:16:00 +0100 Lines: 36 Sender: daemon@mserv1.dl.ac.uk Distribution: bionet Message-ID: <30j11g$qlg@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk Folk stories abound with claims that garlic has some anti-ageing effects. Some research has shown that it has some anti-cancer and anti-platelet aggregation effects. No anti-ageing effects of garlic have been studied or published in the scientific literature. Although lots of garlic products are being sold in the market for the treatment of everything including ageing. But here is the first published research paper, of course, by our group!!! Svendsen, Rattan & Clark (1994) Testing garlic for its anti-ageing effects on human fibroblasts in culture. Journal of Ethnopharmacology, vol 43, pp 125-133 (June-July issue). Our results show that: 1. human cells grown in various concentrations of aquous garlic extract maintain some of the youthful characteristics for a longer duration. 2. Same concentrations are generally toxic for cancer cells of various types, and these cells cannot be grown in the presence of garlic for more than a few days as compared with 300-400 days for normal diploid fibroblasts. 3. At some concentrations there can be a slight increase in the proliferative lifespan of normal cells. 4. Unlike kinetin (reported previously) the effects of garl>ic are more subtle and appear to be best as a general maintenance compound. Of course, these are the studies performed on cells in culture and these results may or may not be extrapolatable directly. Yet we think that the way garlic consumption as a regular component of food may work by maintaining the general health of the normal cells while stopping the uncontrolled growth of any newly developing cancerous or immortal cell. Garlic may not prevent ageing, but it may help to reduce cancer formation and perhaps prevent the onset of other age-related pathologies and impairments. Anyway, we have now some "reductionistic scientific" bases to say that garlic can keep some "devils" of age-related diseases at bay!!! Mechanisms of garlic action as anti-ageing still need to be studied. It may involve any cytokinin activity too, who knows. Keep smelling, you will live healthier and a little bit longer.... Suresh Rattan/Aarhus/Denmark From owner-ageing@net.bio.net Tue Jul 19 23:00:00 1994 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!swrinde!howland.reston.ans.net!spool.mu.edu!torn!nermal.cs.uoguelph.ca!herman.cs.uoguelph.ca!nxu From: nxu@uoguelph.ca (Nanfel Xu) Newsgroups: bionet.molbio.ageing Subject: Re: Anti-ageing news Date: 20 Jul 1994 21:34:38 GMT Organization: University of Guelph Lines: 41 Distribution: bionet Message-ID: <30k59e$ius@nermal.cs.uoguelph.ca> References: <30j11g$qlg@mserv1.dl.ac.uk> NNTP-Posting-Host: herman.cs.uoguelph.ca X-Newsreader: TIN [version 1.2 PL2] I heard some people say that garlic can reduce allergy reactions. Is there any proves of this. RATTAN@kemi.aau.dk wrote: : Folk stories abound with claims that garlic has some anti-ageing : effects. Some research has shown that it has some anti-cancer and : anti-platelet aggregation effects. No anti-ageing effects of garlic have : been studied or published in the scientific literature. Although lots of : garlic products are being sold in the market for the treatment of everything : including ageing. But here is the first published research paper, of course, : by our group!!! : Svendsen, Rattan & Clark (1994) Testing garlic for its anti-ageing effects : on human fibroblasts in culture. Journal of Ethnopharmacology, vol 43, : pp 125-133 (June-July issue). : Our results show that: : 1. human cells grown in various concentrations of aquous garlic extract : maintain some of the youthful characteristics for a longer duration. : 2. Same concentrations are generally toxic for cancer cells of various : types, and these cells cannot be grown in the presence of garlic for more : than a few days as compared with 300-400 days for normal diploid fibroblasts. : 3. At some concentrations there can be a slight increase in the proliferative : lifespan of normal cells. : 4. Unlike kinetin (reported previously) the effects of garl>ic are more : subtle and appear to be best as a general maintenance compound. : Of course, these are the studies performed on cells in culture and these : results may or may not be extrapolatable directly. Yet we think that the way : garlic consumption as a regular component of food may work by maintaining : the general health of the normal cells while stopping the uncontrolled : growth of any newly developing cancerous or immortal cell. Garlic may not : prevent ageing, but it may help to reduce cancer formation and perhaps : prevent the onset of other age-related pathologies and impairments. : Anyway, we have now some "reductionistic scientific" bases to say that : garlic can keep some "devils" of age-related diseases at bay!!! : Mechanisms of garlic action as anti-ageing still need to be studied. : It may involve any cytokinin activity too, who knows. : Keep smelling, you will live healthier and a little bit longer.... : Suresh Rattan/Aarhus/Denmark From owner-ageing@net.bio.net Sat Jul 23 23:00:00 1994 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!munnari.oz.au!ariel.ucs.unimelb.EDU.AU!ariel!andy From: andy@ariel.ucs.unimelb.EDU.AU (Andrew Jarvis) Newsgroups: bionet.molbio.ageing Subject: mail list entitled "AMYLOID" Date: 25 Jul 1994 09:34:14 +1000 Organization: University of Melbourne Lines: 13 Message-ID: NNTP-Posting-Host: ariel.ucs.unimelb.edu.au Summary: setting up of a new list Keywords: Alzheimer's disease research I am planning to set up in the next few days a mail list entitled "AMYLOID", which will be the prototype of a future newsgroup. The aim of the mail list is to provide subscribers will a discussion forum for recent results in the field of Alzheimer's disease research and to provide a means of rapidly advertising meeting, research findings etc. If you are interested in subscribing to **AMYLOID**, please send your full name and E-mail address to david_small@muwayf.unimelb.edu.au. Or post the information to Dr. David Small, Dept. of Pathology, University of Melbourne, Parkville, Victoria, 3052, Australia. ****!!!! PLEASE NOTE: DO NOT REPLY BY RETURN MAIL TO THE ADDRESS FROM WHICH THIS MESSAGE WAS SENT AS I WILL NOT RECEIVE IT !!!!**** From owner-ageing@net.bio.net Mon Jul 25 23:00:00 1994 Path: biosci!rutgers!concert!news-feed-1.peachnet.edu!news.duke.edu!godot.cc.duq.edu!newsfeed.pitt.edu!uunet!munnari.oz.au!sol.ccs.deakin.edu.au!pc02-slip.ccs-stub.deakin.edu.au!drierac From: drierac@deakin.edu.au (Chris Driver) Newsgroups: bionet.molbio.ageing Subject: How to measure aging in vitro Date: Tue, 26 Jul 1994 11:48:34 Organization: Deakin University Lines: 22 Message-ID: NNTP-Posting-Host: pc02-slip.ccs-stub.deakin.edu.au X-Newsreader: Trumpet for Windows [Version 1.0 Rev A] I have seen a number of papers in which substances will alter the lifespan of cells in culture. One thing that appears to be a common feature in these reports is that repeat runs of apparently identical conditions are not particularly reproduceable. Robin Halliday in his paper comments on this and suggests that a clonal succession may occur, where old cell lines are dominated by clones arising from the odd cell that is rather less senescent than their sibling cells. In theory it should be possible to detect senescent cells arising in cultures in about midpassage and quantify them. Has anyone any thoughts on this matter? An alternative, but less useful approach may be to use markers for senescence in the total cell mass. Has anyone any suggestions for good markers? Chris Driver Chris Driver, Ph D School of Biology and Chemistry, Rusden Campus Deakin University 662 Blackburn Rd Clayton, VIC, 3168 AUSTRALIA From owner-ageing@net.bio.net Thu Jul 28 23:00:00 1994 Path: biosci!agate!doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Re: How to measure aging in vitro Date: 29 Jul 1994 12:43:39 GMT Organization: University of Sussex Lines: 56 Message-ID: <31athr$s36@infa.central.susx.ac.uk> References: NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] Chris Driver (drierac@deakin.edu.au) wrote: : I have seen a number of papers in which substances will alter the lifespan of : cells in culture. One thing that appears to be a common feature in these : reports is that repeat runs of apparently identical conditions are not : particularly reproduceable. Robin Halliday in his paper comments on this and : suggests that a clonal succession may occur, where old cell lines are : dominated by clones arising from the odd cell that is rather less senescent : than their sibling cells. We have done quite a lot of work on this. Originally J. Smith et al showed that it was true that successive waves of cell clones emerge during the lifespan of human cells. He showed that in clonies that were short-lived there were cells that could generate bigger colonies than the parent clone. We have subsequently confirmed this, and have directly measured the fraction of growing cells in an ageing population; we found that there is always a fraction of senescent cells, even in a young population. What changes with ageing is the fraction of non-dividing, senescent cells in the population. From the beginning of the culture there are some senescent cells present; as the culture divides the fraction of non-dividing, senescent cells increases until the fraction of new-born cells which are non-dividers, that means reproductively sterile, is greater than 50%. At this point the culture will inevitably begin to decline. Because although there are dividing cells in the population, each set of new-born cells has fewer fertile cells thatn the last generation. Clearly, eventually, the fraction of new-born cells able to divide will eventually reach zero and the culture will be entirely post-mitotic. : In theory it should be possible to detect senescent cells arising in cultures : in about midpassage and quantify them. Has anyone any thoughts on this matter? We have precisely this. At the moment there is not available yet a reliable easy marker for senescent cells, although recently a number of potential candidates have come to light. What we have done then is to score all the cells in a population with antibodies to proteins which are characteristic of dividing cells; or we have used bromo-deoxyuridine incorporation (to simulate thymidine) to measure DNA synthesis. In this way we measured the fraction of cells throughtout the lifespan that were dividers, and by difference the remainder of the population are non-dividing, that is senescent cells. : An alternative, but less useful approach may be to use markers for senescence : in the total cell mass. Has anyone any suggestions for good markers? : Chris Driver : Chris Driver, Ph D : School of Biology and Chemistry, Rusden Campus : Deakin University : 662 Blackburn Rd : Clayton, VIC, 3168 : AUSTRALIA -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Telephone: +44.273.67.83.03 FAX: +44.273.67.84.33 From owner-ageing@net.bio.net Thu Jul 28 23:00:00 1994 Path: biosci!URIACC.URI.EDU!DPEARL From: DPEARL@URIACC.URI.EDU Newsgroups: bionet.molbio.ageing Subject: Pycnogenol Date: 29 Jul 1994 09:29:31 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 21 Sender: daemon@net.bio.net Distribution: world Message-ID: <199407291629.JAA22066@net.bio.net> NNTP-Posting-Host: net.bio.net Does anyone know of any *real* research done on an FDA-approved food-additive called Pycnogenol, supposedly a super antioxidant whose primary active ingredient comes from certain cultivated pine trees in France? It is marketed in this country under a KAIRE brand name and is being touted, rather aggressively, as among other things an anti-aging potion 50 times more powerful than other known antioxidants and a great facilitator of vitamin C absorption. It is supposed to have restorative effects on skin, blood vessels, vision, etc. The "research" I've been handed is clearly company-supported. The pills themselves are rather expensive, and it is possible that a lot of people are being taken advantage of in being sold something suspiciously like a "panacea" (it's even supposed to have anti-cancer properties). Is this a known scam, and I'm simply not aware of it? Please post replies either to the list or to me personally, Dan Pearlman, at dpearl@uriacc.uri.edu Thanks.