From owner-ageing@net.bio.net Thu Jun 01 23:00:00 1995 Path: biosci!bcm!cs.utexas.edu!swrinde!gatech!bloom-beacon.mit.edu!senator-bedfellow.mit.edu!athena.mit.edu!seto From: seto@athena.mit.edu (Arnold H Seto) Newsgroups: bionet.molbio.ageing Subject: Re: Do unicellular organisms age? Date: 2 Jun 1995 00:29:29 GMT Organization: Massachusetts Institute of Technology Lines: 19 Distribution: world Message-ID: <3qlm19$k43@senator-bedfellow.MIT.EDU> NNTP-Posting-Host: w20-575-51.mit.edu Oliver Bogler writes: >I agree witht the first point - bacteria, for example, do not age as there >*must* be an unbroken chain of cells from the beginning of the bacterial >life to today. The germline of higher organisms can be seen similarly as >an "immortal" clone. (Immortal is in quotes because there was a heated >debate in this group about the appropriateness of using that word to talk >about cells - it is used purely in its narrow biological sense). I believe a distinction must be made between the immortality of bacterial colonies and cell lines and the immortality of the _individual_ organism. Colonies may appear immortal and appear to have a single genotype, but the actual, single bacterium (if it could be isolated) might be found to die after a limited number of divisions. In yeast, careful separation of mother and daughter cells has shown that the mother cell stops dividing after budding and eventually dies. Arnold Seto seto@mit.edu From owner-ageing@net.bio.net Thu Jun 01 23:00:00 1995 Path: biosci!BIOTOP.UMCS.LUBLIN.PL!TCHORZ From: TCHORZ@BIOTOP.UMCS.LUBLIN.PL ("Marek Tchorzewski") Newsgroups: bionet.molbio.ageing Subject: RE: Do unicellular organisms age? Date: 2 Jun 1995 02:01:56 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 20 Sender: daemon@net.bio.net Distribution: world Message-ID: <5D096D2AE3@biotop.umcs.lublin.pl> NNTP-Posting-Host: net.bio.net Hi Dmitri > Why do you think it is age process? I thought mother cell and > daughter cell absolutely identical, are they? > Yours truly > Dmitri O no, you are not right. The division of a yeast ( S.cerevisiae) cell budding give rise to two cells which are identifiable, that is, the mother cell from which the bud arose, and the daughter cell which developed from the bud. Therefore, yeast cell (S.c.) produce a finite number of daughters during their life span, which are elaborated on the surface of mother cell as a bud. The number of buds produced by mother, one during each cell division cycle, is the metric of the life span and as I sad before is finite (26-30 bud). Marek From owner-ageing@net.bio.net Thu Jun 01 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!gatech!newsxfer.itd.umich.edu!news.cic.net!infoserv.illinois.net!io.org!nobody From: fissure@io.org (Fissure) Newsgroups: bionet.molbio.ageing Subject: Re: Do unicellular organisms age? Date: 2 Jun 1995 11:04:02 -0400 Organization: Internex Online, Toronto, Ontario, Canada (416 363 3783) Lines: 16 Message-ID: <3qn992$ob9@ionews.io.org> References: <3qlm19$k43@senator-bedfellow.MIT.EDU> NNTP-Posting-Host: wink.io.org >I believe a distinction must be made between the immortality of bacterial >colonies and cell lines and the immortality of the _individual_ organism. >Colonies may appear immortal and appear to have a single genotype, but the >actual, single bacterium (if it could be isolated) might be found to die after a >limited number of divisions. > >In yeast, careful separation of mother and daughter cells has shown that the >mother cell stops dividing after budding and eventually dies. > >Arnold Seto >seto@mit.edu do you know if any research was done into the telomere length of the mother cell and "her" lifespan? do the telomeres of the mother cell get cut off during reproduction as in mammalian cell? From owner-ageing@net.bio.net Fri Jun 02 23:00:00 1995 Path: biosci!FREENET.TORONTO.ON.CA!bk772 From: bk772@FREENET.TORONTO.ON.CA (Dmitri Chamchad) Newsgroups: bionet.molbio.ageing Subject: Re: Do unicellular organisms age? Date: 3 Jun 1995 02:17:03 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 27 Sender: daemon@net.bio.net Distribution: world Message-ID: References: <3qlm19$k43@senator-bedfellow.MIT.EDU> NNTP-Posting-Host: net.bio.net On 2 Jun 1995, Arnold H Seto wrote: > Oliver Bogler writes: > >I agree witht the first point - bacteria, for example, do not age as there > >*must* be an unbroken chain of cells from the beginning of the bacterial > >life to today. The germline of higher organisms can be seen similarly as > >an "immortal" clone. (Immortal is in quotes because there was a heated > >debate in this group about the appropriateness of using that word to talk > >about cells - it is used purely in its narrow biological sense). > I believe a distinction must be made between the immortality of bacterial > colonies and cell lines and the immortality of the _individual_ organism. > Colonies may appear immortal and appear to have a single genotype, but the > actual, single bacterium (if it could be isolated) might be found to die after a > limited number of divisions. > In yeast, careful separation of mother and daughter cells has shown that the > mother cell stops dividing after budding and eventually dies. > In human organism we have the same cell line - germ cells. I think this pull do not age, just somatic environment can't keep this pull alive. Spematogenic layer very looks like bacterial clon. And we have to find difference between germ and somatic cells. Yours truly Dmitri From owner-ageing@net.bio.net Fri Jun 02 23:00:00 1995 Newsgroups: bionet.molbio.ageing Path: biosci!bloom-beacon.mit.edu!gatech!newsfeed.pitt.edu!godot.cc.duq.edu!ddsw1!infoserv.illinois.net!io.org!torfree!bl859 From: bl859@torfree.net (Kwokyin Hui) Subject: Re: Do unicellular organisms age? Message-ID: Organization: Toronto FreeNet X-Newsreader: TIN [version 1.2 PL2] References: <3qd1fe$bl5@adelbert11.Stanford.EDU> Date: Sat, 3 Jun 1995 21:10:03 GMT Lines: 30 Christopher Kashinath Patil (cpatil@leland.Stanford.EDU) wrote: : Do unicellular organisms age? : I'd be interested to know what other people's thoughts were on this subject. : It seems unlikely to me that unicellular organisms would age (as it would : result in the extinction of clones that did undergo aging), but it also seems : difficult to understand how certain kinds of age-related damage (buildup of : metabolic by-products, etc.) could be avoided by these organisms. : On related notes: : 1) Do unicellular organisms that pass through haploid and diploid stages : repair age-related damage in one or both of these stages? : 2) Do all multicellular organisms age? If not, what is the complexity thresh- : hold for aging? : I would be interested to hear thoughts on this subject; needless to say, if : you have references to relevant articles, please include those in your : response as well. I guess it would depend on what you mean by "age." If you mean aging in the sense like humans do, then unicellular animals don't age. But if you mean that they age because of defective machinery, then they do age. You could look into cellular aging if you're interested in the latter topic. The word apoptosis is what you might associate with cellular aging. Sorry, no references, but do do a medline search on apoptosis and cell death. -- ^ ^ ^**^ ( o o ) ( o o ) Pigs in a pen. ( (oo)) ((oo) ) From owner-ageing@net.bio.net Sat Jun 03 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!gatech!newsfeed.pitt.edu!godot.cc.duq.edu!ddsw1!infoserv.illinois.net!io.org!nobody From: fissure@io.org (Fissure) Newsgroups: bionet.molbio.ageing Subject: Re: Do unicellular organisms age? Date: 4 Jun 1995 00:44:58 -0400 Organization: Internex Online, Toronto, Ontario, Canada (416 363 3783) Lines: 16 Message-ID: <3qrdoa$smk@ionews.io.org> References: <5D096D2AE3@biotop.umcs.lublin.pl> NNTP-Posting-Host: nudge.io.org >O no, you are not right. The division of a yeast ( S.cerevisiae) cell >budding give rise to two cells which are identifiable, that is, the mother >cell from which the bud arose, and the daughter cell which developed >from the bud. >Therefore, yeast cell (S.c.) produce a finite number of daughters during >their life span, which are elaborated on the surface of mother cell as a >bud. >The number of buds produced by mother, one during each cell division >cycle, is the metric of the life span and as I sad before is finite (26-30 >bud). > >Marek has any research been done to measure possble telomere length reduction over this lifespan? do yeast telomeres shrink as the mother cell divides? From owner-ageing@net.bio.net Sun Jun 04 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!gatech!news.sprintlink.net!news.gate.net!sarfl-2.gate.net!rlrlaz From: rlrlaz@gate.net (Richard L. Rossi) Newsgroups: bionet.molbio.ageing Subject: Gray hair as aging marker. Date: Mon, 5 Jun 1995 15:20:34 Lines: 6 Message-ID: NNTP-Posting-Host: sarfl-2.gate.net X-Newsreader: Trumpet for Windows [Version 1.0 Rev A] I know this is very non-technical and probably not worth your time to comment but I was wondering if gray hair is a biomarker? for aging. I mean does the amount of gray hair directly correlate to an aged body? Or is it not so significant? Thanks. RR From owner-ageing@net.bio.net Tue Jun 06 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!usc!news.cerf.net!newsserver.sdsc.edu!news.tc.cornell.edu!travelers.mail.cornell.edu!newsstand.cit.cornell.edu!NewsWatcher!user From: pts3@cornell.edu (phil) Newsgroups: bionet.molbio.ageing Subject: Help!! Paper Wasps Needed Followup-To: bionet.molbio.ageing Date: 7 Jun 1995 02:48:13 GMT Organization: cornell Lines: 24 Sender: pts3@cornell.edu (Verified) Message-ID: NNTP-Posting-Host: cu-dialup-0615.cit.cornell.edu Hello. My name is Phil Starks. I am a graduate student at Cornell University in the field of NeuroBiology and Behavior. I am currently examining paper wasps, specifically Polistes dominulus. I am evaluating their nesting behavior and population genetics. I want to compare animals from different regions -- mostly from the Northeast in areas between Boston, MA and Ithaca, NY. My problem is finding these critters. They tend to congregate in the eves of man-made structures. I have searched state parks and some universities but have only found 4 usable sites. A usable site is one that has been relatively undisturbed (not sprayed with insecticides) for a few years and contains 18 or more colonies. These wasps make un-enveloped nests -- you can plainly see the cells of the comb (it looks much like a gray honeycomb). P. dominulus is the more yellow and smaller of the 2 Polistes species in this region (P. fuscatus is dark brown and the larger of the two animals). At this time of year you may see colonies with anywhere from 1 to 10 individuals, and nests that may contain 8 to 100 cells. If you know of any potential sites please email me. I am offering a $20.00 finder fee for useful sites. Thanks for reading this message Phil Starks (pts3@cornell.edu) From owner-ageing@net.bio.net Tue Jun 06 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!usc!elroy.jpl.nasa.gov!swrinde!howland.reston.ans.net!news-e1a.megaweb.com!newstf01.news.aol.com!newsbf02.news.aol.com!not-for-mail From: akbalin@aol.com (Akbalin) Newsgroups: bionet.molbio.ageing Subject: Re: Gray hair as aging marker. Date: 6 Jun 1995 23:18:34 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 9 Sender: root@newsbf02.news.aol.com Message-ID: <3r35qa$i4i@newsbf02.news.aol.com> References: Reply-To: akbalin@aol.com (Akbalin) NNTP-Posting-Host: newsbf02.mail.aol.com There is a correlation between the incidence of grey hair and the age of the individual. Data from Keogh, E.V. and Walsh, R.J. Nature. 207, 877, 1965 reported the incidence of grey hair in an Australian population. Male 25-34 Any greying 22%, complete greying 0.23%; Male 35-44, Any 61%, complete 2.2%, Male 45-54 Any89%, complete13%, Male 55+, Any 94%, complete 30%. Parallel data for females. For more complete information see my chapter"Skin changes as a reflection of biologic age" in Practical Handbook of Human Biologic Age Determination , AK Balin, ed. CRC Press 1994, 525 pages. From owner-ageing@net.bio.net Tue Jun 06 23:00:00 1995 Path: biosci!rutgers!uwm.edu!cs.utexas.edu!news.sprintlink.net!pipex!sunsite.doc.ic.ac.uk!lyra.csx.cam.ac.uk!mrc-lmb.cam.ac.uk!tm1 From: tm1@mrc-lmb.cam.ac.uk (Myles T.) Newsgroups: bionet.molbio.ageing Subject: antioxidants Date: 7 Jun 1995 11:42:20 GMT Organization: MRC Laboratory of Molecular Biology, Cambridge UK Lines: 2 Distribution: world Message-ID: <3r43as$586@lyra.csx.cam.ac.uk> NNTP-Posting-Host: al.mrc-lmb.cam.ac.uk Timothy Myles From owner-ageing@net.bio.net Wed Jun 07 23:00:00 1995 Path: biosci!bcm!cs.utexas.edu!swrinde!hookup!interlog.com!news From: "Anti-Aging International Inc." Newsgroups: bionet.molbio.ageing Subject: INTRODUCING CELLEX-C COMPLEX Date: 8 Jun 1995 21:33:11 GMT Organization: Interlog Internet Services -Voice (416) 975-2655 -Data 515-1414 Lines: 11 Message-ID: <3r7qao$2f9@steel.interlog.com> NNTP-Posting-Host: cellex.interlog.com INTRODUCING CELLEX-C COMPLEX - a revolutionary skin care product that by all indications it may soon be hailed as the skincare breakthrough of the century. Half face pictorial studies are available via our home page. Picture at this site illustrate the long term effectsof using CELLEX-C SERUM. Subjects are shownunder normal ligthing and UV wavelengths. ANTI-AGING SKINCARE ONLINE HOME PAGE: http//tantech.com/antiaging/CELLEXHP.html ASSOCIATED PAGES: http//tantech.com/antiaging/PICTURES.html http//tantech.com/antiaging/NORDERPG.html EMAIL: cellex@interlog.com From owner-ageing@net.bio.net Wed Jun 07 23:00:00 1995 Path: biosci!bcm!cs.utexas.edu!swrinde!hookup!interlog.com!news From: "Anti-Aging International Inc." Newsgroups: bionet.molbio.ageing Subject: INTRODUCING CELLEX-C COMPLEX Date: 8 Jun 1995 21:33:30 GMT Organization: Interlog Internet Services -Voice (416) 975-2655 -Data 515-1414 Lines: 11 Message-ID: <3r7qba$2os@steel.interlog.com> NNTP-Posting-Host: cellex.interlog.com INTRODUCING CELLEX-C COMPLEX - a revolutionary skin care product that by all indications it may soon be hailed as the skincare breakthrough of the century. Half face pictorial studies are available via our home page. Picture at this site illustrate the long term effectsof using CELLEX-C SERUM. Subjects are shownunder normal ligthing and UV wavelengths. ANTI-AGING SKINCARE ONLINE HOME PAGE: http//tantech.com/antiaging/CELLEXHP.html ASSOCIATED PAGES: http//tantech.com/antiaging/PICTURES.html http//tantech.com/antiaging/NORDERPG.html EMAIL: cellex@interlog.com From owner-ageing@net.bio.net Wed Jun 07 23:00:00 1995 Path: biosci!bcm!news.msfc.nasa.gov!sol.ctr.columbia.edu!news.mindlink.net!vanbc.wimsey.com!fonorola!interlog.com!news From: "Anti-Aging International Inc." Newsgroups: bionet.molbio.ageing Subject: INTRODUCING CELLEX-C COMPLEX Date: 8 Jun 1995 21:33:20 GMT Organization: Interlog Internet Services -Voice (416) 975-2655 -Data 515-1414 Lines: 11 Message-ID: <3r7qb0$2oq@steel.interlog.com> NNTP-Posting-Host: cellex.interlog.com INTRODUCING CELLEX-C COMPLEX - a revolutionary skin care product that by all indications it may soon be hailed as the skincare breakthrough of the century. Half face pictorial studies are available via our home page. Picture at this site illustrate the long term effectsof using CELLEX-C SERUM. Subjects are shownunder normal ligthing and UV wavelengths. ANTI-AGING SKINCARE ONLINE HOME PAGE: http//tantech.com/antiaging/CELLEXHP.html ASSOCIATED PAGES: http//tantech.com/antiaging/PICTURES.html http//tantech.com/antiaging/NORDERPG.html EMAIL: cellex@interlog.com From owner-ageing@net.bio.net Sat Jun 10 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!spool.mu.edu!usenet.eel.ufl.edu!noc.netcom.net!news.sprintlink.net!sjuvm!yprlbio Nntp-Posting-Host: 149.68.2.20 Date: Fri, 9 Jun 1995 09:30:44 -0400 From: "LOCKSHIN, RICHARD A" Newsgroups: bionet.molbio.ageing Subject: Re: Do unicellular organisms age? Message-ID: <09JUN95.10261743.0018@sjumusic.stjohns.edu> References: <3qd1fe$bl5@adelbert11.Stanford.EDU> Sender: usenet@sjumusic.stjohns.edu Organization: St. John's University Lines: 39 check Michal Jazwinski for articles on aging in yeast, Joan Smith-Sonneborn (a few years back) for aging in paramecium. Apopotosis is not really cell aging. It is cell death. Check Klaus Bayereuther for senescence (maturation) of fibroblasts in culture. In article bl859@torfree.net (Kwokyin Hui) writes: >Christopher Kashinath Patil (cpatil@leland.Stanford.EDU) wrote: >: Do unicellular organisms age? > >: I'd be interested to know what other people's thoughts were on this subject. >: It seems unlikely to me that unicellular organisms would age (as it would >: result in the extinction of clones that did undergo aging), but it also seems >: difficult to understand how certain kinds of age-related damage (buildup of >: metabolic by-products, etc.) could be avoided by these organisms. > >: On related notes: >: 1) Do unicellular organisms that pass through haploid and diploid stages >: repair age-related damage in one or both of these stages? >: 2) Do all multicellular organisms age? If not, what is the complexity thresh- >: hold for aging? > >: I would be interested to hear thoughts on this subject; needless to say, if >: you have references to relevant articles, please include those in your >: response as well. > >I guess it would depend on what you mean by "age." If you mean aging in >the sense like humans do, then unicellular animals don't age. But if you >mean that they age because of defective machinery, then they do age. You >could look into cellular aging if you're interested in the latter topic. >The word apoptosis is what you might associate with cellular aging. > >Sorry, no references, but do do a medline search on apoptosis and cell death. >-- > ^ ^ ^**^ > ( o o ) ( o o ) Pigs in a pen. > ( (oo)) ((oo) ) >. >. From owner-ageing@net.bio.net Tue Jun 13 23:00:00 1995 Path: biosci!rutgers!uwm.edu!cs.utexas.edu!news.sprintlink.net!pipex!sunsite.doc.ic.ac.uk!daresbury!not-for-mail From: rattan@kemi.aau.dk (Suresh Rattan) Newsgroups: bionet.molbio.ageing Subject: An article on gerontogenes Date: 14 Jun 1995 10:47:17 +0100 Lines: 350 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <3rmb75$5c7@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk I am posting an article about the nature of genes involved in ageing. This article has already been published in the FASEB Journal, vol. 9, pp. 284-286, 1995 (February issue) under the category of "Hypothesis". I thought it might be of interest to a wider readership: ________________________________________ Gerontogenes: real or virtual ? Suresh I. S. Rattan Laboratory of Cellular Ageing, Department of Chemistry, Aarhus University, DK-8000 Aarhus-C, Denmark. Summary: The view that lifespan of an organism is intrinsically limited and is largely species-specific necessarily involves certain notions of genetic elements of regulation. The term gerontogenes refers to any such genetic elements that are involved in the regulation of aging and lifespan. The existence of genes for programmed aging is generally discounted on the basis of evolutionary arguments against the notion of adaptive nature of aging. It is suggested here that the concept of gerontogenes be linked with the idea of genes involved in homeostasis and longevity assurance, which is not contradictory to the non-adaptive nature of aging. Since these genes were not originally selected as real genes for aging, their involvement in aging is an emergent property making them virtual gerontogenes. Some experimental evidence is available that suggests that sets of genes involved in the maintenance and repair of various cellular functions are the primary candidates qualifying as virtual gerontogenes. Key Words: Aging * lifespan * homeostasis * virtual genes Sooner or later, all individuals die. There may or may not be any genetic program that determines the exact time of death, but there appears to be an evolutionary constraint in terms of maximum achievable lifespan within a species. The view that lifespan of an organism is intrinsically limited and lies largely within a species-specific range involves necessarily certain notions of genetic elements of regulation. In this context, the term gerontogenes (1) refers to any such genetic elements that are involved in aging. The idea of gerontogenes does not contradict the non-adaptive nature of aging. Rather, it reasserts the importance of the genetic mechanisms of somatic maintenance in assuring germ line continuity, as envisaged by both antagonistic pleiotropy theory and disposable-soma theory of the evolution of aging and lifespan (2, 3). Since the existence of gerontogenes as genes for programmed self-destruction is on the whole discounted on the basis of evolutionary arguments against the notion of adaptive nature of aging (4, 5), the concept of gerontogenes is intimately linked with the idea of genes involved in homeostasis and longevity assurance, instead of certain special genes for aging. the nature of gerontogenes The term "gerontogenes" does not refer to a tangible physical reality of real genes for aging but to an emergent functional property of a number of genes which may influence aging. For this purpose, the term "virtual" gerontogenes has been suggested (6, 7) in which "virtual" is defined, as in the Shorter Oxford Dictionary, as something that "is so in essence or effect although not formally or actually; admitting of being called by the name so far as the effect or result is concerned". In science, the term "virtual" is used for entities that it is helpful to regard as being present although they have no physical existence. The paradigm of such an entity is the virtual image of optics. Another example is the currently fashionable "virtual reality", which fulfills the same definition. The concept of virtual genes therefore refers to the emergent property of several genes whose functions are tightly coupled and whose combined action and interaction resembled the effect of one gene. Treating such a group as a virtual gene is a useful conceptual tool while the search continues for the genetic elements of regulation of complex biological processes, such as aging. Although differentiation and development are good examples of highly complicated and complex systems involving a large number of genes, the concept of virtual genes may be inappropriate to apply to them because these processes are under direct genetic control and have evolved as a result of natural selection. This situation is unlike aging where no natural selection for any specific genes is envisaged. Therefore, the concept of virtual genes is appropriate only for phenomena such as aging where a genetic involvement is expected without direct genetic control open to natural selection. The idea of gerontogenes as being virtual implies that every time a gene is discovered which appears to have a role in the process of aging, it will, on sequencing and identification, turn out to be a familiar normal gene with a defined function. Its role as a gerontogene can only be realised in the context of its emergent property in relation to several other genes which influence its activity and interactivity. Such genes cannot be hidden, because their identities can in principle become well known. Individually, the functions of such genes can in principle be clearly established. Yet, as a result of concerted action and interaction, the combined effect of these genes resembles that of a "gene for aging" although these were not specially designed or naturally selected for causing aging. This idea of virtual gerontogenes is in line with the evloutionary explanation of the process of aging as being an emergent phenomenon owing to the lack of eternal maintenance and repair instead of it being an active and adaptive process. EVIDENCE for candidate gerontogenes Obviously, not every gene is potentially a virtual gerontogene. However, potentially every gene can affect the survival of an organism. Therefore, a distinction must be made between the immediate survival or death and the process of aging. Knocking out any essential gene will result in the death of an organism without having anything to do with the process of aging. For virtual gerontogenes, one could narrow down the possibilities to sets of genes involved in the maintenance and repair of the cellular and sub-cellular components as the primary candidates for qualification as virtual gerontogenes. This is because almost all theories of aging imply directly or indirectly that the progressive failure of homeostatic mechanisms is crucial for the process of aging. For example, theories emphasising the accumulation of somatic mutations, the build-up of oxidative damage in macromolecules, the accumulation of abnormal, erroneous and defective proteins, deficiency of the signal transduction pathways, deficiency of the immune system and several other similar hypotheses all point to the failure of maintenance at all levels of organization as a crucial determinant of aging and lifespan (8-10). Evidence for the hypothesis that candidate virtual gerontogenes operate through one or more of the mechanisms of somatic maintenance and repair comes from experiments performed to slow down aging and to increase the lifespan of organisms. For example, anti-aging and life-prolonging effects of calorie restriction are seen to stimulate various maintenance mechanisms. These include increased efficiency in DNA repair (11), increased fidelity of genetic information transfer (12, 13), more efficient protein synthesis (14-16), more efficient protein degradation (17), more effective cell replacement and regeneration, improved cellular responsiveness (18), fortification of the immune system and enhanced protection from free-radical- and oxidation-induced damage (19-21). Genetic selection of Drosophila for longer lifespan also appears to work mainly through an increase in the efficiency of maintenance mechanisms, such as antioxidation potential (2, 22-24). An increase in lifespan of transgenic Drosophila containing extra copies of Cu-Zn superoxide dismutase (SOD) and catalase genes is primarily due to enhanced defences against oxidative damage (25). Similarly, anti-aging effects of a dipeptide, carnosine (26) and a cytokinin, kinetin (27) on human diploid fibroblasts also appear to be due to the effect of these chemicals on maintaining the efficiency of defence mechanisms, including efficient protein synthesis and turnover and the removal of oxidative damage. Attempts at identifying determinants of longevity by finding a correlation between maximum lifespan of a species and certain biological characteristics have also shown that it is the efficiency of various defence mechanisms that correlates best with longevity (28). Some of the well-known maintenance mechanisms whose activity levels and efficiencies are directly correlated with species lifespan include DNA repair (29-31), cell proliferative capacity (32, 33) and antioxidative potential (34-37). Further experimental evidence in favour of the concept of virtual gerontogenes comes from several studies to identify senescence-specific genes in old cells and tissues. Almost all such studies have resulted in the identification of genes, such as those of the components of the extracellular matrix, which are known to have other functions in cell metabolism and physiology (38-41). Studies on the extension of lifespan and slowing-down of various age-related biochemical and functional alterations of D. melanogaster by simultaneous overexpression of Cu-Zn-SOD and catalase (25) indicate that these free-radical-scavenging and antioxidant genes are part of the gerontogene family by virtue of their role in influencing aging and lifespan. The identification of the long-lived mutants of the nematode Caenorhabditis elegans, involving the age-1 (38, 42-44), dauer-constitutive daf-2 (45) and spermatogenesis defective spe-26 (46) genes may provide other examples of virtual gerontogenes. Although the exact nature of the final protein products of these genes is at present unknown, characterization of the age-1 mutant strain of C. elegans has shown increased resistance to hydrogen peroxide-induced oxidative damage and an increase in the activities of SOD and catalase enzymes in the mutants (47). Other possibilities may be found in the complex regulatory mechanisms known to exist in connection with the end-replication problem of telomeres (48) and the post-replicative processing of DNA, such as methylation (49). Molecular studies using a comparative approach, including the use of transgenic organisms, will be useful to identify most important genes in this respect and can form the basis of developing appropriate strategies for future gerontological research. Implications for aging research The objective of this article is to develop the concept of virtual genes in aging as an emergent property of several functionally-coupled genes which were not naturally selected to cause aging, but whose combined action and interaction reveals their role as gerontogenes. Therefore, in order to unravel the genetic elements regulating the aging process, studies should be directed towards understanding the mechanisms of interaction and inter-dependence of various genes involved in maintenance and repair. The phenomenology of aging is rich in empirical data showing that individually no tissue, organ or system becomes functionally exhausted even in very old organisms, yet it is their combined interaction and inter-dependence that determines the survival of the whole. The same logic needs to be applied for studies on the molecular and genetic levels. Searching for an all-encompassing aging gene(s) is unlikely to be successful. Estimates of the number of genes which could influence aging and lifespan run up to a few hundred out of about one hundred thousand genes, and their allelic variants, in mammalian systems (50). A search for universal biomarkers of aging is likely to remain unsuccessful because of the astronomical number of ways in which such interactive units or networks can manifest stochastic alterations. Therefore, manipulating any single gene or a few genes that show some effects on aging and lifespan will help to identify genes that might qualify as being a part of the virtual gerontogene family. Of course, such studies will be valuable to find ways to "fine-tune" the network and to prevent the onset of various age-related diseases and impairments by maintaing the efficiency of homeostatic processes. In the short term, such studies will also result in developing a variety of so-called anti-aging products by concentrating on the individual members of the gerontogene family. In contrast, direct gene therapy of the total aging process seems to hold little promise. In order to unravel the molecular basis of aging and modulate the process, the most promising research strategies will incorporate an analysis of the formation and functioning of maintenance and repair networks. The concept of virtual gerontogenes can be useful to design new experiments and help to search for the genetic "hand of cards" that provides the best possible combination to prevent succumbing to perturbations from internal and external sources. Acknowledgement: I am grateful to Dr. Paul Woolley for several discussions and critical reading of the manuscript. REFERENCES 1. Rattan, S. I. S. (1985) Beyond the present crisis in gerontology. BioEssays, 2, 226-228 2. Rose, M. R., and Graves, J. L. (1990) Evolution of aging. Rev. Biol. Res. Aging, 4, 3-14 3. Kirkwood, T. B. L., and Holliday, R. (1979) The evolution of ageing and longevity. Proc. R. Soc. Lond. B, 205, 531-546 4. Rose, M. R. (1991) Evolutionary Biology of Aging. Oxford University Press, New York. 5. Kirkwood, T. B. L. (1992) Biological origins of ageing. In Oxford textbook of geriatric medicine. (Edited by Evans, J. G. , and Williams, T. =46.), pp. 35-40, Oxford University Press, Oxford. 6. Rattan, S. I. S. (1989) DNA damage and repair during cellular aging. Int. Rev. Cytol., 116, 47-88 7. Rattan, S. I. S. (1991) Aging and disease: proteins as the molecular link. Persp. Biol. Med., 34, 526-533 8. Holliday, R. (1988) Towards a biological understanding of the ageing process. Persp. Biol. Med., 32, 109-123 9. Medvedev, Z. A. (1990) An attempt at a rational classification of theories of ageing. Biol. Rev., 65, 375-398 10. Rattan, S. I. S., and Clark, B. F. C. (1988) Ageing: a challenge for biotechnology. Trends Biotech., 6, 58-62 11. Weraarchakul, N., Strong, R., Wood, W. G., and Richardson, A. (1989) The effect of aging and dietary restriction on DNA repair. Exp. Cell Res., 181, 197-204 12. Srivastava, V. K., Tilley, R. D., Hart, R. W., and Busbee, D. L. (1991) Effect of dietary restriction on the fidelity of DNA polymerases in aging mice. Exp. Gerontol., 26, 453-466 13. Srivastava, V., Tilley, R., Miller, S., Hart, R., and Busbee, D. (1992) Effects of aging and dietary restriction on DNA polymerases: gene expression, enzyme fidelity, and DNA excision repair. Exp. Gerontol., 27, 593-613 14. Merry, B. J., Goldspink, D. F., and Lewis, S. E. M. (1991) The effect of age and chronic restricted feeding on protein synthesis and growth of the large intestine of the rat. Comp. Biochem. Physiol., 98A, 559-562 15. Merry, B. J., and Holehahn, A. M. (1991) Effect of age and restricted feeding on polypeptide chain assembly kinetics in liver protein synthesis in vivo. Mech. Ageing Develop., 58, 139-150 16. Merry, B. J., Lewis, S. E. M., and Goldspink, D. F. (1992) The influence of age and chronic restricted feeding on protein synthesis in the small intestine of the rat. Exp. Gerontol., 27, 191-200 17. Ishigami, A., and Goto, S. (1990) Effect of dietary restriction on the degradation of proteins in senescent mouse liver parenchymal cells in culture. Arch. Biochem. Biophys., 283, 362-366 18. Chatterjee, B., Fernandes, G., Yu, B. P., Song, C., Kim, J. M., Demyan, W., and Roy, A. K. (1989) Calorie restriction delays age-dependent loss in androgen responsiveness of the rat liver. FASEB J., 3, 169-173 19. Youngman, L. D., Park, J.-Y. K., and Ames, B. N. (1992) Protein oxidation associated with aging is reduced by dietary restriction of protein or calories. Proc. Natl. Acad. Sci. USA, 89, 9112-9116 20. Youngman, L. D. (1993) Protein restriction (PR) and caloric restriction (CR) compared: effects on DNA damage, carcinogenesis, and oxidative damage. Mutat. Res., 295, 165-179 21. Yu, B. P. (1990) Food restriction research: past and present status. Rev. Biol. Res. Aging, 4, 349-371 22. Arking, R., Buck, S., Wells, R. A., and Pretzlaff, R. (1988) Metabolic rates in genetically based long lived strains of Drosophila. Exp. Gerontol., 23, 59-76 23. Arking, R. (1988) Genetic analysis of aging processes in Drosophila. Exp. Aging Res., 14, 125-135 24. Luckinbill, L. S. (1993) Prospective and retrospective tests of evolutionary theories of senescence. Arch. Gerontol. Geriatr., 16, 17-32 25. Orr, W. C., and Sohal, R. S. (1994) Extension of life-span by overexpression of superoxide dismutase and catalase in Drosophila melanogaster. Science, 263, 1128-1130 26. McFarland, G. A., and Holliday, R. (1994) Retardation of the senescence of cultured human diploid fibroblasts by carnosine. Exp. Cell Res., 212, 167-175 27. Rattan, S. I. S., and Clark, B. F. C. (1994) Kinetin delays the onset of ageing characteristics in human fibroblasts. Biochem. Biophys. Res. Commun., 201, 665-672 28. Holliday, R. (1992) The ancient origins and causes of ageing. News Physiol. Sci., 7, 38-40 29. Grube, K., and B=FCrkle, A. (1992) Poly(ADP-ribose) polymerase activit= y in mononuclear leukocytes of 13 mammalian species correlates with species-specific life span. Proc. Natl. Acad. Sci. USA, 89, 11759-11763 30. Hart, R. W., and Turturro, A. (1981) Evolution and longevity-assurance processes. Naturwissenschaften., 68, 552-557 31. Whitehead, I., and Grigliatti, T. A. (1993) A correlation between DNA repair capacity and longevity in adult Drosophila melanogaster. J. Gerontol., 48, B124-B132 32. Hayflick, L. (1991) Aging under glass. Mutat. Res., 256, 69-80 33. Macieira-Coelho, A. (1993) Contributions made by the studies of cells in vitro for understanding of the mechanisms of aging. Exp. Gerontol., 28, 1-16 34. Cutler, R. G. (1985) Antioxidants and longevity of mammalian species. In Molecular Biology of Aging. (Edited by Woodhead, A. D., Blackett, A. D. , and Hollaender, A.), pp. 15-73, Plenum Press, New York. 35. Cutler, R. G. (1985) Dysdifferentiation hypothesis of aging: a review. In Molecular Biology of Aging: gene stability and gene expression. (Edited by Sohal, R. S., Birnbaum, L. S. , and Cutler, R. G.), pp. 307-340, Raven Press, New York. 36. Sacher, G. A. (1982) Evolutionary theory in gerontology. Persp. Biol. Med., 25, 339-353 37. Sohal, R. S., Agarwal, S., Dubey, A., and Orr, W. C. (1993) Protein oxidative damage is associated with life expectancy of houseflies. Proc. Natl. Acad. Sci. USA, 90, 7255-7259 38. Friedman, D. B., and Johnson, T. E. (1988) A mutation in the age-1 gene in Caenorhabditis elegans lengthens life and reduces hermaphrodite fertility. Genetics, 118, 75-86 39. Nuell, M. J., McClung, J. K., Smith, J. R., and Danner, D. B. (1989) Approach to the isolation of antiproliferative genes. Exp. Gerontol., 24, 469-476 40. Smith, J. R. (1992) Inhibitors of DNA synthesis derived from senescent human diploid fibroblasts. Exp. Gerontol., 27, 409-412 41. Thweatt, R., Lumpkin, C. K., and Goldstein, S. (1992) A novel gene encoding a smooth muscle protein is overexpressed in senescent human fibroblasts. Biochem. Biophys. Res. Commun., 187, 1-7 42. Friedman, D. B., and Johnson, T. E. (1988) Three mutants that extend both mean and maximum life span of the nematode, Caenorhabditis elegans, define the age-1 gene. J. Gerontol., 43, B102-109 43. Johnson, T. E. (1988) Genetic specification of life span: processes, problems, and potentials. J. Gerontol., 43, B87-92 44. Johnson, T. E. (1990) Increased life-span of age-1 mutants in Caenorhabditis elegans and lower Gompertz rate of aging. Science, 249, 908-912 45. Kenyon, C., Chang, J., Gensch, E., Rudner, A., and Tabtiang, R. (1993) A C. elegans mutant that lives twice as long as wild type. Nature, 366, 461-464 46. Van Voorhies, W. A. (1992) Production of sperm reduces nematode lifespan. Nature, 360, 456-458 47. Larsen, P. L. (1993) Aging and resistance to oxidative damage in Caenorhabditis elegans. Proc. Natl. Acad. Sci. USA, 90, 8905-8909 48. Levy, M. Z., Allsopp, R. C., Futcher, A. B., Greider, C. W., and Harley, C. B. (1992) Telomere end-replication problem and cell aging. J. Mol. Biol., 225, 951-960 49. Holliday, R. (1987) The inheritance of epigenetic defects. Science, 238, 163-170 50. Martin, G. M. (1992) Biological mechanisms of ageing. In Oxford Textbook of Geriatric Medicine. (Edited by Evans, J. G. , and Williams, T. =46.), pp. 41-48, Oxford Univ. Press, Oxford. Suresh I.S. Rattan Laboratory of Cellular Ageing Department of Chemistry Aarhus University DK-8000 Aarhus-C, Denmark. Phone: +45 8942 3956; Fax: +45 8619 6199 From owner-ageing@net.bio.net Wed Jun 14 23:00:00 1995 Path: biosci!rutgers!uwm.edu!lll-winken.llnl.gov!apple.com!mac1015.kip.apple.com!user From: u4484@nes.nersc.gov (The Old Ghost) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: "Black box" kills old people? Date: 15 Jun 1995 01:15:17 GMT Organization: Blind Alley Services Lines: 51 Message-ID: References: NNTP-Posting-Host: mac1015.kip.apple.com Xref: biosci bionet.molbio.ageing:1813 sci.life-extension:5716 Please excuse me if I am out of line, but I have to speak up. I am considering all of the arguments I have heard about age and aging and death being one process. This is, however, not true. Age has nothing to do, intrinsically, with aging. There are some minor physiological signs that will occur, causing someone to appear "aged", but one can be as active at 90 as 30 depending on the physical condition of the subject. No one has ever died of old age. This is ludicrous to consider. There is no anatomical precedent to death of old age. Study the carp - they can be kept in captivity for years, kept and well fed and will not die! The oldest in captivity was 71 years old, and showed no untoward signs of deteoration. Man need not die - at least not simply because he has lived a long while; the gerontoligists will accede to this fact. They will not define themselves out of a job, but make their current profession one of true endeavour. *Not* meant to disrespect anyone... In article , steve@chambers.ak.planet.co.nz (Steve Chambers) wrote: > I'm just reviewing "How and Why We Age" by Leonard Hayflick. In > Chapter 4 he argues that: > > diseases associated with old age are NOT part of the normal aging > process ... diseases, unlike aging, are not normal. > > later he says: > > The cause of death in old people is a mysterious "black box." > Usually some standard cause of death is chosen from an approved > list in order to comply with legal requirements. > > Please forgive my impudence, I know LH is one of the giants of > gerontology, but this comment seems like a desperate attempt to stitch > up a paradigm of aging that is falling apart at the seams. > > I see his problem. If the diseases of age are not aging then one can > only conclude that (without this mysterious black box) nobody ever dies > of old age! > > LH and those of similar thinking are in danger of defining themselves out > of a job. > > Who amongst you shall be their champion? > > Steve > > -- > ________________________ > (I_lurk,_therefore_I_am!_\ ,,, Steve Chambers > (o o) steve@chambers.ak.planet.co.nz > ----------------------oOO--(_)--OOo----------------------------- From owner-ageing@net.bio.net Thu Jun 15 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!news.starnet.net!wupost!howland.reston.ans.net!vixen.cso.uiuc.edu!news.uoregon.edu!ntuix.ntu.ac.sg!raffles.technet.sg!nuscc.nus.sg!phcelee From: phcelee@leonis.nus.sg (Edmund Lee Jon Deoon) Newsgroups: bionet.molbio.ageing Subject: test - don't read Date: 16 Jun 1995 08:01:16 GMT Organization: National University of Singapore Lines: 1 Message-ID: <3rrdoc$7pq@nuscc.nus.sg> NNTP-Posting-Host: phcelee@leonis.nus.sg X-Newsreader: TIN [version 1.2 PL2] just testing From owner-ageing@net.bio.net Thu Jun 15 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!usc!howland.reston.ans.net!vixen.cso.uiuc.edu!news.uoregon.edu!ntuix.ntu.ac.sg!raffles.technet.sg!nuscc.nus.sg!phcelee From: phcelee@leonis.nus.sg (Edmund Lee Jon Deoon) Newsgroups: bionet.molbio.ageing Subject: Re: test - don't read Date: 16 Jun 1995 08:06:34 GMT Organization: National University of Singapore Lines: 4 Message-ID: <3rre2a$7rm@nuscc.nus.sg> References: <3rrdoc$7pq@nuscc.nus.sg> NNTP-Posting-Host: phcelee@leonis.nus.sg X-Newsreader: TIN [version 1.2 PL2] test2: Edmund Lee Jon Deoon (phcelee@leonis.nus.sg) wrote: : just testing From owner-ageing@net.bio.net Thu Jun 15 23:00:00 1995 Path: biosci!agate!howland.reston.ans.net!swrinde!elroy.jpl.nasa.gov!ames!waikato!canterbury.ac.nz!southern.co.nz!equinox.gen.nz!equinox!not-for-mail From: Brian_Sandle@equinox.gen.nz (Brian Sandle) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: "Black box" kills old people? Followup-To: bionet.molbio.ageing,sci.life-extension Date: 16 Jun 1995 12:26:55 GMT Organization: Southern InterNet Services Lines: 20 Message-ID: <3rrtaf$fk5@southern.co.nz> References: NNTP-Posting-Host: equinox.gen.nz X-Newsreader: TIN [AMIGA 1.3 950520BETA PL0] Xref: biosci bionet.molbio.ageing:1816 sci.life-extension:5741 The Old Ghost (u4484@nes.nersc.gov) wrote: : Please excuse me if I am out of line, but I have to speak up. I am : considering all of the arguments I have heard about age and aging and : death being one process. This is, however, not true. Age has nothing to : do, intrinsically, with aging. There are some minor physiological signs : that will occur, causing someone to appear "aged", but one can be as : active at 90 as 30 depending on the : physical condition of the subject. No one has ever died of old age. This : is ludicrous to consider. There is no anatomical precedent to death of : old age. Perhaps I've been botching it a little, but I've been trying to talk on alt.support.euthanasia about the psychological changes which occur with old age. I suppose in men the testosterone decreases, there will be a less 'grasping' psychology. Wouldn't death occur at a time governed by the hormones the same way a boy loses his high voice is governed? Brian_Sandle@equinox.gen.nz From owner-ageing@net.bio.net Thu Jun 15 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!gatech!howland.reston.ans.net!Germany.EU.net!EU.net!news.sprintlink.net!sjuvm!yprlbio Nntp-Posting-Host: 149.68.2.20 Date: Fri, 16 Jun 1995 07:22:14 -0400 From: "LOCKSHIN, RICHARD A" Newsgroups: bionet.cellbiol,bionet.immunology,bionet.drosophila,bionet.celegans,bionet.molbio.ageing,bionet.neuroscience Subject: NYC Area Cell Death Club Meeting Message-ID: <16JUN95.07959891.0020@sjumusic.stjohns.edu> Sender: usenet@sjumusic.stjohns.edu Organization: St. John's University Lines: 19 Xref: biosci bionet.cellbiol:2430 bionet.immunology:4556 bionet.drosophila:1148 bionet.celegans:427 bionet.molbio.ageing:1817 bionet.neuroscience:8423 NYC Area Cell Death Club (Death Poets' Society) Next meeting: Wednesday June 28, 1995 7-8:30 PM Rockefeller University, 1230 York Ave., Tower Bldg Room 301 Free Parking after 5PM at 66th St. & York Ave (Please carpool as parking space is limited) Speakers: 1. Thomas Mammone, St. Johns Univ & Estee Lauder, Programmed cell death in human epidermal keratinocytes 2. Adriana Haimovitz-Friedman NYU Skirball), Radiation- induced cell death in endothelial cells. To help plan for pizza call lab of Dr. Zahra Zakeri, 718: 997-3429 and let them know the number coming for pizza, talk, and if you need parking. Please RSVP by 6/26/95. Organizers: Zahra Zakeri, Fax 718: 997-3445 Phone 718: 997-3417 Raymond Birge: Fax 212 327-7943; Phone 212: 327-7412 From owner-ageing@net.bio.net Fri Jun 16 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!news.kei.com!news.mathworks.com!europa.chnt.gtegsc.com!news.sprintlink.net!demon!longevb.demon.co.uk!John From: John de Rivaz Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: "Black box" kills old people? Date: 17 Jun 1995 10:47:37 +0100 Organization: Myorganisation Lines: 25 Sender: news@news.demon.co.uk Message-ID: <537801039wnr@longevb.demon.co.uk> References: <3rrtaf$fk5@southern.co.nz> Reply-To: John@longevb.demon.co.uk NNTP-Posting-Host: dispatch.demon.co.uk X-Newsreader: Newswin Alpha 0.7 X-Posting-Host: longevb.demon.co.uk Xref: biosci bionet.molbio.ageing:1818 sci.life-extension:5756 In article: <3rrtaf$fk5@southern.co.nz> Brian_Sandle@equinox.gen.nz (Brian Sandle) writes: > Wouldn't death occur at a time governed by the hormones the same way a boy > loses his high voice is governed? > But sometimes these hormones don't work and a boy doesn't turn into a man. However such people still die of old age. Once could suggest that different hormones create old age. But if this is so why isn't there occasionally a deficiency disorder that prevents this happening, just as in the boy/man transformation? If there was only one biological system in this universe that isn't subject to occasional failure, then that would have profound scientific, philosophical and theological implications. -- Sincerely, **************************************** * Publisher of Longevity Report * John de Rivaz * Fractal Report * * details on request * **************************************** **** What is the point of life if it ends in death? **** From owner-ageing@net.bio.net Fri Jun 16 23:00:00 1995 Path: biosci!galaxy.ucr.edu!library.ucla.edu!csulb.edu!nic-nac.CSU.net!usc!elroy.jpl.nasa.gov!lll-winken.llnl.gov!decwrl!svc.portal.com!portal.com!cup.portal.com!Floyd_-_Meyer From: Floyd_-_Meyer@cup.portal.com Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: "Black box" kills old people? Date: 17 Jun 1995 09:20:04 -0700 Organization: The Portal System (TM) Lines: 24 Sender: pccop@unix.portal.com Message-ID: <140720@cup.portal.com> References: <3rrtaf$fk5@southern.co.nz> <537801039wnr@longevb.demon.co.uk> NNTP-Posting-Host: news1.unix.portal.com Xref: biosci bionet.molbio.ageing:1819 sci.life-extension:5763 Could aging be from lack of intake. If we lost vitamin C we would all get scurvy and think it was normal. I suggest that after an extinction the earths magnetic field was moving as much as 200,000 times as fast as is now. It is now moving in a easterly direction at the rate of one revolution faster than the crust every 2,000 years. This ongoing, non reversing moving magnetic field could have supplied the energy for origin of life and chirality. It would also force negative water vapor high to forma band of ice crystals around the earth. this band of ice crystals would procect living things from solar radiation and be broken up to release oxygen and hydrogen. The oxygen the oxygen stayed and the hydrogen escaped. During this time evolution bloomed and molecules were made that are no longer available. Aging could be one or more intake ailments due to these missing molecules. When the movement between the crust and the magnetic field slowed, the ice crystals fell in and caused the flood. We now have , mostly, stopped evolving and are actually degenerating. Waiting on the next meteor impact to stir things up. Floyd From owner-ageing@net.bio.net Sun Jun 18 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!spool.mu.edu!uwm.edu!lll-winken.llnl.gov!enews.sgi.com!decwrl!waikato!comp.vuw.ac.nz!canterbury.ac.nz!southern.co.nz!equinox.gen.nz!equinox!not-for-mail From: Brian_Sandle@equinox.gen.nz (Brian Sandle) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: "Black box" kills old people? Followup-To: bionet.molbio.ageing,sci.life-extension Date: 18 Jun 1995 23:36:57 GMT Organization: Southern InterNet Services Lines: 39 Message-ID: <3s2dap$in9@southern.co.nz> References: <3rrtaf$fk5@southern.co.nz> <537801039wnr@longevb.demon.co.uk> NNTP-Posting-Host: equinox.gen.nz X-Newsreader: TIN [AMIGA 1.3 950520BETA PL0] Xref: biosci bionet.molbio.ageing:1820 sci.life-extension:5779 John de Rivaz (John@longevb.demon.co.uk) wrote: : In article: <3rrtaf$fk5@southern.co.nz> Brian_Sandle@equinox.gen.nz (Brian : Sandle) writes: : > Wouldn't death occur at a time governed by the hormones the same way a boy : > loses his high voice is governed? : > : : But sometimes these hormones don't work and a boy doesn't turn into a man. : However such people still die of old age. Yes, but think in terms of the whole picture including the thymic hormones. The thymus is no longer thought of as only related to youth, though it does reduce at puberty. : : Once could suggest that different hormones create old age. But if this is so : why isn't there occasionally a deficiency disorder that prevents this : happening, just as in the boy/man transformation? Or lack of the hormones - the switching off of the control triggers. : : If there was only one biological system in this universe that isn't subject : to occasional failure, then that would have profound scientific, : philosophical and theological implications. : My point, or rather my question, is asking whether death might be timetabled like puberty, menopause etc, by some body clock. It might be possible to postpone death, as it is possible to block sexual maturation, but would it be a whole and healthy thing to do? Puberty is getting earlier, possibly with extended lighting hours from electric light, and this produces problems for some. Postponing death beyond the normal year ratios of other mammals for gestation:puberty:menopause:death when they are unstressed for food and light etc not over calorie supplied or restricted, may be illogical. Brian_Sandle@equinox.gen.nz From owner-ageing@net.bio.net Sun Jun 18 23:00:00 1995 Path: biosci!bloom-beacon.mit.edu!gatech!news.sprintlink.net!howland.reston.ans.net!news.moneng.mei.com!news.ecn.bgu.edu!movietone.ils.nwu.edu!newsfeed.acns.nwu.edu!news.cc.uic.edu!uicvm.uic.edu!ruhnke Message-ID: <19950619.023846.591861.NETNEWS@UICVM.UIC.EDU> Nntp-Posting-Host: slip3-13.dialin.uic.edu Date: Mon, 19 Jun 1995 00:32:16 +0000 Newsgroups: bionet.molbio.ageing From: ruhnke@uiuc.edu (Earle Ruhnke) Subject: Help! Please? X-Newsreader: News Xpress Version 1.0 Beta #3 Lines: 8 Does anyone have the latest revision of "Internet and E-Mail Resources on Aging" compiled by Joyce A. Post? If so could you please eith post it or e-mail it to me (ruhnke@uiuc.edu). I have an incomplete copy and would like to review the whole document. Thank you, Earle Ruhnke ruhnke@uiuc.edu From owner-ageing@net.bio.net Mon Jun 19 23:00:00 1995 Path: biosci!daresbury!trane.uninett.no!nac.no!Norway.EU.net!EU.net!howland.reston.ans.net!news.starnet.net!wupost!newspump.wustl.edu!news.miami.edu!usenet.ufl.edu!maple.circa.ufl.edu!DATA From: data@maple.circa.ufl.edu Newsgroups: bionet.molbio.ageing Subject: Searching Date: 20 Jun 1995 14:36:06 GMT Organization: University of Florida - CIRCA Lines: 5 Message-ID: <3s6mcm$60t@no-names.nerdc.ufl.edu> Reply-To: data@maple.circa.ufl.edu NNTP-Posting-Host: maple.circa.ufl.edu I also would be interested in a copy of "Internet and E-Mail Resources on Aging" compiled by Joyce A. Post. If at all possible could you please eithe rpost it or e-mail it to me at Data@ufcc.ufl.edu Thank you From owner-ageing@net.bio.net Wed Jun 21 23:00:00 1995 Path: biosci!daresbury!trane.uninett.no!Norway.EU.net!EU.net!howland.reston.ans.net!nntp.crl.com!acara.snsnet.net!polo.iquest.com!usenet From: Jane Hays Newsgroups: bionet.molbio.ageing Subject: Searching Date: 22 Jun 1995 17:15:11 GMT Organization: interQuest: Fuel for the Mind Lines: 11 Distribution: world Message-ID: <3sc8ev$1k6@polo.iquest.com> References: <3s6mcm$60t@no-names.nerdc.ufl.edu> NNTP-Posting-Host: 199.172.89.92 > I also would be interested in a copy of "Internet and E-Mail Resources on > Aging" compiled by Joyce A. Post. If at all possible could you please > eithe rpost it or e-mail it to me at Data@ufcc.ufl.edu > Thank you > Me too!! jhays@colsa.com Thanks! From owner-ageing@net.bio.net Thu Jun 22 23:00:00 1995 Path: biosci!FREENET.TORONTO.ON.CA!bk772 From: bk772@FREENET.TORONTO.ON.CA (Dmitri Chamchad) Newsgroups: bionet.molbio.ageing Subject: Re: Searching Date: 22 Jun 1995 16:55:12 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 15 Sender: daemon@net.bio.net Distribution: world Message-ID: References: <3sc8ev$1k6@polo.iquest.com> On 22 Jun 1995, Jane Hays wrote: > > I also would be interested in a copy of "Internet and E-Mail Resources on > > Aging" compiled by Joyce A. Post. If at all possible could you please > > eithe rpost it or e-mail it to me at Data@ufcc.ufl.edu > > Thank you > > > > > Me too!! jhays@colsa.com > Don't forget about me! bk772@freenet.toronto.on.ca Yours truly Dmitri From owner-ageing@net.bio.net Thu Jun 22 23:00:00 1995 Path: biosci!bcm!cs.utexas.edu!howland.reston.ans.net!Germany.EU.net!EU.net!Portugal.EU.net!news.rccn.net!master.di.fc.ul.pt!skull.cc.fc.ul.pt!bjoao From: Joao Rodrigues Newsgroups: bionet.molbio.ageing Subject: Re: Searching Date: Fri, 23 Jun 1995 14:07:37 +0200 Organization: Faculdade de Ciencias da Universidade de Lisboa Lines: 13 Message-ID: References: <3s6mcm$60t@no-names.nerdc.ufl.edu> NNTP-Posting-Host: skull.cc.fc.ul.pt Mime-Version: 1.0 Content-Type: TEXT/PLAIN; charset=US-ASCII In-Reply-To: <3s6mcm$60t@no-names.nerdc.ufl.edu> On 20 Jun 1995 data@maple.circa.ufl.edu wrote: > I also would be interested in a copy of "Internet and E-Mail Resources on > Aging" compiled by Joyce A. Post. If at all possible could you please > eithe rpost it or e-mail it to me at Data@ufcc.ufl.edu > Thank you > > >I am also interested in that. If posible, send me a copy to bjoao@skull.cc.fc.ul.pt Thanks in advance From owner-ageing@net.bio.net Thu Jun 22 23:00:00 1995 Newsgroups: bionet.molbio.ageing Path: biosci!bcm!cs.utexas.edu!howland.reston.ans.net!spool.mu.edu!agate!sunsite.doc.ic.ac.uk!warwick!bsmail!usenet From: Harry.Witchel@bristol.ac.uk Subject: Where is E-mail resources on Aging? Message-ID: Sender: usenet@uns.bris.ac.uk (Usenet news owner) Nntp-Posting-Host: rm2.pys.bris.ac.uk Reply-To: harry.witchel@bristol.ac.uk Organization: Medical School, Bristol X-Newsreader: WinVN 0.91.4 References: <3s6mcm$60t@no-names.nerdc.ufl.edu> Date: Fri, 23 Jun 1995 15:58:15 GMT Lines: 18 In article <3sc8ev$1k6@polo.iquest.com>, Jane Hays says: > >> I also would be interested in a copy of "Internet and E-Mail Resources on >> Aging" compiled by Joyce A. Post. If at all possible could you please >> eithe rpost it or e-mail it to me at Data@ufcc.ufl.edu >> Thank you >> > > >Me too!! jhays@colsa.com > >Thanks! > So would I! Harry.Witchel@bristol.ac.uk From owner-ageing@net.bio.net Sun Jun 25 23:00:00 1995 Path: biosci!daresbury!trane.uninett.no!Norway.EU.net!EU.net!howland.reston.ans.net!vixen.cso.uiuc.edu!uwm.edu!psuvax1!news.eecs.nwu.edu!newsfeed.acns.nwu.edu!news.cc.uic.edu!uicvm.uic.edu!ruhnke Message-ID: <19950623.233424.766727.NETNEWS@UICVM.UIC.EDU> Nntp-Posting-Host: slip3-21.dialin.uic.edu Date: Fri, 23 Jun 1995 18:50:44 +0000 Newsgroups: bionet.molbio.ageing From: ruhnke@uiuc.edu (Earle Ruhnke) Subject: Internet and e-mail Resources on Aging X-Newsreader: News Xpress Version 1.0 Beta #3 Lines: 3 gopher.os.dhhs.gov and look under resources by organization, administration on aging, administration on aging (AoA), finally, internet and e-mail resources on aging. From owner-ageing@net.bio.net Sun Jun 25 23:00:00 1995 Path: biosci!daresbury!trane.uninett.no!Norway.EU.net!EU.net!howland.reston.ans.net!gatech!hubcap.clemson.edu!bigbird.csd.sc.edu!usenet From: danker@phar2.pharm.sc.edu (Walt Danker) Newsgroups: bionet.molbio.ageing Subject: Re: Searching Date: Mon, 26 Jun 1995 15:29:31 GMT Lines: 16 Message-ID: <3sm9am$16e@bigbird.csd.sc.edu> References: <3s6mcm$60t@no-names.nerdc.ufl.edu> <3sc8ev$1k6@polo.iquest.com> NNTP-Posting-Host: 129.252.72.53 X-Newsreader: Forte Free Agent v0.55 Jane Hays wrote: >> I also would be interested in a copy of "Internet and E-Mail Resources on >> Aging" compiled by Joyce A. Post. If at all possible could you please >> eithe rpost it or e-mail it to me at Data@ufcc.ufl.edu >> Thank you >> Me too!! Thanks! Walt Walt Danker@phar2.pharm.sc.edu From owner-ageing@net.bio.net Sun Jun 25 23:00:00 1995 Path: biosci!daresbury!trane.uninett.no!nac.no!Norway.EU.net!EU.net!news.sprintlink.net!europa.chnt.gtegsc.com!gatech!newsfeed.pitt.edu!dsinc!netnews.upenn.edu!cronkite.ocis.temple.edu!astro.ocis.temple.edu!devisett From: devisett@astro.ocis.temple.edu (DN (Narasimha Devisetty)) Newsgroups: bionet.molbio.ageing Subject: Internet & E-mail resources on aging Date: 26 Jun 1995 14:05:10 GMT Organization: Temple University, Academic Computer Services Lines: 15 Message-ID: <3smeqm$2pq@cronkite.ocis.temple.edu> NNTP-Posting-Host: astro.ocis.temple.edu X-Newsreader: TIN [version 1.2 PL2] I saw lot of people requesting for Joyce Post's "Internet & E-mail resources on Aging". I have access to one of her versions. But I am not sure if it is the latest. But I could tell where to reach Joyce Post. She could be reached at post@shrsys.hslc.org. Sorry, Ms. Post if I am not supposed to post your address here. Good Luck DN **************************************************************************** If u think nobody cares if you're alive;try missing a couple of car payments. ***************************************************************************** From owner-ageing@net.bio.net Tue Jun 27 23:00:00 1995 Path: biosci!SINGER.ASRI.EDU!MANEV From: MANEV@SINGER.ASRI.EDU Newsgroups: bionet.molbio.ageing Subject: Symposium Registration in Progress Date: 28 Jun 1995 09:45:13 -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 International Symposium on Oxidative Stress, Apoptosis and Brain Damage, September 21 to 24, 1995; Pittsburgh, PA, USA. Registration is in progress. For information and registration please call: + 412-359-4952 or fax to Ms. Kathleen Hrdlicka, Continuing Medical Education, AGH, 412-359-8218. From owner-ageing@net.bio.net Wed Jun 28 23:00:00 1995 Newsgroups: bionet.molbio.ageing Path: biosci!rutgers!gatech!news.sprintlink.net!cs.utexas.edu!news.tamu.edu!news.utdallas.edu!corpgate!bcarh189.bnr.ca!nott!cunews!freenet.carleton.ca!FreeNet.Carleton.CA!bz355 From: bz355@FreeNet.Carleton.CA (Jennifer Dyer) Subject: Re: Searching Message-ID: Sender: bz355@freenet3.carleton.ca (Jennifer Dyer) Organization: The National Capital FreeNet, Ottawa, Ontario, Canada Date: Thu, 29 Jun 1995 16:44:47 GMT Lines: 5 I would also like a copy of this guide. Fax me at 613-761-5334 or e-mail me at bz355@freenet.carleton.ca. Thanks! Jen Calhoun From owner-ageing@net.bio.net Thu Jun 29 23:00:00 1995 Path: biosci!daresbury!not-for-mail From: rattan@kemi.aau.dk (Suresh Rattan) Newsgroups: bionet.molbio.ageing Subject: Doctor of Science in Ageing Date: 30 Jun 1995 10:20:37 +0100 Lines: 28 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <3t0fl5$5cc@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk I would like to share with the readers of this group my happiness on the award of the degree of Doctor of Science (Or: Doctor Scientiarum, as they say it in Denmark) in the field of biology of ageing by the Faculty of Natural Sciences, University of Aarhus, Denmark. This award (which to the best of our knowledge is the first one in the field of biology of ageing) also acknowledges the fact that the research area of cellular and molecular biology of ageing has now matured enough to be worthy of recognition with the highest academic degree. For me personally, it is the culmination of my formal "training and education" in the field of ageing, which began with my initiation through an MSc (Hons) research thesis on aspects of insect ageing, G.N.D. University, Amritsar, India (1977); MPhil thesis on the development and ageing of hydra, J.N.U., New Delhi, India (1979); PhD thesis on human fibroblast ageing, at the National Institute for Medical resrach, Mill Hill, London, UK (1982); and now the post-PhD degree for my research on the translational regulation of gene expression during ageing and for the development of certain ideas about the nature of gerontogenes. Hopefully, such a recognition of the field will make it more attractive for young beginners to consider doing research in the field of ageing. Dr. Suresh I.S. Rattan, PhD; DSc Laboratory of Cellular Ageing Department of Chemistry Aarhus University DK-8000 Aarhus-C, Denmark. Phone: +45 8942 3956; Fax: +45 8619 6199 From owner-ageing@net.bio.net Thu Jun 29 23:00:00 1995 Path: biosci!daresbury!bioftp.unibas.ch!citi2.fr!jussieu.fr!oleane!cam.news.pipex.net!pipex!edi.news.pipex.net!pipex!howland.reston.ans.net!news.cac.psu.edu!news.pop.psu.edu!hudson.lm.com!godot.cc.duq.edu!news.duke.edu!solaris.cc.vt.edu!swiss.ans.net!prodigy.com!usenet From: SRPJ89A@prodigy.com (Art Moore) Newsgroups: bionet.molbio.ageing Subject: Re: Searching Date: 30 Jun 1995 12:21:17 GMT Organization: Prodigy Services Company 1-800-PRODIGY Lines: 4 Distribution: world Message-ID: <3t0q7t$v7s@usenetw1.news.prodigy.com> References: <3s6mcm$60t@no-names.nerdc.ufl.edu> <3sc8ev$1k6@polo.iquest.com> <3sm9am$16e@bigbird.csd.sc.edu> NNTP-Posting-Host: inugap2.news.prodigy.com X-Newsreader: Version 1.2 I would like a copy too please! Art Moore srpj89a@prodigy.com Thanks From owner-ageing@net.bio.net Fri Jun 30 23:00:00 1995 Path: biosci!lhc!darwin.sura.net!www.uno.edu!uno.edu!KGPL From: kgpl@uno.edu Newsgroups: bionet.molbio.ageing Subject: Pineal Gland Output Date: 1 Jul 1995 04:35:27 GMT Organization: University of New Orleans Lines: 7 Message-ID: <3t2jaf$9i0@www.uno.edu> Reply-To: kgpl@uno.edu NNTP-Posting-Host: jazz.ucc.uno.edu There has been a lot of stuff recently about the possible effects of melatonin on ageing. Does the pineal gland put out anything other than melatonin? If so, what? And what effect does whatever else it puts out have when given to ageing rats? Thanks, Kevin