From owner-ageing@net.bio.net Fri Mar 01 22:00:00 1996 Path: biosci!TENET.EDU!dashley From: dashley@TENET.EDU (Don Ashley) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 2 Mar 1996 03:02:44 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 32 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net ---------- Forwarded message ---------- Date: Fri, 1 Mar 1996 09:45:02 CST From: Edward Friedlander, M.D. To: Multiple recipients of list TALK-MAN Subject: Re: Learned Helplessness About Immortality (fwd) > Consider the discovery of telomerase, the 'immortality' enzyme in cancer > cells. If telomerase is manipulated into healthy cells, we may literally > be able to stop aging. Anybody who's still taking this seriously is a sucker. I'm still hearing these telomerase claims (and was the first guy at my medical school to present the original discovery of the loss of telomeres, during lecture). The ends of chromosomes (telomeres) shorten with cell division under some circumstances, but it seems preposterous to think that this is happening in the reserve cells of skin, marrow, gut epithelium, and so forth. Nor is it reasonable to believe that these cells can divide only fifty times (the "Hayflick phenomenon"). Further, the cells that bear the brunt of aging (i.e., the brain cells) don't even divide. The other familiar changes of aging are obviously programmed genetically (I'm thinking, for example, of the loss of receptors from the erectile tissues, which are also made up of non-dividing cells). I appreciate anybody who wants to offer hope to others. Sorry, but this particular hope is vain. Our bodies are programmed to wear out. From owner-ageing@net.bio.net Fri Mar 01 22:00:00 1996 Path: biosci!TENET.EDU!dashley From: dashley@TENET.EDU (Don Ashley) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 2 Mar 1996 03:03:57 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 44 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net ---------- Forwarded message ---------- Date: Fri, 01 Mar 1996 14:48:16 +0000 From: David Kipling To: ageing@net.bio.net Subject: Re: Learned Helplessness About Immortality (fwd) > Consider the discovery of telomerase, the 'immortality' enzyme in cancer > cells. If telomerase is manipulated into healthy cells, we may literally > be able to stop aging. Hi There is a big leap of faith here. Telomerase may ne necessary for tumor cells to continue growing but that does *not* mean that the reason normal, somatic cells stop growing normally has anything to do with telomeres and telomerase. To put it bluntly, in vivo many cells cease growth before the equivalent # of generations that they would undergo in vitro (Hayflick limit). This is terminal differentiation. Good examples of this comes from the behaviour of cells in multistage carcinogenesis systems. The first oncogenic transformation overcomes the differentiation/arrest signal and allows the cells to continue growing - without telomerase activation. Later on, as even more divisions are required, telomerase is sometimes seen to be up-regulated. The point is that the cells stopped dividing in the first place not because of a lack of telomerase, but because of normal cellular differentiation. If this is true, then ageing problems will come down more to questions of cellular regeneration (getting out of my field here). David Kipling Edinburgh ########################################## Quick plug for a couple of reviews: Kipling, D (1995) Telomerase: immortality enzyme or oncogene? Nature Genetics 9:104 Kipling, D (1995) The Telomere. Oxford University Press. From owner-ageing@net.bio.net Fri Mar 01 22:00:00 1996 Path: biosci!TENET.EDU!dashley From: dashley@TENET.EDU (Don Ashley) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 2 Mar 1996 03:25:17 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 56 Sender: daemon@net.bio.net Distribution: world Message-ID: References: <199602272126.PAA12190@formby.tenet.edu> NNTP-Posting-Host: net.bio.net On Tue, 27 Feb 1996, Charles Flannery wrote: > > Actually, that is what I was asking the group. Why would people want to live > > for an extended period of time. On 2/10/96 via this thread you posted many > > reasons people might 'resist' the idea of living forever. I simply wanted to > > know why people are promoting the idea of living forever. What is there to > > gain? > > > > Karen > > > I am asking the same question. What is there to gain from living > forever? Forever is unconceivable. Stopping the ageing process will get us an extra 100 years. We still have choices of careless, overconsumptive, inadequately coping lifestyles that will eventually snuff us if we stop ageing. >Life was meant to end.... Life was meant to be lived, not to end. > and trying to make it an eternal thing > would upset the balance of nature. Anything man invents or develops upsets the balance of nature. >I don't feel our world is such a great > place that we would want to stay on it forever, do you? The world is a great place. Our attitudes (which are changable) can give us a depressing or exciting outlook about the world. I would like to > hear some opinions on this subject. > > > You have just read an important e-mail message from: > Charles Flannery > Ramapo College > cflanner@ramapo.edu > > > > DO NOT PUT OFF UNTIL TOMORROW WHAT CAN BE DONE NEXT WEEK!!!! > (or the week after that or next month or 3 months from now or > next year...........) > > > Do not go where the path may lead, > instead go where there is no path and leave a trail. > From owner-ageing@net.bio.net Fri Mar 01 22:00:00 1996 Path: biosci!NJ1.AAE.COM!nmig From: nmig@NJ1.AAE.COM (Nicholas Migliozzi) Newsgroups: bionet.molbio.ageing Subject: (no subject) Date: 2 Mar 1996 14:28:57 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 17 Sender: daemon@net.bio.net Distribution: world Message-ID: <199603022218.QAA09986@ns.aae.com> NNTP-Posting-Host: net.bio.net Hello, I throw out a question for your consideration. I would appreciate an answer from someone who thinks he or she knows the answer. I certainly don't. What IS old age? Thank you, NickM From owner-ageing@net.bio.net Fri Mar 01 22:00:00 1996 Path: biosci!bcm.tmc.edu!news.msfc.nasa.gov!newsfeed.internetmci.com!panix!news.columbia.edu!bonjour.cc.columbia.edu!tac2 From: tac2@bonjour.cc.columbia.edu (Todd A Carter) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 2 Mar 1996 16:14:31 GMT Organization: Columbia University Lines: 23 Message-ID: <4h9s57$86e@apakabar.cc.columbia.edu> References: NNTP-Posting-Host: bonjour.cc.columbia.edu >Subject: Re: Learned Helplessness About Immortality (fwd) > >Actually, that is what I was asking the group. Why would people want to live >for an extended period of time. On 2/10/96 via this thread you posted many >reasons people might 'resist' the idea of living forever. I simply wanted to >know why people are promoting the idea of living forever. What is there to >gain? Many people argue that it would not be enjoyable to live forever, that a certain boredom or disinterest would set in. This, I suppose, is a definite possibility. I, personally would prefer the option of living for, if not forever, than an extremely long time. There are more things to do and see on this planet than I could possibly do in a single normal human lifespan. There is also more to learn and experience. And, if you add the possibility of accessable space travel someday, you can throw the magnitude of the universe into the bucket. Basically, a combination of curiosity about the universe and about the future provides the motivation for an increased life span. --Todd Carter From owner-ageing@net.bio.net Fri Mar 01 22:00:00 1996 Path: biosci!TENET.EDU!dashley From: dashley@TENET.EDU (Don Ashley) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 2 Mar 1996 04:06:31 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 64 Sender: daemon@net.bio.net Distribution: world Message-ID: References: <199602280212.UAA23632@formby.tenet.edu> NNTP-Posting-Host: net.bio.net On Tue, 27 Feb 1996, Kaye Hartzler wrote: > actually you are asking a very hard question, and I am curious why. The question is asked because: The concept of living an extra hundred years can be liberating and exhilerating without promoting irresponsibility. I enjoy sharing new insights. The concept is reflective of a positive mental attitude and I like to interact with others who enjoy PMA. Discussing anti-ageing concepts helps to break down the barriers to progress about research in the area. Funding from the gov't and the private sector are severly limited due to the 'flat world' mentality that there is no hope. To achieve breakthoughs in science will require significant financial support. Lifestyles are polluted with the notion that after age '65' there is no reason to learn new careers or languages or avocations because we are already 'spent' and we are hopelessly waiting out our genetically programmed sentence to the gallows. Such resignation contributes to physical and mental inactivity and lack of stimulation. The concept that we might get to live an extra hundred years is more credible than eternity, which is inconceivable. It is fun to think of the advances in all the technologies that we might get to experience if we stay around even 50 more years. Look at the advances in the last 100 years. It is motivating to keep our bodies and attitudes in peak condition so that we have a better chance to be around when the breakthroughs in anti-ageing technology occur. Health attitudes and bodies extend lives for a few years. Maybe just long enough to get the advantage of the scientific 'cure of the old age disease'. Taking risks in traffic is more significant when we think that we may be risking an extra hundred years of our own lives as well as the lives of others. Consuming delicious toxins that are available on every street and in every store and restaurant may be given second thought. Overconsumptive, lethargic lifestyles may rob us of more than we could have ever imagined when thinking about anti-ageing possibilities. Pointless conflicts at home or work tend to reduce optimum health. When thinking of life 100 years from now, the conflicts and issues that we waste energy on today become trivial instead of paramount. It is a challenge to explore new concepts in a world that promotes negativity and pessimism. > I want to > live a very long time, maybe forever, and the only reason I can give you is > that I just want to. I love being around people, new and old friends. I love > hiking and anything with nature, except driving in snow. I want to live and > enjoy the growing mentally. I believe in life after life, and reincarnation, > and people tell me that another life may be better. I don't really want to go > into another life, I want to enjoy this one a long long time. > From owner-ageing@net.bio.net Sat Mar 02 22:00:00 1996 Path: biosci!internet!biosci!not-for-mail From: biohelp (BIOSCI Administrator) Newsgroups: bionet.molbio.ageing Subject: IMPORTANT - BIOSCI Fundraising Update! Date: 3 Mar 1996 02:00:28 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 149 Sender: daemon@net.bio.net Distribution: world Message-ID: <199603031000.CAA12378@net.bio.net> NNTP-Posting-Host: net.bio.net I'm interrupting the usual monthly posting of the BIOSCI miniFAQ to bring you up to date on BIOSCI fundraising progress, a topic of concern to your future use of this resource. Thank you in advance for taking the time to read this message carefully. Last year we announced that BIOSCI was going to adopt the U.S. Public Broadcasting System model to fund its operations after our DOE/NSF grant runs out later this year. Unlike PBS, we are not soliciting contributions from users; we are only selling ads on our Web pages solely to cover our operating costs. Our goal is to seek sponsorships until we build up an operating reserve of about $100,000 and then cease further promotions until we need to build the reserve back up. (The accountants among our readership will be familiar with the problem of deferred revenue which we can not safely utilize until ads have been displayed for a period of time.) We have three sponsors to date with a couple more pending. The process is time-consuming, however, and we need your help as explained further below. Our operating costs consist of our network connection, phone lines, hardware maintenance (we hope to have new and faster hardware soon!), plus 0.7 FTE of salaries covering UNIX systems admin, technical support, quality assurance, i.e., testing, of our system, and administrative costs (such as the time it takes to actually find/write/call potential sponsors and raise money!). Although the BIOSCI staff does get compensated for a portion of the work that they do, this project has always received a lot of free after-hours and "vacation" time labor, so we hope that no one will begrudge the time that we do charge to the project to serve you. All of the three part-time staff members, Dave Mack, Julie Lawrence, and myself, have full time day jobs and families in addition to working hard to keep this service running for all of you. Julie and Dave Mack are subcontractors for BIOSCI; my time that is charged to the project defrays a portion of my regular salary instead of adding to my income. Besides having to relocate the project, we were very busy this last year building new infrastructure such as our WWW hypermail interface to the system. This was released last December along with scores of WAIS indices for the newsgroups. Virtually everything is complete, although we do continue to find and fix bugs (many through your helpful feedback!). We are still having some problems with our WAIS indexing. The archives continue to grow rapidly. We are running over 100 indexes now versus three previously and any systems crashes cause greater havoc with the indexing than before! We are still working to fix this as fast as our resources permit and appreciate your patience, but we have been able to automate a lot of the infrastructure to reduce labor as compared to past requirements. We have also implemented new software to make moderation of BIOSCI/bionet newsgroups much easier and combat the growing problem of Internet junk mail and USENET "spamming." About 20% of our groups are now moderated, many of them by the BIOSCI staff! This, for example, made a major difference last year in the quality of content in our EMPLOYMENT/bionet.jobs.offered newsgroup which many commercial concerns and recruiting firms are using **without charge** to recruit candidates for positions in the biological sciences. We are also now in a position to have sponsors for individual newsgroups as you will have noticed if you have visited http://www.bio.net/ and clicked on "Access the BIOSCI/bionet newsgroups" recently. So, how can you help?? ---------------------- As noted above it can take a lot of time to contact potential sponsors if I have to do it all myself. Our request is quite simple. You can do two important things which will take very little time for you individually. First, please use our WWW system at http://www.bio.net/ to access the archives. You can now post or reply to messages via your Web browser. Your usage helps attract sponsors. If you contact any of our sponsors, please be sure to thank them for supporting BIOSCI. It is critical for them to get this feedback if they are to continue their sponsorship for the long term. Second, if you work for a company or organization that provides products or services of interest to the biology community, please pass this message on to your marketing or marketing communications department or other appropriate group. Please ask them to help support BIOSCI by sponsoring our Web site and explain the uses and benefits of the system to the biology community. If they are interested, they can then contact us for further information at our tech support address, biosci-help@net.bio.net. Our hope is to quickly raise several large corporate/institutional sponsors on our heavily-used WWW locations (some stats appended below), and then end this sponsorship campaign so that our resources can continue to be used for service provision, not fundraising. Many of our specialty newsgroup WWW archives are still used by small communities of scientists (and they haven't been heavily promoted yet). While these may be valuable niche markets to some advertisers, it will generate more labor and overhead having to find these sponsors, fairly price the locations, and deal with lots of smaller sponsorships than fewer mid-to large sponsors. We are striving to keep our operation as lean and efficient as possible since we are not trying to make careers out of running BIOSCI. We are trying if at all possible to avoid the administrative overhead entailed with processing lots of small payments to reach our fundraising goals. I'd like to thank all of you for your help in advance. In helping us, you are also helping yourselves, not only in keeping this resource available for all of the both large and small research communities that we serve, but also by alleviating the need for us to go back and compete with researchers for tight grant dollars! We promised NSF when we were awarded the BIOSCI grant that we would carry out this mission to make the service self-supporting. With your help, we will succeed in continuing BIOSCI's work into its second decade. Thank you very much! Sincerely, Dave Kristofferson BIOSCI/bionet Manager biosci-help@net.bio.net A list of our prime WWW sponsorship locations follow. Statistics are for the four week period from 22 Jan. - 18 Feb. 1996 and usage continues to grow. ---------------------------------------------------------------------- The overall BIOSCI WWW pages are currently visited by users from close to 5000 unique computer hosts per week. Web servers only log the Internet computer/host name and frequently more than one individual can connect to us from a particular host. Main home page, http://www.bio.net, visited recently by about 2100 unique hosts per week Main Newsgroups archives page, http://www.bio.net/archives.html, visited recently by about 1200 Unique hosts per week BIO-JOURNALS archive page, http://www.bio.net/BIO-JOURNALS.html, visited recently by about 1000 unique hosts per week. EMPLOYMENT archive pages: http://www.bio.net:80/hypermail/EMPLOYMENT/ and monthly header pages, visited recently by about 600 unique hosts per week. Address database search page, http://www.bio.net/addrsearch.html, visited recently by about 450 unique hosts per week. Methods newsgroup archive pages, http://www.bio.net:80/hypermail/METHDS- REAGNTS/ and monthly header pages, visited recently by about 350 unique hosts per week. ---------------------------------------------------------------------- From owner-ageing@net.bio.net Sat Mar 02 22:00:00 1996 Path: biosci!NJ1.AAE.COM!nmig From: nmig@NJ1.AAE.COM (Nicholas Migliozzi) Newsgroups: bionet.molbio.ageing Subject: Kinetin Date: 3 Mar 1996 12:41:39 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 8 Sender: daemon@net.bio.net Distribution: world Message-ID: <199603032031.OAA18593@ns.aae.com> NNTP-Posting-Host: net.bio.net Hi, What is kinetin? And how does it help in anti-ageing? Nick M. From owner-ageing@net.bio.net Sat Mar 02 22:00:00 1996 Path: biosci!bcm.tmc.edu!cs.utexas.edu!howland.reston.ans.net!tank.news.pipex.net!pipex!dispatch.news.demon.net!demon!mail2news.demon.co.uk!longevb.demon.co.uk From: John de Rivaz Newsgroups: bionet.molbio.ageing Subject: Re: Old Age Date: Sun, 03 Mar 1996 17:08:25 +0100 Organization: Myorganisation Lines: 31 Message-ID: <698438805wnr@longevb.demon.co.uk> References: <199603022218.QAA09986@ns.aae.com> Reply-To: John@longevb.demon.co.uk X-NNTP-Posting-Host: longevb.demon.co.uk X-Newsreader: Newswin Alpha 0.9.1 X-Mail2News-Path: disperse.demon.co.uk!post.demon.co.uk!longevb.demon.co.uk In article: <199603022218.QAA09986@ns.aae.com> nmig@NJ1.AAE.COM (Nicholas Migliozzi) writes: > > Hello, > > I throw out a question > for your consideration. > I would appreciate an > answer from someone who > thinks he or she knows the > answer. I certainly don't. > > What IS old age? A disease, possibly of the immune system, that causes the body's self repair system to fail. Every human suffers from the disease, which is probably genetic in origin. -- Sincerely, **************************************** * Publisher of Longevity Report * John de Rivaz * Fractal Report * * details on request * **************************************** In the information age, sharing can increase world wealth enormously, because giving information does not decrease your information. http://ourworld.compuserve.com/homepages/JohndeR Fast loading, very few slow pictures From owner-ageing@net.bio.net Sun Mar 03 22:00:00 1996 Path: biosci!agate!newsxfer2.itd.umich.edu!chi-news.cic.net!nntp.coast.net!harbinger.cc.monash.edu.au!news.mel.connect.com.au!munnari.OZ.AU!news.uwa.edu.au!newsman.murdoch.edu.au!usenet From: Jim Cummins Newsgroups: bionet.molbio.ageing Subject: mtDNA database Date: 4 Mar 1996 04:25:55 GMT Organization: Murdoch University Lines: 15 Message-ID: <4hdrcj$ljd@newsman.murdoch.edu.au> NNTP-Posting-Host: vetmac3.murdoch.edu.au Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 1.1N (Macintosh; I; 68K) X-URL: news:bionet.molbio.ageing Hi: Wallace et al's searchable database on human mtDNA is now up on WWW page http://www.gen.emory.edu/mitomap.html Kogelnik AM, Lott MT, Brown MD, Navathe SB, Wallace DC. Mitomap - a human mitochondrial genome database. Nucleic Acids Research 1996;24(1):177-179. Jim Cummins, Associate Professor in Veterinary Anatomy, Murdoch University, Western Australia 6150. TEL +61-9-360 2668 FAX +61-9-310 4144 From owner-ageing@net.bio.net Sun Mar 03 22:00:00 1996 Path: biosci!TENET.EDU!dashley From: dashley@TENET.EDU (Don Ashley) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 4 Mar 1996 04:59:56 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 36 Sender: daemon@net.bio.net Distribution: world Message-ID: References: <4h9s57$86e@apakabar.cc.columbia.edu> NNTP-Posting-Host: net.bio.net On 2 Mar 1996, Todd A Carter wrote: > >Subject: Re: Learned Helplessness About Immortality (fwd) > > > >Actually, that is what I was asking the group. Why would people want to live > >for an extended period of time. On 2/10/96 via this thread you posted many > >reasons people might 'resist' the idea of living forever. I simply wanted to > >know why people are promoting the idea of living forever. What is there to > >gain? > > Many people argue that it would not be enjoyable to live forever, that a > certain boredom or disinterest would set in. This, I suppose, is a > definite possibility. One does not have to live forever to experience 'certain boredom or disinterest'. There are many opportunities to waste time like that in our traditional life expectancy of less than 100 years. > I, personally would prefer the option of living > for, if not forever, than an extremely long time. > > There are more things to do and see on this planet than I could possibly > do in a single normal human lifespan. There is also more to learn and > experience. And, if you add the possibility of accessable space travel > someday, you can throw the magnitude of the universe into the bucket. > > Basically, a combination of curiosity about the universe and about the > future provides the motivation for an increased life span. > > --Todd Carter > > > From owner-ageing@net.bio.net Sun Mar 03 22:00:00 1996 Path: biosci!TENET.EDU!dashley From: dashley@TENET.EDU (Don Ashley) Newsgroups: bionet.molbio.ageing Subject: Re: Immortality Date: 4 Mar 1996 05:52:15 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 31 Sender: daemon@net.bio.net Distribution: world Message-ID: References: <199602291959.LAA11490@desiree.teleport.com> NNTP-Posting-Host: net.bio.net On Thu, 29 Feb 1996, Mary Montgomery wrote: > At 11:44 AM 2/26/96 +0800, cheehoe@pop2.jaring.my wrote: > > >I do not want to hear from those who are endogenously depressed. They should > >go get ECT. > >From: Ratan Singh, address: cheehoe@pop2.jaring.my > > Why? So that they can't remember WHY they ever wanted to live or die? Not > a good joke in my book. > > I'm not depressed, love life, live it to the fullest, an nearing "Senior > Citizen" status at the mall and am perfectly willing to exit this life in > the next 20 to 40 years. Forced innocualtions for immortality treatments are many years further away than the actual breakthroughs in anti-aging technology. People will still have choices to live dangerous, overconsumptive, inadequately coping lifestyles. Remember, naps while driving prevent old age. > > Mary > Mary Montgomery > > > From owner-ageing@net.bio.net Sun Mar 03 22:00:00 1996 Path: biosci!daresbury!nntp-trd.UNINETT.no!newsfeed.sunet.se!news00.sunet.se!sunic!mn6.swip.net!plug.news.pipex.net!pipex!tube.news.pipex.net!pipex!dish.news.pipex.net!pipex!tank.news.pipex.net!pipex!newsfeed.internetmci.com!mr.net!news.mr.net!visi.com!usenet From: "Richard E. McClain" Newsgroups: bionet.molbio.ageing Subject: Alheimer's Date: Mon, 04 Mar 1996 15:55:06 -0600 Organization: Vector Internet Services, Inc. Lines: 6 Message-ID: <313B66BA.60AD@visi.com> NNTP-Posting-Host: ppp23.visi.com Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.0GoldB1 (Win95; I) There's a new book available about a woman who lost her mother, two sisters and two brothers to Alzheimer's. Very informative for caregivers. http://choicemall.com/minnesota/mn001-01 R. McClain From owner-ageing@net.bio.net Mon Mar 04 22:00:00 1996 Path: biosci!agate!cgl!itssrv1.ucsf.edu!itsa!cpatil From: cpatil@itsa.ucsf.edu (Chris Patil) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 5 Mar 1996 03:37:00 GMT Organization: UCSF, ITS Computing Facility Lines: 56 Message-ID: <4hgcss$12t7@itssrv1.ucsf.edu> References: NNTP-Posting-Host: itsa.ucsf.edu In article dashley@TENET.EDU (Don Ashley) writes: >The ends of chromosomes (telomeres) shorten with cell division under >some circumstances, but it seems preposterous to think that this is >happening in the reserve cells of skin, marrow, gut epithelium, and >so forth. Nor is it reasonable to believe that these cells can >divide only fifty times (the "Hayflick phenomenon"). Telomeres absolutely do shorten in vivo, in all dividing cell lineages other than those in the germ line. This is far from preposterous. It still doesn't mean that telomere shortening causes aging, that telomere shortening is in any way responsible for the Hayflick limit, or that the Hayflick limit has anything to do with the aging process. >Further, the cells that bear the brunt of aging (i.e., the brain >cells) don't even divide. The other familiar changes of aging are >obviously programmed genetically (I'm thinking, for example, of the >loss of receptors from the erectile tissues, which are also made up >of non-dividing cells). > >I appreciate anybody who wants to offer hope to others. Sorry, but >this particular hope is vain. Our bodies are programmed to wear out. Aging isn't "obviously" programmed genetically, except to the trivial extent that different organisms have different genomes and different lifespans. The question of whether aging is part of a developmental program, the consequence of accumulated damage to somatic tissues, or some combination of these factors is by all means an open question Population biology does predict that aging will evolve in a population that has a separation between soma and germ line, and in which genes influence fitness to different extents at different times in the life cycle (an "age-structured population" in which reproductively mature individuals can be phenotypically distinguished on the basis of age); however, it doesn't say anything about the mechanism by which aging needs to take place. The model is open to the possibility that alleles that act to increase reproductive success at later ages simply have less of an impact on overall fitness (the intuitive explanation for this being the observation that when two organisms are otherwise identical, the one with the shorter generation time is more fit), and therefore aren't as vigorously selected for. Alternatively (but hardly mutually exclusively), if there are alleles which confer early reproduction at the expense of later survival, these alleles will still be positively selected (a situation referred to as "antagonistic pleiotropy"). Neither of these classes of "aging genes" necessarily amounts to a developmental program which actively results in aging. An interesting question that may or may not reduce to a question of semantics is whether there's a difference between an active developmental program that results in senescence, and senescence due to a lack of effort put into maintenance (where such lack evolved as a result either of antagonistic pleiotropy or decay of late-acting alleles by neutral selection). From owner-ageing@net.bio.net Mon Mar 04 22:00:00 1996 Path: biosci!daresbury!yama.mcc.ac.uk!peer-news.britain.eu.net!newsfeed.ed.ac.uk!news From: David Kipling Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: Tue, 05 Mar 1996 12:28:57 +0000 Organization: MRC Human Genetics Unit Lines: 78 Message-ID: <313C3389.5ABB@hgu.mrc.ac.uk> References: <4hgcss$12t7@itssrv1.ucsf.edu> NNTP-Posting-Host: purdeys.hgu.mrc.ac.uk Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.0 (Win16; I) To: Chris Patil CC: mwest@geron.com I think Chris has made a very valid set of comments here. > Chris Patil wrote: > > In article dashley@TENET.EDU (Don Ashley) writes: > > >The ends of chromosomes (telomeres) shorten with cell division under > >some circumstances, but it seems preposterous to think that this is > >happening in the reserve cells of skin, marrow, gut epithelium, and > >so forth. Nor is it reasonable to believe that these cells can > >divide only fifty times (the "Hayflick phenomenon"). (in reply to original post) Why is it preposterous? 50 divisions of a single cell produces about 1,000,000,000,000,000 offspring. A pea-sized bit of tissue contains something of the order of 100,000,000 cells. 50 divisions therefore gives enough cells to make about 10 million pea-sized bits of tissue. That's a lot of slack for development and regeneration to play with. > Telomeres absolutely do shorten in vivo, in all dividing cell lineages > other than those in the germ line. This is far from preposterous. It > still doesn't mean that telomere shortening causes aging, that telomere > shortening is in any way responsible for the Hayflick limit, or that the > Hayflick limit has anything to do with the aging process. This of course is the crucial point, to what extent the Hayflick limit impacts upon organismal ageing. It may in some tissues, whereas in other tissues damage to non-mitotic cells could be the major determinant (for point of argument). Organismal ageing is probably too complex to be put down to a single mechanism. > Aging isn't "obviously" programmed genetically, except to the trivial > extent that different organisms have different genomes and different > lifespans. The question of whether aging is part of a developmental > program, the consequence of accumulated damage to somatic tissues, or > some combination of these factors is by all means an open question The way I had it explained to me goes something like this: An animal takes in resources (in the form of food). These can be used for two main processes: repair to the somatic cells, and for producing offspring (e.g. growth of the embryo, post-natal care and feeding, etc.). For every calorie you use for somatic repair, that's one less for the offspring. On top of this you have the problem of predation. So, if one is a mouse, there is no point in devoting vast amounts of resources to somatic repair - why live for 100 years if you are more than likely to be eaten in 12 months? Better for you to devote more of those precious resources to making offspring as fast as possible. In short, there is no selective advantage for a mouse to live for 100 years, but there is a selective *disadvantage* for it to use resources which would otherwise have been used for reproduction on useless somatic repair. Note here that species with low levels of predation have longer lifespans - for example, ostriches are particularly short-lived birds (cannot fly so get eaten more often). And so forth. This is the "disposable soma" theory and suggests that ageing is a non-selected by-product of maximising the reproduction v. predation lifehistory, and also the fact that life is a compromise: you cannot have maximum reproductive rates *and* maximum life spans at the same time. > Neither of these classes of "aging genes" necessarily amounts to a > developmental program which actively results in aging. An interesting > question that may or may not reduce to a question of semantics is whether > there's a difference between an active developmental program that results > in senescence, and senescence due to a lack of effort put into > maintenance (where such lack evolved as a result either of antagonistic > pleiotropy or decay of late-acting alleles by neutral selection). The other thing we should remember as a general point is that ageing is probably a fairly recent process in human evolution. We popularly think of age-related processes occurring in middle-age onwards, yet consider the fact that until the last few thousand years human life-spans have been very low. Stone-age man was lucky to get past his early 20s by all accounts. It is not until recent years that cultural advances have allowed massively extended lifespans, and with them ageing in the popularist definition. In short, what we think of as "ageing" never really happened much during human evolution, so it is hard to see that it was actively "selected for" or "genetically programmed". Better to imagine it as an unavoidable side-effect of other things being selected for, like reproductive success versus somatic repair. David Kipling MRC HGU Edinburgh From owner-ageing@net.bio.net Tue Mar 05 22:00:00 1996 Path: biosci!daresbury!bioftp.unibas.ch!infobiogen.fr!jussieu.fr!oleane!tank.news.pipex.net!pipex!newsfeed.internetmci.com!newsxfer2.itd.umich.edu!uunet!in2.uu.net!svc.portal.com!portal.com!cup.portal.com!Floyd_-_Meyer From: Floyd_-_Meyer@cup.portal.com Newsgroups: bionet.molbio.ageing Subject: Re: Old Age Date: 6 Mar 1996 05:20:03 -0800 Organization: The Portal System (TM) Lines: 30 Sender: pccop@unix.portal.com Message-ID: <150821@cup.portal.com> References: <199603022218.QAA09986@ns.aae.com> <698438805wnr@longevb.demon.co.uk> NNTP-Posting-Host: news1.unix.portal.com Old age might not be a disease. It might be a intake defficency. Scurvy, rickets, beri beri and palagra are intake defficencies. If nothing on earth made vitamin C we would all get scurvy and think it normal. IMHO we lived longer before the flood due to the earth's magnetic field moving from west to east about 10,000 times faster than it is now (one extra revolution every 2,000 years). Actually the speed of the magnetic field stays about the same. The earth's crust turns slower for a period of time after a meteor impact. Genesis would be the history of the Jewish People from the last extinction to the last flood. The order would be: 1. Meteor impact causes the mantle to ring like a bowl of jelly. 2. Earth's crust shifts and the gyroscopic action causes the crust to "REEL". 3. Mass extinction. 4. Sun stands still, races around sky and/or rises in the west. 5. Earth's Crust stabalizes, turns slower due to having lost energy. 6. Earth's magnetic fielf turns with the core, out-races the crust. 7. Moving magnetic field provides energy for origin of life and chirality. Also forces negative ionized water vapor high forming a band of ice crystals around the earth. Positive water vapor is forced low to form the heavy dew. 8. Plants make molecules they do not make now. People live longer. 9. Friction between the core and crust drags the crust up to speed reducing the effect of the moving field. 10. Ice crystals fall in causing the flood. 11. We do not live as long, waiting for the next meteor impact. Floyd From owner-ageing@net.bio.net Tue Mar 05 22:00:00 1996 Path: biosci!ilr.rc.ac.ru!ageing From: ageing@ilr.rc.ac.ru ("Leonid A.Gavrilov") Newsgroups: bionet.molbio.ageing Subject: Mechanisms of Life Shortening in Humans Born by Old Parents Date: 6 Mar 1996 09:08:57 -0800 Organization: A.N.Belozersky Institute Lines: 108 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Dear Colleagues, We have developed research project under the title: MECHANISMS OF LIFE SHORTENING IN HUMANS BORN BY OLD PARENTS. and we would like to discuss it with those who might be interested in it. Any comments and suggestions to the text printed below would be greatly appreciated. Thank you in advance. Dr.Leonid A.Gavrilov, Ph.D. Director, Center for Longevity Research Moscow State University Moscow, Russia ********************************************************************** MECHANISMS OF LIFE SHORTENING IN HUMANS BORN BY OLD PARENTS. The general trend in modern societies is that more people now postpone the birth of the child to older ages. People are too busy by their business career, more people are surviving now to the advanced ages and because of population aging there is a shift to higher age at reproduction. Also, progress in medicine made it technically possible to have children at very old ages. What is the risk associated with these changes in human reproductive age ? What will be the health and longevity of the children born by old parents ? These are the problems that will be studied in this research project. The unique and novel feature of the project is that it is not restricted by studies on relatively rare congenital malformations that become more often for the offspring of old parents (and that is well-known), but is mainly focused on the long-term effects of parental age on the longevity of the major part of adult people who do not have obvious congenital conditions. The purpose of this study is to find out whether the paternal and maternal age at reproduction has long-term effects on longevity of their children. Our preliminary studies have demonstrated that there is a specific life-shortening effect of paternal age at reproduction on longevity of daughters only. Since only daughters inherite paternal X chromosome, this observation indicates that critical targets (genes) affected by age-related accumulation of mutational load in paternal germ cells might be located in X chromosome. These preliminary results were presented and discussed by the authors of this project at the III European Congress of Gerontology in Amsterdam (August-September, 1995) and published in more details in Longevity Report (vol.10, No.54, pp.7-15, 1996). The purpose of this project is to develop these preliminary studies further, to reconfirm previous results and to investigate the effect of maternal age at reproduction too, with special emphasis on the mechanisms of life shortening in humans born by old parents. Specifically, we shall collect and computerize the genealogical longevity data of about 100,000 persons in addition to genealogical longevity database for 10,000 persons we already have. This significant increase in the sample size is of critical importance because this is the only way to make statistically significant conclusions taking into account great variation in life span and relatively small proportion of progeny born by old parents in human population. Life span for each particular person will be studied as a function of both maternal and paternal age at reproduction controlling for other confounding factors such as parental longevity, sex, ethnicity, social status, geographical location, etc. In order to check the hypothesis that critical targets (genes) for life shortening are located in X chromosome, the specific effect of the age of the grandfather from mother's side will be studied (since grandfather's X chromosome is inherited from mother's side only). The significance of the proposed research with regard to the understanding of the biological basis of aging is determined by the fact that this will be the first comprehensive study on the importance of age-related accumulation of the mutational load in parental germ cells for the longevity of the offspring in humans. In particular, if the mitochondrial theory of aging (hypothesis that mitochondrial DNA is a critical target in age-related oxidative damage during aging) is correct, one can expect that high maternal age at reproduction is associated with low offspring longevity (expected as a result of age-related accumulation of oxidative damage to mitochondrial DNA in maternal germ cells). Another prediction that will be tested in this study is whether maternal longevity is more important predictor for offspring longevity than paternal one (because of maternal inheritance of mitochomdrial DNA). The significance of the proposed research with regard to clinical applications is determined by the fact that the population groups at risk will be identified. For example, our preliminary studies indicate that in the case of high paternal age at reproduction the the risk group is restricted by daughters only born by fathers at age higher than 50 years. These preliminary studies should be reconfirmed on the samples of larger size and by taking into account other confounding factors. The effect of mother's reproductive age should be also studied in this research. The results of this research project will have potential commercial value for life insurance market and for improving life insurance technology, since the detailed life tables will be constructed for persons born by parents of different ages and the age-sex-specific relative risks will be calculated as a function of parental age at reproduction. ****************************THE END*************************************  From owner-ageing@net.bio.net Wed Mar 06 22:00:00 1996 Path: biosci!KB.USM.MY!ratan From: ratan@KB.USM.MY (Ratan Singh) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 6 Mar 1996 19:38:21 -0800 Organization: Universiti Sains Malaysia Lines: 14 Sender: daemon@net.bio.net Distribution: world Message-ID: References: NNTP-Posting-Host: net.bio.net I will like to live for ever to see what is in store in the future of humans. I will like to go to other planets. Those of us who do not wish immortality because they are scared of boredom are either using denial mechanism (because they know they cannot be immortal, so sweeten the situation by saying: Who wants it anyway), or are bored already. Life is too interesting to lose. There is a planet 35 light years away that has water, and its two moons have more water than it itself. Scietists have also seen the cosmic dance: Planets being born in galaxies ! Simply beautiful. If I am not I but That (pure consciousness, the basis of all, the Brahman of the Vedas), then I can never die because I was never born. Beautiful that life is elsewhere also. This gives me a feeling of immortality already and deep joy like I will survive by my progeny elsewhere ! From: Ratan Singh, address: Ratan@kb.usm.my From owner-ageing@net.bio.net Thu Mar 07 22:00:00 1996 Path: biosci!CS.Arizona.EDU!noao!ennfs.eas.asu.edu!gatech!newsxfer2.itd.umich.edu!chi-news.cic.net!mr.net!umn.edu!newsstand.tc.umn.edu!hiv.med.umn.edu!selby From: selby@hiv.med.umn.edu (Scott Selby (Med-Hem)) Newsgroups: bionet.cellbiol,bionet.molbio.ageing,bionet.molbio.methds-reagnts,bionet.molbio.proteins Subject: single-strand DNA break detection Date: 6 Mar 1996 18:17:03 GMT Organization: University of Minnesota Lines: 26 Message-ID: <4hkkqv$c97@epx.cis.umn.edu> NNTP-Posting-Host: hiv.med.umn.edu Keywords: DNA damage, p53 X-Newsreader: TIN [version 1.2 PL2] Xref: biosci bionet.cellbiol:4258 bionet.molbio.ageing:2549 bionet.molbio.methds-reagnts:41507 bionet.molbio.proteins:7275 I'm wondering if anyone could direct me toward proteins that might be involved in recognition of single-stranded DNA breaks (SSB). The cell line I'm working with has a decrease response to single-stranded DNA damage, as evidenced by Western blottig, of p53. The p53 is wild-type, and I'm curious as to whether the defect is in a regulatory region of p53 upstream somewhere, or whether the actual detection of single-stranded breaks is faulty. Does anyone have knowledge as to what proteins are specifically involved in detection SSBs? I'd love to hear any discussion about other possible causes of this muted p53 response. Thanks, in advance. ______________________________________________________________________________ || Scott A. Selby 6098)o%:::%o(860 ==== Univ. of Minnesota 098)o%:::%o(8609 | |__ Dept. of Med/Hematology 6o%:%o(86098) | |-.\ Box 480 UMHC (86098)o |__| \\ Minneapolis, MN 55455 6098)o%::%o9 || || 098)o%::::::%o9 ======__| selby@lenti.med.umn.edu 6o%::::::%o(860 ________||__ 6o%::%o(8609 /____________\ o(86098) ^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^ From owner-ageing@net.bio.net Thu Mar 07 22:00:00 1996 Path: biosci!CS.Arizona.EDU!math.arizona.edu!noao!ennfs.eas.asu.edu!gatech!newsfeed.internetmci.com!tank.news.pipex.net!pipex!dispatch.news.demon.net!demon!mail2news.demon.co.uk!longevb.demon.co.uk From: John de Rivaz Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: Fri, 08 Mar 1996 14:56:24 +0100 Organization: Myorganisation Lines: 33 Message-ID: <108224398wnr@longevb.demon.co.uk> References: Reply-To: John@longevb.demon.co.uk X-NNTP-Posting-Host: longevb.demon.co.uk X-Newsreader: Newswin Alpha 0.9.1 X-Mail2News-Path: disperse.demon.co.uk!post.demon.co.uk!longevb.demon.co.uk I hope you also read sci.cryonics In article: ratan@KB.USM.MY (Ratan Singh) writes: > > I will like to live for ever to see what is in store in the future of > humans. I will like to go to other planets. > Those of us who do not wish immortality because they are scared of > boredom are either using denial mechanism (because they know they cannot > be immortal, so sweeten the situation by saying: Who wants it anyway), or > are bored already. Life is too interesting to lose. > There is a planet 35 light years away that has water, and its two moons > have more water than it itself. Scietists have also seen the cosmic > dance: Planets being born in galaxies ! Simply beautiful. If I am not I > but That (pure consciousness, the basis of all, the Brahman of the > Vedas), then I can never die because I was never born. Beautiful that > life is elsewhere also. This gives me a feeling of immortality already > and deep joy like I will survive by my progeny elsewhere ! From: Ratan > Singh, address: Ratan@kb.usm.my > > -- Sincerely, **************************************** * Publisher of Longevity Report * John de Rivaz * Fractal Report * * details on request * **************************************** In the information age, sharing can increase world wealth enormously, because giving information does not decrease your information. http://ourworld.compuserve.com/homepages/JohndeR Fast loading, very few slow pictures From owner-ageing@net.bio.net Sun Mar 10 22:00:00 1996 Path: biosci!CS.Arizona.EDU!noao!ennfs.eas.asu.edu!gatech!newsfeed.internetmci.com!in1.uu.net!fdn.fr!jussieu.fr!citi2.fr!news From: truman@citi2.fr (J-P Truman) Newsgroups: bionet.molbio.ageing Subject: Premature Ageing Date: 11 Mar 1996 11:42:33 GMT Organization: CITI2 - Universite Rene Descartes, Paris Lines: 9 Message-ID: <4i13j9$go6@bisance.citi2.fr> NNTP-Posting-Host: rpc5.citi2.fr Mime-Version: 1.0 Content-Type: Text/Plain; charset=US-ASCII X-Newsreader: WinVN 0.99.7 I am an immunologist by profession, so I'm not an expert on ageing. However, recently I heard about children who were prematurely aged. This was on TV, so I don't have any scientific facts on this. Do any of you know more about this, and it's mechanisms and causes ? Thank you in advance. J-P. From owner-ageing@net.bio.net Sun Mar 10 22:00:00 1996 Path: biosci!agate!howland.reston.ans.net!gatech!newsfeed.internetmci.com!in2.uu.net!news1.digital.com!decwrl!lll-winken.llnl.gov!fnnews.fnal.gov!nntp-server.caltech.edu!mac1554.bio.caltech.edu!user From: grovesa@starbase1.caltech.edu (Andy Groves) Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: Mon, 11 Mar 1996 14:00:16 -0800 Organization: California Institute of Technology Lines: 40 Message-ID: References: <4i13j9$go6@bisance.citi2.fr> NNTP-Posting-Host: mac1554.bio.caltech.edu In article <4i13j9$go6@bisance.citi2.fr>, truman@citi2.fr (J-P Truman) wrote: > I am an immunologist by profession, so I'm not an expert on ageing. > However, recently I heard about children who were prematurely aged. > This was on TV, so I don't have any scientific facts on this. Do any of > you know more about this, and it's mechanisms and causes ? > > Thank you in advance. There is a condition known as Werner syndrome that causes people to age at an accelerated rate. Sydney Shall (who used to post here occasionally) has published tissue culture studies on samples from Werner syndrome patients. I reproduce below an abstract from a paper of his from 1993 in PNAS v90 pp12030-12034: "Werner syndrome is a rare, autosomal, recessive condition that is frequently studied as a model of some aspects of human aging, although the behavioral changes that are usually associated with old age are only seen very infrequently. A most striking aspect of the phenotype of Werner syndrome, presumably arising from the same gene defect, is a dramatic shortening of the replicative life-span of dermal fibroblasts in vitro. The finite replicative life-span of human cells in vitro is due to the stochastic loss of replicative ability in a continuously increasing fraction of newborn cells at every generation. Normal human fibroblasts achieve almost-equal-to 60 population doublings in culture, while Werner syndrome cells usually only achieve almost-equal-to 20 population doublings. We describe an analysis of the replicative ability of fibroblasts from Werner syndrome patients and demonstrate that the cells in these cultures usually exit, apparently irreversibly, from the cell cycle at a faster rate than do normal cells, although they mostly start off with a good replicative ability. We propose that the Werner syndrome gene is a ''counting'' gene controlling the number of times that human cells are able to divide before terminal differentiation." -- Andy Groves Division of Biology, 216-76 California Institute of Technology From owner-ageing@net.bio.net Tue Mar 12 22:00:00 1996 Path: biosci!bcm.tmc.edu!news.msfc.nasa.gov!newsfeed.internetmci.com!in2.uu.net!news.sprintlink.net!jupiter.planet.net!usenet From: ssr@planet.net@mailhost2.planet.net Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: 13 Mar 1996 11:39:50 GMT Organization: Planet Access Networks - Stanhope, NJ Lines: 18 Message-ID: <4i6c67$mg7@jupiter.planet.net> References: <4i13j9$go6@bisance.citi2.fr> Reply-To: ssr@planet.net@mailhost2.planet.net NNTP-Posting-Host: stan7.planet.net X-Newsreader: IBM NewsReader/2 v1.2 In <4i13j9$go6@bisance.citi2.fr>, truman@citi2.fr (J-P Truman) writes: >I am an immunologist by profession, so I'm not an expert on ageing. >However, recently I heard about children who were prematurely aged. >This was on TV, so I don't have any scientific facts on this. Do any of >you know more about this, and it's mechanisms and causes ? > >Thank you in advance. > >J-P. > There are distinct medical conditions notably progeria, accompanied by accelerated development of stigmata of aging. These may be reviewed on MEDLINE, in pediatric texts. BTW, do you work with macrophages? Steve From owner-ageing@net.bio.net Wed Mar 13 22:00:00 1996 Path: biosci!daresbury!bioftp.unibas.ch!infobiogen.fr!jussieu.fr!oleane!tank.news.pipex.net!pipex!swrinde!howland.reston.ans.net!usc!usc!not-for-mail From: william@neuro.usc.edu (William Sun) Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: 13 Mar 1996 16:04:42 -0800 Organization: University of Southern California, Los Angeles, CA Lines: 9 Sender: william@neuro.usc.edu Message-ID: <4i7nqq$4ve@neuro.usc.edu> References: <4i13j9$go6@bisance.citi2.fr> <4i6c67$mg7@jupiter.planet.net> NNTP-Posting-Host: neuro.usc.edu On a related topic, anyone know if there is an animal model (like mouse) of Werner's Syndrome? -- William Sun, Ph.D. Phone: (213)740-3406 University of Southern California FAX: (213)740-5687 Los Angeles, CA 90089-2520 http://rana.usc.edu:8376/~wisun/ From owner-ageing@net.bio.net Wed Mar 13 22:00:00 1996 Path: biosci!rutgers!uwm.edu!newsfeed.internetmci.com!in2.uu.net!newstf01.news.aol.com!newsbf02.news.aol.com!not-for-mail From: nspctrgdgt@aol.com (NspctrGdgt) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 14 Mar 1996 05:44:11 -0500 Organization: America Online, Inc. (1-800-827-6364) Lines: 10 Sender: root@newsbf02.news.aol.com Message-ID: <4i8t9r$b7d@newsbf02.news.aol.com> References: <108224398wnr@longevb.demon.co.uk> Reply-To: nspctrgdgt@aol.com (NspctrGdgt) NNTP-Posting-Host: newsbf02.mail.aol.com I must wholeheartedly cast my vote with those who would be immortal. At this phase of my college career my intentions are towards research in cell biology, programmed cell death, ageing, etc. I am also one of the fortunate ones that are capable of feeling the raging fire that life can be. I don't want to give up my time here...certainly I would love to see others worlds if possible, dabble in bionics a little maybe. I am of the opinion that immortality IS a possibility, in one form or another, and also that a lengthy life would not necessarily be a boring drag. Boredom is a symptom of the uninterested and dwells most deeply in those persons who merely exist but do not LIVE ! From owner-ageing@net.bio.net Wed Mar 13 22:00:00 1996 Path: biosci!rutgers!gatech!newsfeed.internetmci.com!in2.uu.net!news.icanect.net!news From: didatec@icanect.net (Victor Floresmeyer) Newsgroups: bionet.molbio.ageing Subject: Melatonin Sale Date: Thu, 14 Mar 1996 22:26:25 GMT Organization: Internet Communications of America Lines: 10 Message-ID: <31489d04.84494532@news.icanect.net> NNTP-Posting-Host: ascend04-23.icanect.net X-Newsreader: Forte Agent .99d/16.182 $6.00/ 60 capsules 3 mg. bottle Surplus for a cancell order of MelatoninI will be glad to send you as much as you want. I am a wholesaler and can get you the 60 capsules bottle of 3 mg. at $6.00 USD FOB Californa. Min. Qty 24 bottles. let me know. Victor Floresmeyer didatec@icanect.com From owner-ageing@net.bio.net Thu Mar 14 22:00:00 1996 Path: biosci!agate!howland.reston.ans.net!newsfeed.internetmci.com!in2.uu.net!news.u.washington.edu!homer25.u.washington.edu!hubio543 From: Pharmacology Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: Fri, 15 Mar 1996 10:12:14 -0800 Organization: University of Washington Lines: 27 Message-ID: References: <108224398wnr@longevb.demon.co.uk> <4i8t9r$b7d@newsbf02.news.aol.com> NNTP-Posting-Host: homer25.u.washington.edu Mime-Version: 1.0 Content-Type: TEXT/PLAIN; charset=US-ASCII NNTP-Posting-User: hubio543 In-Reply-To: <4i8t9r$b7d@newsbf02.news.aol.com> On 14 Mar 1996, NspctrGdgt wrote: > I must wholeheartedly cast my vote with those who would be immortal. At > this phase of my college career my intentions are towards research in cell > biology, programmed cell death, ageing, etc. I am also one of the > fortunate ones that are capable of feeling the raging fire that life can > be. I don't want to give up my time here...certainly I would love to see > others worlds if possible, dabble in bionics a little maybe. I am of the > opinion that immortality IS a possibility, in one form or another, and > also that a lengthy life would not necessarily be a boring drag. Boredom > is a symptom of the uninterested and dwells most deeply in those persons > who merely exist but do not LIVE ! > > Once had a professor who told me something that really struck a chord with me: "There are no uninteresting things in the world [I would say Universe], only uninterested people." Still, I am all for recycling at an appropriate time, and when it is time, the container we call a body can be recycled - and that is appropriate for the ecosystem we call Earth, for a wide variety of reasons. From owner-ageing@net.bio.net Thu Mar 14 22:00:00 1996 Path: biosci!ihnp4.ucsd.edu!munnari.OZ.AU!news.ecn.uoknor.edu!news.ysu.edu!usenet.ins.cwru.edu!gatech!newsfeed.internetmci.com!howland.reston.ans.net!psinntp!psinntp!psinntp!psinntp!usenet From: yo_doc@usa.pipeline.com(Richard A. Lockshin) Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: 15 Mar 1996 20:30:09 GMT Organization: Pipeline USA Lines: 22 Message-ID: <4ick0h$8h3@news1.h1.usa.pipeline.com> References: <4i7nqq$4ve@neuro.usc.edu> NNTP-Posting-Host: 38.8.60.2 X-PipeUser: yo_doc X-PipeHub: usa.pipeline.com X-PipeGCOS: (Richard A. Lockshin) X-Newsreader: Pipeline USA v3.4.0 There have been attempts to create mice transgenic for familial Alzheimer's, but there was a bit of trouble with the reliability of what was reported. Some biotech companies claim to have good mice but are not circulating them or the data. On Mar 13, 1996 16:04:42 in article , 'william@neuro.usc.edu (William Sun)' wrote: >On a related topic, anyone know if there is an animal model (like mouse) >of Werner's Syndrome? > > >-- >William Sun, Ph.D. Phone: (213)740-3406 >University of Southern California FAX: (213)740-5687 >Los Angeles, CA 90089-2520 http://rana.usc.edu:8376/~wisun/ > -- Richard A. Lockshin From owner-ageing@net.bio.net Sat Mar 16 22:00:00 1996 Path: biosci!bloom-beacon.mit.edu!senator-bedfellow.mit.edu!m37-312-38.MIT.EDU!owen From: owen@mit.edu (Owen Hughes) Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: 17 Mar 1996 23:06:29 GMT Organization: Massachvsetts Institvte of Technology Lines: 11 Sender: owen@m37-312-38.MIT.EDU (Owen Hughes) Message-ID: <4ii5tl$1m7@senator-bedfellow.MIT.EDU> References: <4i13j9$go6@bisance.citi2.fr> <4i6c67$mg7@jupiter.planet.net> <4i7nqq$4ve@neuro.usc.edu> NNTP-Posting-Host: m37-312-38.mit.edu Hi, In reply to William Sun's question: >On a related topic, anyone know if there is an animal model (like mouse) >of Werner's Syndrome? Check out animal models for ataxia telangiectasia. ;-) Owen From owner-ageing@net.bio.net Sun Mar 17 22:00:00 1996 Path: biosci!ihnp4.ucsd.edu!agate!howland.reston.ans.net!swrinde!newsfeed.internetmci.com!iol!tank.news.pipex.net!pipex!sunsite.doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: Source for mortality rates/life expec by occupation? Followup-To: bionet.molbio.ageing,sci.life-extension Date: 18 Mar 1996 13:31:09 GMT Organization: University of Sussex Lines: 25 Message-ID: <4ijoit$qr1@infa.central.susx.ac.uk> References: NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] Xref: biosci bionet.molbio.ageing:2565 sci.life-extension:11352 Steve Chambers (steve@chambers.ak.planet.co.nz) wrote: : Does anyone know a good source for data on mortality rates or life expectancy : by occupational group? : Thanks in advance :-) : Steve : -- : ________________________ : (I_lurk,_therefore_I_am!_\ ,,, Steve Chambers : (o o) steve@chambers.ak.planet.co.nz : -----------------------oOO--(_)--OOo------------------------------------ I suggest that you ask any big Life-Insurance Company. Clearly their actuaries must have access to such data. When you find out, will you please tell us all. Sydney Shall -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Tel:+44.273.67.83.03 FAX:+44.273.67.84.33; E-Mail:Janet:S.Shall@uk.ac.sussex Elsewhere:S.Shall@sussex.ac.uk EARN/BITNET:S.Shall%sussex@ukacrl From owner-ageing@net.bio.net Sun Mar 17 22:00:00 1996 Path: biosci!galaxy.ucr.edu!library.ucla.edu!info.ucla.edu!newsfeed.internetmci.com!solaris.cc.vt.edu!news.mathworks.com!tank.news.pipex.net!pipex!sunsite.doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: Short men have higher heart risk? Followup-To: bionet.molbio.ageing,sci.life-extension Date: 18 Mar 1996 13:29:46 GMT Organization: University of Sussex Lines: 25 Message-ID: <4ijoga$qpe@infa.central.susx.ac.uk> References: NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] Xref: biosci bionet.molbio.ageing:2566 sci.life-extension:11353 Steve Chambers (steve@chambers.ak.planet.co.nz) wrote: : This by-line headed an article in yesterday's local rag. Not much detail - : but a Donna Parker of Memorial Hospital in Rhode Island was quoted and : a German study was also mentioned in passing. : Anyone know any more detail? These results seem counter-intuitive to me : given established relationships between mortality and size, calorie : restriction and lifespan increase etc. : Steve : -- : ________________________ : (I_lurk,_therefore_I_am!_\ ,,, Steve Chambers : (o o) steve@chambers.ak.planet.co.nz : -----------------------oOO--(_)--OOo------------------------------------ I wonder whether there is data correlating adult height and life-span. If anybody knows of such data could they please give a reference. Sydney Shall -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Tel:+44.273.67.83.03 FAX:+44.273.67.84.33; E-Mail:Janet:S.Shall@uk.ac.sussex Elsewhere:S.Shall@sussex.ac.uk EARN/BITNET:S.Shall%sussex@ukacrl From owner-ageing@net.bio.net Sun Mar 17 22:00:00 1996 Path: biosci!galaxy.ucr.edu!library.ucla.edu!info.ucla.edu!agate!howland.reston.ans.net!nntp.coast.net!harbinger.cc.monash.edu.au!news.mel.connect.com.au!news.syd.connect.com.au!news.bri.connect.com.au!grissom.powerup.com.au!usenet From: rgay@powerup.com.au (vincent henry guerrini) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: Live shortening effects of sport Date: 18 Mar 1996 10:19:18 GMT Organization: Power Up Lines: 58 Message-ID: <4ijdb6$k22@grissom.powerup.com.au> References: <4fb2tm$bj9@altrade.nijmegen.inter.nl.net> <4ffmjj$mdo@epx.cis.umn.edu> Reply-To: rgay@powerup.com.au NNTP-Posting-Host: ts0310.powerup.com.au Mime-Version: 1.0 X-Newsreader: WinVN 0.93.11 Xref: biosci bionet.molbio.ageing:2563 sci.life-extension:11348 In article <4ffmjj$mdo@epx.cis.umn.edu>, selby@lenti.med.umn.edu says... > >H.O.van.den.Berg@Inter.NL.net wrote: > >[lots of false conjecture deleted] > >: So I think it's reasonable to assume that sports progresses the >: aging process. Probably even a lot of "lean muscle tissue" >: does the same (consuming more oxygen). > >: Is muscle tissue and sports activity the reason for the fact >: that women live longer ? > >: Yes, I know about the finish study of ski-sportsmen. But they were >: compared to their collegue sports, not a control group of couch >: potatoes. > >: And if we pay this price for sports, what sport would give >: the best physical results for the lowes oxygen price ? > >You have ignored numerous human studies where sedentary lifestyles >coincide with increased risk for heart disease, stroke, etc. etc. and a >study done on rowers in the late 70's that showed that these athletes >(many of whom continued their sport after college) outlived there >classmates by 10-12 years. > >This physiobabble is the same thing sighted by trash newspapers every so >often about the deleterious effects of exercise. What you fail to >recognize is that in evolutionary terms, our vigorous types are probably >very sedentary compared to the gathering/hunting lifestyle of prehistoric >peoples. > >Drawing parallels between fruit flys and human behaviour is ludicrous. >Paralysis in humans (the ultimate in non-activity) results in a decrease >in life-span of 5-20 years depending on the extend of injury. While this >is complicated by the other health issues involved in spinal cord injury, >the 200% figure you sight in fruit flies should outweigh the deleterious >effects of spinal cord injury. While my reasoning in this argument is >ridiculous, at best, it shows the danger of taking wildly disperate >species studies and drawing conclusions about supposed health benefits or >deleterious effects. > >I'll continue my fitness and diet regimes, and you just lay around the >house. I promise to come to your funeral and NOT say, "I told you so!" >This is the first time I use this system! Really interesting this >argument whether EXCESSIVE exercize shortens your life! Of course it >must because you burn more oxygen but the day to day quality of life improves due to good oxygenation and use of biohardware. Who wants to live to 100 anyway!Free radical damage is obviously responsible for long term damage. Its a bit like a fire the more fuel you pour on it the faster and BETTER it burns From owner-ageing@net.bio.net Sun Mar 17 22:00:00 1996 Path: biosci!agate!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!in2.uu.net!comp.vuw.ac.nz!waikato!kcbbs!planet!chambers!steve From: steve@chambers.ak.planet.co.nz (Steve Chambers) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Source for mortality rates/life expec by occupation? Message-ID: Date: Mon, 18 Mar 96 11:41:23 +1200 Organization: PlaNet (Auckland New Zealand) Lines: 13 Xref: biosci bionet.molbio.ageing:2562 sci.life-extension:11342 Does anyone know a good source for data on mortality rates or life expectancy by occupational group? Thanks in advance :-) Steve -- ________________________ (I_lurk,_therefore_I_am!_\ ,,, Steve Chambers (o o) steve@chambers.ak.planet.co.nz -----------------------oOO--(_)--OOo------------------------------------ From owner-ageing@net.bio.net Sun Mar 17 22:00:00 1996 Path: biosci!agate!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!in2.uu.net!comp.vuw.ac.nz!waikato!kcbbs!planet!chambers!steve From: steve@chambers.ak.planet.co.nz (Steve Chambers) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Short men have higher heart risk? Message-ID: Date: Mon, 18 Mar 96 11:38:05 +1200 Organization: PlaNet (Auckland New Zealand) Lines: 15 Xref: biosci bionet.molbio.ageing:2561 sci.life-extension:11341 This by-line headed an article in yesterday's local rag. Not much detail - but a Donna Parker of Memorial Hospital in Rhode Island was quoted and a German study was also mentioned in passing. Anyone know any more detail? These results seem counter-intuitive to me given established relationships between mortality and size, calorie restriction and lifespan increase etc. Steve -- ________________________ (I_lurk,_therefore_I_am!_\ ,,, Steve Chambers (o o) steve@chambers.ak.planet.co.nz -----------------------oOO--(_)--OOo------------------------------------ From owner-ageing@net.bio.net Sun Mar 17 22:00:00 1996 Path: biosci!agate!howland.reston.ans.net!tank.news.pipex.net!pipex!sunsite.doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: 18 Mar 1996 13:27:44 GMT Organization: University of Sussex Lines: 42 Message-ID: <4ijocg$qga@infa.central.susx.ac.uk> References: <4i7nqq$4ve@neuro.usc.edu> <4ick0h$8h3@news1.h1.usa.pipeline.com> NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] Richard A. Lockshin (yo_doc@usa.pipeline.com) wrote: : There have been attempts to create mice transgenic for familial : Alzheimer's, but there was a bit of trouble with the reliability of what : was reported. Some biotech companies claim to have good mice but are not : circulating them or the data. : : On Mar 13, 1996 16:04:42 in article , : 'william@neuro.usc.edu (William Sun)' wrote: : : : >On a related topic, anyone know if there is an animal model (like mouse) : >of Werner's Syndrome? : > : > : >-- : >William Sun, Ph.D. Phone: (213)740-3406 : >University of Southern California FAX: (213)740-5687 : >Los Angeles, CA 90089-2520 http://rana.usc.edu:8376/~wisun/ : > : -- : : Richard A. Lockshin To the best of my knowledge there is NO animal model of Werner's syndrome in Humans. Such rodents would presumably only live for about 1 year. Perhaps such variants [?mutants] would be discarded by the animal house staff. I do not know how to generate such animals. Since the gene for Werner's syndrome in humans will be cloned, the possibility will then exist to determine whether rodents have this gene, and if they do, what they would be like if this gene was mutated or deleted. If anyone knows of or has heard talk of an animal model of Werner's syndrome in humans, I would be extremely anxious and delighted to be told about it; however, tenuous the information may be. Sydney Shall -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Tel:+44.273.67.83.03 FAX:+44.273.67.84.33; E-Mail:Janet:S.Shall@uk.ac.sussex Elsewhere:S.Shall@sussex.ac.uk EARN/BITNET:S.Shall%sussex@ukacrl From owner-ageing@net.bio.net Sun Mar 17 22:00:00 1996 Path: biosci!daresbury!bioftp.unibas.ch!infobiogen.fr!jussieu.fr!oleane!tank.news.pipex.net!pipex!swrinde!sgigate.sgi.com!enews.sgi.com!decwrl!waikato!waikato.ac.nz!hawthorn From: hawthorn@waikato.ac.nz Newsgroups: bionet.molbio.ageing Subject: Re: Short men have higher heart risk? Message-ID: <1996Mar19.094124.42529@waikato.ac.nz> Date: 19 Mar 96 09:41:24 +1200 References: Organization: University of Waikato, Hamilton, New Zealand Lines: 21 In article , steve@chambers.ak.planet.co.nz (Steve Chambers) writes: > This by-line headed an article in yesterday's local rag. Not much detail - > but a Donna Parker of Memorial Hospital in Rhode Island was quoted and > a German study was also mentioned in passing. > > Anyone know any more detail? These results seem counter-intuitive to me > given established relationships between mortality and size, calorie > restriction and lifespan increase etc. Short men are usually smaller over all, which means smaller diameter blood vessels. These are more easily clogged than larger diameter ones. So it makes sense. The rate of formation of arterial plaques is going to depend on blood composition, and is probably not going to be lower for short men. Hence their arteries will clog faster Furthermore short and fat are not mutually exclusive. It is weight for size that is significant. Not weight overall. Ian H A short man, latest in a line of short men, most of whom have died from heart attacks. From owner-ageing@net.bio.net Mon Mar 18 22:00:00 1996 Path: biosci!bcm.tmc.edu!news.tamu.edu!news.utdallas.edu!news.starnet.net!wupost!waikato!celebrian.otago.ac.nz!adi005.adi.co.nz!user From: tillno@bifrost.otago.ac.nz (Till Noever) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: Tue, 19 Mar 1996 16:14:12 +1200 Organization: University of Otago Lines: 13 Message-ID: References: <108224398wnr@longevb.demon.co.uk> <4i8t9r$b7d@newsbf02.news.aol.com> NNTP-Posting-Host: adi005.adi.co.nz In article , Pharmacology wrote: > I am all for recycling at an appropriate time, and when it is > time, the container we call a body can be recycled - and that is > appropriate for the ecosystem we call Earth, for a wide variety of reasons. That may be so, but the question is: is it appropriate for the *individual*? :) -- Till (a.k.a. tillno@bifrost.otago.ac.nz or till@adi.co.nz) From owner-ageing@net.bio.net Mon Mar 18 22:00:00 1996 Path: biosci!agate!howland.reston.ans.net!newsfeed.internetmci.com!news.fibr.net!nntp.news.primenet.com!news.primenet.com!news.primenet.com!not-for-mail From: keving@primenet.com (Kevin Goldstein) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: Live shortening effects of sport Date: 19 Mar 1996 00:42:01 -0700 Organization: Primenet Services for the Internet Lines: 20 Sender: root@primenet.com Message-ID: <4ilog9$68@nnrp1.news.primenet.com> References: <4fb2tm$bj9@altrade.nijmegen.inter.nl.net> <4ffmjj$mdo@epx.cis.umn.edu> <4ijdb6$k22@grissom.powerup.com.au> X-Posted-By: kg.com X-Newsreader: Forte Free Agent 1.0.82 Xref: biosci bionet.molbio.ageing:2569 sci.life-extension:11374 rgay@powerup.com.au (vincent henry guerrini) wrote: >In article <4ffmjj$mdo@epx.cis.umn.edu>, selby@lenti.med.umn.edu says... >> >>H.O.van.den.Berg@Inter.NL.net wrote: >> >>[lots of false conjecture deleted] >> >>: So I think it's reasonable to assume that sports progresses the >>: aging process. Probably even a lot of "lean muscle tissue" >>: does the same (consuming more oxygen). >> You can assume whatever you please. Without any supporting evidence, your assumption is about as useful as any other opinion, which is to say, at best useless, at worse misleading. -Kevin From owner-ageing@net.bio.net Mon Mar 18 22:00:00 1996 Path: biosci!TENET.EDU!dashley From: dashley@TENET.EDU (Don Ashley) Newsgroups: bionet.molbio.ageing Subject: Re: Learned Helplessness About Immortality (fwd) Date: 19 Mar 1996 03:57:13 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 21 Sender: daemon@net.bio.net Distribution: world Message-ID: References: NNTP-Posting-Host: net.bio.net It gives me no sense of satisfaction or benevolence to think that my body through early death (before 100 years) will benefit society or nature by being recycled thru the ecosystem. On Tue, 19 Mar 1996, Till Noever wrote: > In article > , > Pharmacology wrote: > > I am all for recycling at an appropriate time, and when it is > > time, the container we call a body can be recycled - and that is > > appropriate for the ecosystem we call Earth, for a wide variety of reasons. > > That may be so, but the question is: is it appropriate for the *individual*? :) > > -- > > Till (a.k.a. tillno@bifrost.otago.ac.nz or till@adi.co.nz) > > > From owner-ageing@net.bio.net Mon Mar 18 22:00:00 1996 Path: biosci!VMHOST.CDP.STATE.NE.US!DPI3375 From: DPI3375@VMHOST.CDP.STATE.NE.US Newsgroups: bionet.molbio.ageing Subject: NO SUBJECT Date: 19 Mar 1996 06:55:48 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 4 Sender: daemon@net.bio.net Distribution: world Message-ID: <199603191455.GAA13314@net.bio.net> NNTP-Posting-Host: net.bio.net From: Art Machado Subject: Please unsubscribe me. Thanks. From owner-ageing@net.bio.net Mon Mar 18 22:00:00 1996 Path: biosci!ns1.faseb.org!lamarck.sura.net!newsfeed.internetmci.com!tank.news.pipex.net!pipex!dish.news.pipex.net!pipex!bbc!news From: KathyBarnby Newsgroups: bionet.molbio.ageing Subject: BBC TV Natural History of the Human Body Date: 19 Mar 1996 16:36:55 GMT Organization: BBC Lines: 29 Message-ID: <4imnr7$6ld@bbcnews.rd.bbc.co.uk> NNTP-Posting-Host: 132.185.52.216 Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 1.22 (Windows; I; 16bit) BBC Needs Help With Natural History of Human Body The BBC are making a series of programmes about the Human Body. They will illustrate what science can currently tell us about how the human body works and how it evolved. If you have research that you think would help us to visualise human biological processes in a new and enlightening way, please contact me at kathy.barnby@bbc.co.uk *+44.181.752.6210 and fax +44.181.752 6810 in London. I would love to see examples of images created by new technologies such as magnetic resonance imaging, ultrasound, computer analysis of X-ray and PET scans. Also film or video images, no matter how old, which show the processes of our bodies. We want to illustrate human life from conception, through foetal development, into babyhood, childhood, before and after puberty, the ageing process, death and beyond. Examples of the moments we might capture on film are: 1 Light microscope or electron micrograph images of the ageing process in the skin structure and cells 2 MRI or PET scans which show the effect of ageing on brain functions 3 How is it that although some people age prematurely, noone has ever not died? - is it possible to demonstrate something on film (cell division?) which would answer this question. From owner-ageing@net.bio.net Thu Mar 21 22:00:00 1996 Path: biosci!ns1.faseb.org!lamarck.sura.net!ra.nrl.navy.mil!europa.chnt.gtegsc.com!news.kreonet.re.kr!news.dacom.co.kr!vyzynz!news1.cris.com!liberator.cris.com!news From: George Kuiper Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: Short men have higher heart risk? Date: 21 Mar 1996 23:54:11 GMT Organization: Cosmic Sales & Mkt., Inc. Lines: 5 Message-ID: <4isq73$r6m@tribune.cris.com> References: NNTP-Posting-Host: cnc028044.concentric.net Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 1.2 (Windows; U; 16bit) Xref: biosci bionet.molbio.ageing:2573 sci.life-extension:11452 They also are the last to know when it's raining! -- gk From owner-ageing@net.bio.net Thu Mar 21 22:00:00 1996 Path: biosci!daresbury!bioftp.unibas.ch!infobiogen.fr!jussieu.fr!oleane!tank.news.pipex.net!pipex!newsfeed.internetmci.com!in1.uu.net!nctuccca.edu.tw!news.cc.nctu.edu.tw!thccx4!eusapia.nthu!nthuls From: mjhsieh.bbs@bbs.life.nthu.edu.tw (謝孟叡) Newsgroups: bionet.molbio.ageing Subject: Re: Short men have higher heart risk? Date: 22 Mar 1996 17:01:40 GMT Organization: 清大生科系 BBS Lines: 19 Message-ID: <3BgS4b$LiH@bbs.life.nthu.edu.tw> NNTP-Posting-Host: bbs.life.nthu.edu.tw X-Filename: ageing/M.827514085.A In article, hawthorn@waikato.ac.nz, wrote: : Short men are usually smaller over all, which means smaller diameter blood : vessels. These are more easily clogged than larger diameter ones. So it : makes sense. The rate of formation of arterial plaques is going to depend : on blood composition, and is probably not going to be lower for short men. : Hence their arteries will clog faster : Furthermore short and fat are not mutually exclusive. It is : weight for size that is significant. Not weight overall. : Ian H : A short man, latest in a line of short men, : most of whom have died from heart attacks. What is the defenition of "ShortMan"? -- Francis M. J. Hsieh, NTHU, Taiwan Republic. (謝孟叡，台灣清華大學) 生科系同學不可不玩的 BBS : bbs.life.nthu.edu.tw (140.114.98.61) -- ※ Origin: 清華大學生命科學系 ◆ From: phoenix.csie.nctu.edu.tw From owner-ageing@net.bio.net Fri Mar 22 22:00:00 1996 Path: biosci!news.Stanford.EDU!nntp-hub2.barrnet.net!news1.digital.com!decwrl!elroy.jpl.nasa.gov!swrinde!newsfeed.internetmci.com!babylon.fcl.net!usenet From: Justin Lindemann Newsgroups: bionet.molbio.ageing Subject: Alzheimers, ageing and cortical thickness? Date: 23 Mar 1996 19:44:18 GMT Organization: FCI TheNet - Global Internet Access Lines: 8 Message-ID: <4j1kai$q6u@babylon.fcl.net> NNTP-Posting-Host: 194.130.29.45 Does anyone know of any published studies investigating the relationship between cortical thickness and age in a group that includes both "normal" subjects AND those that go on to develop ALD/AD? Thanks in advance. From owner-ageing@net.bio.net Fri Mar 22 22:00:00 1996 Path: biosci!daresbury!bioftp.unibas.ch!infobiogen.fr!jussieu.fr!oleane!tank.news.pipex.net!pipex!iol!imci2!news.internetMCI.com!newsfeed.internetmci.com!in2.uu.net!news2.compulink.com!not-for-mail Newsgroups: bionet.molbio.ageing From: shiner@idirect.com (Andrew Shiner) Subject: Pictures for science fair project Content-Type: Text/Plain; charset=US-ASCII MIME-Version: 1.0 X-Newsreader: WinVN 0.99.6 Reply-To: shiner@idirect.com Followup-to: shiner@idirect.com X-Client-Port: 1077 Message-ID: X-Nntp-Posting-Host: grim.idirect.com Date: 23 Mar 96 08:34:46 GMT Sender: shiner@grim.idirect.com Lines: 12 I am doing a science fair project that involves developing sensors to studdy human movement. Often theas types of sensors are used to study how movement is afected as people age. What I am curently looking for are pictures of people that are having there movement analised. Dose any one know where I could find sutch pictures. I would aprecieat any ideas or sugestions, Sincearly, Andrew Shiner From owner-ageing@net.bio.net Fri Mar 22 22:00:00 1996 Path: biosci!rutgers!uwm.edu!vixen.cso.uiuc.edu!howland.reston.ans.net!swrinde!sgigate.sgi.com!news1.best.com!news.exodus.net!uunet!in1.uu.net!nntp.news.primenet.com!news.primenet.com!news.primenet.com!not-for-mail From: keving@primenet.com (Kevin Goldstein) Newsgroups: bionet.molbio.ageing Subject: Re: Short men have higher heart risk? Date: 22 Mar 1996 20:57:00 -0700 Organization: Primenet Services for the Internet Lines: 32 Sender: root@primenet.com Message-ID: <4ivsqc$mal@nnrp1.news.primenet.com> References: <1996Mar19.094124.42529@waikato.ac.nz> X-Posted-By: kg.com X-Newsreader: Forte Free Agent 1.0.82 hawthorn@waikato.ac.nz wrote: >In article , steve@chambers.ak.planet.co.nz (Steve Chambers) writes: >> This by-line headed an article in yesterday's local rag. Not much detail - >> but a Donna Parker of Memorial Hospital in Rhode Island was quoted and >> a German study was also mentioned in passing. >> >> Anyone know any more detail? These results seem counter-intuitive to me >> given established relationships between mortality and size, calorie >> restriction and lifespan increase etc. >Short men are usually smaller over all, which means smaller diameter blood >vessels. These are more easily clogged than larger diameter ones. So it Is this an assumption based on "common sense," or do you actually facts on vessel size versus height? -Kevin >makes sense. The rate of formation of arterial plaques is going to depend >on blood composition, and is probably not going to be lower for short men. >Hence their arteries will clog faster >Furthermore short and fat are not mutually exclusive. It is >weight for size that is significant. Not weight overall. >Ian H >A short man, latest in a line of short men, >most of whom have died from heart attacks. From owner-ageing@net.bio.net Sat Mar 23 22:00:00 1996 Path: biosci!news.Stanford.EDU!nntp-hub2.barrnet.net!sgigate.sgi.com!swrinde!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!in2.uu.net!uunet.ca!news.uunet.ca!news1.io.org!news From: factory@io.org (factory) Newsgroups: bionet.molbio.ageing Subject: Chemical Structure of Melatonine. Date: 23 Mar 1996 22:17:08 GMT Organization: Internex Online (io.org), Toronto, Ontario, Canada Lines: 15 Message-ID: <4j1t94$bim@news1.io.org> NNTP-Posting-Host: dyna-65.net7b.io.org X-Newsreader: NeoLogic News for OS/2 [version: 4.2] I'm an Graduating Student from Canada. I'm trying to do some reasearch on Melatonin. Can someone please point me to a site/book/reasource for the following information: The chemical composition? How it reacts with the body/mind? What/which glad produces it? How it is produced artificially? thanks... Lloyd Leung, factory@io.org From owner-ageing@net.bio.net Sat Mar 23 22:00:00 1996 Path: biosci!news.Stanford.EDU!nntp-hub2.barrnet.net!sgigate.sgi.com!nntp.coast.net!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!in2.uu.net!uunet.ca!news.uunet.ca!news1.io.org!news From: factory@io.org (factory) Newsgroups: bionet.molbio.ageing Subject: Chemical Structure of Melatonine. Date: 23 Mar 1996 22:17:12 GMT Organization: Internex Online (io.org), Toronto, Ontario, Canada Lines: 15 Message-ID: <4j1t98$bik@news1.io.org> NNTP-Posting-Host: dyna-65.net7b.io.org X-Newsreader: NeoLogic News for OS/2 [version: 4.2] I'm an Graduating Student from Canada. I'm trying to do some reasearch on Melatonin. Can someone please point me to a site/book/reasource for the following information: The chemical composition? How it reacts with the body/mind? What/which glad produces it? How it is produced artificially? thanks... Lloyd Leung, factory@io.org From owner-ageing@net.bio.net Sat Mar 23 22:00:00 1996 Path: biosci!rutgers!uwm.edu!newsspool.doit.wisc.edu!news.doit.wisc.edu!Gosnell Lab From: yracheta@facstaff.wisc.edu (Joseph) Newsgroups: bionet.molbio.ageing Subject: Taboo Subjects Date: 24 Mar 1996 19:55:24 GMT Organization: UW-Madison Lines: 26 Message-ID: <4j49bc$1vok@news.doit.wisc.edu> NNTP-Posting-Host: 144.92.70.91 X-Newsreader: News Xpress Version 1.0 Beta #4 I work in academia in the biological sciences. The Phd.'s I work for and even most I don't work for balk at the notion of immortality or even lengthening the life span to any great degree. They say things like, "Why, what's the point who would want to live for ever anyway." Or things like, "It isn't meant to be, it would be to egotistical and ecologically unsound". It seems that some scientists are working on the problem but never state it in their papers. They usually couch it in terms of cellular senescence, regeneration or oncology. Is it that taboo a subject. Is everyone afraid of being labeled a crackpot. Or is it that the research and the reality are so far removed from each other that we won't see any progress in this area for another 100 years. Moreover, I have not seen any discussion or consensus about the ethical or social issues that such a discovery might bring up. I personally would like to live longer than the current norm and the scientific challenge that the problem poses is very compelling, but when I think of the 'correctness' of such a breakthrough I am at a loss. Is it a selfish egotistical endeavor and would we cause global havoc, or would it really benefit mankind and remove that "the one who dies with the most toys wins" attitude. Are there any ethical treatise or government reports on these ethical potentialities. Joseph Yracheta Dept. Psychiatry University of Wisconsin yracheta@facstaff.wisc.edu From owner-ageing@net.bio.net Sat Mar 23 22:00:00 1996 Path: biosci!news.Stanford.EDU!nntp-hub2.barrnet.net!newsfeed.internetmci.com!news.ycc.yale.edu!minerva!pboduch From: Paul Boduch Newsgroups: bionet.molbio.ageing Subject: Sperms & Ageing Date: Sun, 24 Mar 1996 01:51:56 -0500 Organization: Yale University Lines: 13 Message-ID: NNTP-Posting-Host: minerva.cis.yale.edu Mime-Version: 1.0 Content-Type: TEXT/PLAIN; charset=US-ASCII X-Sender: pboduch@minerva Hey, here's an idea. Someone here once told me that there's "simply too much too replace" referring to DNA replacement in an immortality scheme that would involve replacing entire damaged DNA strands with a fresh master copy. I pointed out that bacteria and viruses replace pieces of DNA (or all of it-I don't know) in host cells routinely, but if they can't replace the entire strand, then they could probably replace parts. O.K. O.K. If that doesn't work, how about sending in modified sperms to do the job? They're perfectly suited for the job. Maybe someone could genetically engineer a phagocytic sperm, one that would devour the existing faulty DNA copy and leave a fresh one in its place? Any thoughts on this? From owner-ageing@net.bio.net Sat Mar 23 22:00:00 1996 Path: biosci!news.Stanford.EDU!nntp-hub2.barrnet.net!sgigate.sgi.com!nntp.coast.net!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!in2.uu.net!uunet.ca!news.uunet.ca!news1.io.org!news From: factory@io.org (factory) Newsgroups: bionet.molbio.ageing Subject: Chemical Structure of Melatonine. Date: 23 Mar 1996 22:17:13 GMT Organization: Internex Online (io.org), Toronto, Ontario, Canada Lines: 15 Message-ID: <4j1t99$bik@news1.io.org> NNTP-Posting-Host: dyna-65.net7b.io.org X-Newsreader: NeoLogic News for OS/2 [version: 4.2] I'm an Graduating Student from Canada. I'm trying to do some reasearch on Melatonin. Can someone please point me to a site/book/reasource for the following information: The chemical composition? How it reacts with the body/mind? What/which glad produces it? How it is produced artificially? thanks... Lloyd Leung, factory@io.org From owner-ageing@net.bio.net Sat Mar 23 22:00:00 1996 Path: biosci!news.Stanford.EDU!nntp-hub2.barrnet.net!sgigate.sgi.com!swrinde!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!in2.uu.net!uunet.ca!news.uunet.ca!news1.io.org!news From: factory@io.org (factory) Newsgroups: bionet.molbio.ageing Subject: Chemical Structure of Melatonine. Date: 23 Mar 1996 22:17:05 GMT Organization: Internex Online (io.org), Toronto, Ontario, Canada Lines: 15 Message-ID: <4j1t91$bim@news1.io.org> NNTP-Posting-Host: dyna-65.net7b.io.org X-Newsreader: NeoLogic News for OS/2 [version: 4.2] I'm an Graduating Student from Canada. I'm trying to do some reasearch on Melatonin. Can someone please point me to a site/book/reasource for the following information: The chemical composition? How it reacts with the body/mind? What/which glad produces it? How it is produced artificially? thanks... Lloyd Leung, factory@io.org From owner-ageing@net.bio.net Sat Mar 23 22:00:00 1996 Path: biosci!news.Stanford.EDU!nntp-hub2.barrnet.net!sgigate.sgi.com!nntp.coast.net!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!in2.uu.net!uunet.ca!news.uunet.ca!news1.io.org!news From: factory@io.org (factory) Newsgroups: bionet.molbio.ageing Subject: Chemical Structure of Melatonine. Date: 23 Mar 1996 22:17:11 GMT Organization: Internex Online (io.org), Toronto, Ontario, Canada Lines: 15 Message-ID: <4j1t97$bil@news1.io.org> NNTP-Posting-Host: dyna-65.net7b.io.org X-Newsreader: NeoLogic News for OS/2 [version: 4.2] I'm an Graduating Student from Canada. I'm trying to do some reasearch on Melatonin. Can someone please point me to a site/book/reasource for the following information: The chemical composition? How it reacts with the body/mind? What/which glad produces it? How it is produced artificially? thanks... Lloyd Leung, factory@io.org From owner-ageing@net.bio.net Sun Mar 24 22:00:00 1996 Path: biosci!rutgers!gatech!newsfeed.internetmci.com!in1.uu.net!hoho.quake.net!xdcrlab.com!user From: xdcrlab@quake.net (Mike Davis) Newsgroups: bionet.molbio.ageing Subject: Re: Melatonin Sale Date: Sun, 24 Mar 1996 18:14:20 -0800 Organization: XdcrLab Lines: 20 Message-ID: References: <31489d04.84494532@news.icanect.net> NNTP-Posting-Host: xdcrlab.com X-Newsreader: Value-Added NewsWatcher 2.0b24.0+ In article <31489d04.84494532@news.icanect.net>, didatec@icanect.net (Victor Floresmeyer) wrote: > $6.00/ 60 capsules 3 mg. bottle Surplus for a cancell order of > MelatoninI will be glad to send you as much as you want. I am a > wholesaler and can get you the 60 capsules bottle of 3 mg. at $6.00 > USD FOB Californa. Min. Qty 24 bottles. > > let me know. > Victor, I think I'll stick with my 120 x 3 mg tabs of Schiff for $6.99 from Costco. -- Articles: Melatonin, Folate, DHEA, etc.; Discount Sources Listing, http://www.quake.net/~xdcrlab/hp.html, the SpringBoard ULTRANET: Ultrasound Technology Graphic Hot Links http://www.quake.net/~xdcrlab/Ultrasound.html Save the BW, I report unsolicited commercial email -> Blacklist of Internet Advertisers: http://www.cco.caltech.edu/~cbrown/BL/ From owner-ageing@net.bio.net Sun Mar 24 22:00:00 1996 Newsgroups: bionet.molbio.ageing Path: biosci!mserv1.dl.ac.uk!yama.mcc.ac.uk!viking.ucsalf.ac.uk!news.salford.ac.uk!aber!bath.ac.uk!bsmail!usenet From: Harry.Witchel@bristol.ac.uk (Harry J. Witchel) Subject: Re: Chemical Structure of Melatonine. Content-Type: Text/Plain; charset=US-ASCII Message-ID: Sender: usenet@uns.bris.ac.uk (Usenet news owner) Nntp-Posting-Host: rm2.pys.bris.ac.uk Reply-To: harry.witchel@bristol.ac.uk Organization: Physiology / Med. School / Bristol X-Newsreader: WinVN 0.99.6 References: <4j1t91$bim@news1.io.org> Mime-Version: 1.0 Date: Mon, 25 Mar 1996 09:54:53 GMT Lines: 26 Lloyd -- Melatonin is made by the pineal gland. Chemically it is an indole. It seems important in the regulation of circadian rhythms, and it is produced in higher quanitity at night. A general reference would be the chapter on the endocrine system in Review of Medical Physiology by W. F. Ganong. Harry In article <4j1t91$bim@news1.io.org>, factory@io.org says... > >I'm an Graduating Student from Canada. > > I'm trying to do some reasearch on Melatonin. > > Can someone please point me to a >site/book/reasource for the following information: > > The chemical composition? > How it reacts with the body/mind? > What/which glad produces it? > How it is produced artificially? > > > thanks... Lloyd Leung, factory@io.org > From owner-ageing@net.bio.net Sun Mar 24 22:00:00 1996 Path: biosci!rutgers!gatech!usenet.eel.ufl.edu!tank.news.pipex.net!pipex!dispatch.news.demon.net!demon!mail2news.demon.co.uk!longevb.demon.co.uk From: John de Rivaz Newsgroups: bionet.molbio.ageing Subject: Re: Taboo Subjects Date: Mon, 25 Mar 1996 10:54:47 +0100 Organization: Myorganisation Lines: 79 Message-ID: <827481061wnr@longevb.demon.co.uk> References: <4j49bc$1vok@news.doit.wisc.edu> Reply-To: John@longevb.demon.co.uk X-NNTP-Posting-Host: longevb.demon.co.uk X-Newsreader: Newswin Alpha 0.9.1 X-Mail2News-Path: disperse.demon.co.uk!post.demon.co.uk!longevb.demon.co.uk You raise some interesting points. You have studied Psychiatry so maybe you can also work out some of the answers. here are some ideas to go on, in no particular order. 1. The established society is based on a birth-live-suffer-die cycle and there are many professions and organisations that would lose thier livings if this was changed. 2. Obsequience to religion or government or profession or other collective provides a comfort level that replaces being a child and having parents (at least in people who donlt think that deeply). Although there are few collectives that wage open warfare against immortalism, many people intuitively feel that they would be against it if asked. 3. The inbuilt desire to look after the next generation includes a powerful sacrifice meme that suggests one should die to make room for another. In article: <4j49bc$1vok@news.doit.wisc.edu> yracheta@facstaff.wisc.edu (Joseph) writes: > > I work in academia in the biological sciences. The Phd.'s I work for and even > most I don't work for balk at the notion of immortality or even lengthening > the life span to any great degree. They say things like, "Why, what's the > point who would want to live for ever anyway." Or things like, "It isn't meant > to be, it would be to egotistical and ecologically unsound". > > It seems that some scientists are working on the problem but never state it in > their papers. They usually couch it in terms of cellular senescence, > regeneration or oncology. Is it that taboo a subject. Is everyone afraid of > being labeled a crackpot. Or is it that the research and the reality are so > far removed from each other that we won't see any progress in this area for > another 100 years. > Moreover, I have not seen any discussion or consensus about the ethical or > social issues that such a discovery might bring up. I personally would like to > live longer than the current norm and the scientific challenge that the > problem poses is very compelling, but when I think of the 'correctness' of > such a breakthrough I am at a loss. Is it a selfish egotistical endeavor and > would we cause global havoc, or would it really benefit mankind and remove > that "the one who dies with the most toys wins" attitude. > Are there any ethical treatise or government reports on these ethical > potentialities. > > Joseph Yracheta > Dept. Psychiatry > University of Wisconsin > yracheta@facstaff.wisc.edu > > -- Sincerely, **************************************** * Publisher of Longevity Report * John de Rivaz * Fractal Report * * details on request * **************************************** In the information age, sharing can increase world wealth enormously, because giving information does not decrease your information. http://ourworld.compuserve.com/homepages/JohndeR Fast loading, very few slow pictures From owner-ageing@net.bio.net Tue Mar 26 22:00:00 1996 Path: biosci!bloom-beacon.mit.edu!gatech!newsfeed.internetmci.com!csn!news-1.csn.net!magnus.acs.ohio-state.edu!lerc.nasa.gov!purdue!haven.umd.edu!cville-srv.wam.umd.edu!theoblit From: theoblit@wam.umd.edu (Jason Taylor) Newsgroups: bionet.molbio.ageing Subject: Re: Short men have higher heart risk? Date: 27 Mar 1996 04:22:18 GMT Organization: University of Maryland College Park Lines: 54 Message-ID: <4jafpq$9aa@cville-srv.wam.umd.edu> References: <1996Mar19.094124.42529@waikato.ac.nz> NNTP-Posting-Host: rac1.wam.umd.edu X-Newsreader: TIN [version 1.2 PL0] hawthorn@waikato.ac.nz wrote: : In article , steve@chambers.ak.planet.co.nz (Steve Chambers) writes: : > This by-line headed an article in yesterday's local rag. Not much detail - : > but a Donna Parker of Memorial Hospital in Rhode Island was quoted and : > a German study was also mentioned in passing. : > : > Anyone know any more detail? These results seem counter-intuitive to me : > given established relationships between mortality and size, calorie : > restriction and lifespan increase etc. : Short men are usually smaller over all, which means smaller diameter blood : vessels. These are more easily clogged than larger diameter ones. So it Assuming this were true, wouldn't capillaries (the smallest arteries) get clogged first? Also, wouldn't rabbits be less likely than mice (rather than more) to develop cardiovascular disease? I had assumed that the correlation between shortness and heart disease was due to the differences in the kcal/kg requirements between short people and average people. Realize, there are very strong social pressures for people to eat ~1700-2700 kcal per day. Both dieters (like me) and body builders are under social pressure from the normal people they frequently eat with to eat closer to the ~2200 kcal mean. Also, numerous studies have suggested that height is largely determined by the quality and quantity of pre-pubescent protein intake. Thus, on the average, short people: (a) used to eat a relatively imbalanced diet and (b) used to eat a relatively low number of calories (assuming caloric intake is crudely correlated to protein intake). Since the basical metabolic rate is roughly constant after puberty, (b) alone implies that short people, if subjected to social norms or personal freedom not experienced as children, would overeat relative to their kcal/day set-point. In this case, their mean triglyceride levels would be higher than the mean of average height people. I had thought this to be sortta obvious really. I'd think that many short women hate to order just because they can't finish any normal meal on their plate without worrying about getting fat. It's catch-22 because they don't want to order just a salad because it would bring up the issue. I'd say that men and tall women are much less likely to feel uncomfortable about eating with others, especially in restaurants. Funny thing is, these people have probably have a much greater maximum life span parameter (see my website for def) if they practiced CR. This only makes the effect stronger, since they are less likely to die of other causes, such a lung disease. --Jason ______________________________________________________________________________ Jason Taylor, Greenbelt, MD USA|"Doctor, don't cut so deep! That's the third http://www.wam.umd.edu/~theoblit| operating table you've ruined this week!" From owner-ageing@net.bio.net Wed Mar 27 22:00:00 1996 Path: biosci!daresbury!nntp-trd.UNINETT.no!newsfeed.sunet.se!news00.sunet.se!sunic!news99.sunet.se!news.chalmers.se!mdstud.chalmers.se!md2nicke From: md2nicke@mdstud.chalmers.se (Niclas Johansson) Newsgroups: bionet.molbio.ageing Subject: How old should you be before start eating Melatonin? Date: 28 Mar 1996 14:23:55 GMT Organization: School of Mathematics and Computing Science Lines: 18 Distribution: world Message-ID: <4je7dr$cie@nyheter.chalmers.se> NNTP-Posting-Host: fraggel25.mdstud.chalmers.se Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit Well the subject says it all: How old should you be before start eating Melatonin? I am 24, is it to early??? Niclas. ~~~~~~~~~~~~~~Niclas johansson~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ http://www.mdstud.chalmers.se/~md2nicke/english.html md2nicke@mdstud.chalmers.se A mind is like a parachute. It doesn't work if it is not open. (Frank Zappa) ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ From owner-ageing@net.bio.net Thu Mar 28 22:00:00 1996 Path: biosci!rutgers!gatech!newsfeed.internetmci.com!in2.uu.net!news.us.world.net!news.aus.world.net!usenet From: GuyD@world.net (Guy Dunphy) Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: Fri, 29 Mar 1996 13:06:51 GMT Organization: AUSNet Services pty. ltd. Lines: 47 Message-ID: <4jgjp5$2u9@sydney1.world.net> References: <4i13j9$go6@bisance.citi2.fr> NNTP-Posting-Host: sydney39.world.net X-Newsreader: Forte Free Agent 1.0.82 grovesa@starbase1.caltech.edu (Andy Groves) wrote: >There is a condition known as Werner syndrome that causes people to age at >an accelerated rate. Sydney Shall (who used to post here occasionally) has >published tissue culture studies on samples from Werner syndrome patients. >I reproduce below an abstract from a paper of his from 1993 in PNAS v90 >pp12030-12034: ...snip Anyone know if more recent work has examined the condition of the telomeres in Werner syndrome patients? Might they have started out shorter than normal in the egg cell, hence the reduced number of potential cell division cycles? Isn't it amazing the number of researchers who are looking into telomeres, 'just for the cancer connection'! What a bunch of funding whimps. Go on, admit it you guys, WE ALL WANT TO BE IMMORTAL. Another thought: Given the prime ageing mechanism may be so simple, just a 'bit of string' that gets shortened till its all gone, then your genes start to fray. Also, cells have a mechanism for preventing this, but its usually switched off. Then isn't it possible that small changes in the human genome in the past could have produced significant (even major) shifts in the species' average lifespan? Perhaps a viral epidemic, or somesuch, could have produced a widespread sudden change in the population's telomere related code, and hence a lifespan change? Now, I'm normally loathe to mention the bible (not a believer, and the whole religion thing gives me the creeps) but what about the bible story that the first humans had much longer lifespans, which were reduced after the 'fall'. Could there be some very old oral legend behind this, and might it have been true? Interesting thought. Can anyone think of any fossil record data that would allow estimation of real 'age at death' of early human fossils? Not just age estimated by comparison of structure to modern humans. Bones don't have age rings like trees, do they? And carbon dating gives time from then till now, not 'lifetime' age. | Just when you are starting to figure out whats going on, you die. | Guy Dunphy Sydney, Australia. Still in my first century. | Computer programmer & hardware engineer. Eager to work in genetics field. PS If you reply to this, _please_ also email a copy to me. My server sucks. From owner-ageing@net.bio.net Thu Mar 28 22:00:00 1996 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!news1.ucsd.edu!usenet From: Oliver Bogler Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: Fri, 29 Mar 1996 11:20:28 -0700 Organization: The University of California at San Diego Lines: 35 Message-ID: <315C29EC.7220@ucsd.edu> References: <4i13j9$go6@bisance.citi2.fr> <4jgjp5$2u9@sydney1.world.net> NNTP-Posting-Host: licr-user003.ucsd.edu Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.0 (Macintosh; I; 68K) Guy Dunphy wrote: > Anyone know if more recent work has examined the condition of the telomeres > in Werner syndrome patients? > Isn't it amazing the number of researchers who are looking into telomeres, > 'just for the cancer connection'! > What a bunch of funding whimps. Go on, admit it you guys, WE ALL WANT TO BE > IMMORTAL. > Another thought: Given the prime ageing mechanism may be so simple, just a 'bit > of string' that gets shortened till its all gone, > Interesting thought. Can anyone think of any fossil record data that would > allow estimation of real 'age at death' of early human fossils? Not just age > estimated by comparison of structure to modern humans. Bones don't have age > rings like trees, do they? And carbon dating gives time from then till now, > not 'lifetime' age. This is all very interesting, but you seem to unaware that there is no evidence of a connection between telomere length/cellular ageing and organismal ageing. Organismal ageing is better discussed in terms of mortality - no one dies of "old age". There is always a "pathology", and that has nothing to do with telomere length. Of course, older people have older cells that may be less good at doing their stuff, contributing to a conditions that kills. Would you really argue that telomere lenght killed George Burns and Sergei Gringkov? Also, the fossil record would look at people with no basic health care or sanitation, that were predated actively. Hardly a fair comparison. In general, in the wild, animals never reach their maximum possible age because they get eaten first! So I guess, most scientists who work on telomeres do so to learn more about tumors, than for the sake of living forever. Also the connection between cellular ageing and telomere length is so far only correlative: no direct evidence of causation has been provided. Oliver Bogler, Ph.D. Ludwig Inst for Cancer Res., UCSD From owner-ageing@net.bio.net Fri Mar 29 22:00:00 1996 Path: biosci!NOVELL2.BHAM.AC.UK!imm3gjg7 From: imm3gjg7@NOVELL2.BHAM.AC.UK ("G.J.Griffiths") Newsgroups: bionet.molbio.ageing Subject: Telomerase Trouble Date: 30 Mar 1996 09:42:05 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 24 Sender: daemon@net.bio.net Distribution: world Message-ID: <315DE2DF.520F@novell2.bham.ac.uk> NNTP-Posting-Host: net.bio.net So if it's true that the telomere length dictates cellular ageing, then what would be the easiest way to maintain it in cells? How would it posible to upregulate telomerase expression? Three methods spring to mind. 1) Find some way of injecting 'neat' telomerase into all cells. This would pose problems as it would not be actively taken up across cellular membranes. The only way around this I can think of is to somehow link it to another component that is hydrophobic and will merge with the membranes and release telomerase into the cell. 2) Insert the DNA sequence into all the cells genomes providing it with an 'inducible?' or constitutive promoter to allow over expression. The use of retroviruses that have been made safe could be employed to carry out this task. 3) Find out how telomerase expression is controlled by the cell. Isolate its promoter that initiates its expression and study it. It may be possible to find a component that will cause its upregulation. If this component is taken up actively by cells then it would simply be a matter of injecting it to give your cells a boost. Does anyone know if any of these tasks have been attempted or if they can think of another way around the problem? Cheers Gareth From owner-ageing@net.bio.net Fri Mar 29 22:00:00 1996 Path: biosci!rutgers!gatech!newsfeed.internetmci.com!in2.uu.net!news.us.world.net!news.aus.world.net!usenet From: GuyD@world.net (Guy Dunphy) Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: Sat, 30 Mar 1996 15:09:44 GMT Organization: AUSNet Services pty. ltd. Lines: 125 Message-ID: <4jjfbj$bsp@sydney1.world.net> References: <4i13j9$go6@bisance.citi2.fr> <4jgjp5$2u9@sydney1.world.net> <315C29EC.7220@ucsd.edu> NNTP-Posting-Host: sydney27.world.net X-Newsreader: Forte Free Agent 1.0.82 Oliver Bogler wrote: >Guy Dunphy wrote: >> Anyone know if more recent work has examined the condition of the telomeres >> in Werner syndrome patients? Well? >> Isn't it amazing the number of researchers who are looking into telomeres, >> 'just for the cancer connection'! >> What a bunch of funding whimps. Go on, admit it you guys, WE ALL WANT TO BE >> IMMORTAL. >> Another thought: Given the prime ageing mechanism may be so simple, just a 'bit >> of string' that gets shortened till its all gone, >> Interesting thought. Can anyone think of any fossil record data that would >> allow estimation of real 'age at death' of early human fossils? Not just age >> estimated by comparison of structure to modern humans. Bones don't have age >> rings like trees, do they? And carbon dating gives time from then till now, >> not 'lifetime' age. >This is all very interesting, but you seem to unaware that there is no evidence of a >connection between telomere length/cellular ageing and organismal ageing. Organismal >ageing is better discussed in terms of mortality - no one dies of "old age". Oddly enough, that was what my grandfather died of. >There is always a "pathology", and that has nothing to do with telomere length. Now who' s making unproven assertions? >Of course, older >people have older cells that may be less good at doing their stuff, contributing to a >conditions that kills. Exactly. Even where infectious disease was the cause of death, perhaps an immune system with a smaller proportion of 'tellomere challenged' cells would have mounted an effective defense. So how do we ever decide whether the root cause of a particular death was short tellomeres. Can't. All we can do is see if an experimental population with 'new, improved' tellomere restoration has longer average lifetimes than a control. >Would you really argue that telomere lenght killed George Burns and >Sergei Gringkov? Sorry, I can't remember what George Burns died of (other than being very old). But probably yes. Who was Sergei Gringkov? >Also, the fossil record would look at people with no basic health care or sanitation, that >were predated actively. Hardly a fair comparison. My point was, that all other things (predation, lifestyle, etc) remaining equal, there may have been a relatively sudden change in average human lifespan. I wondered if any one could examine a human bone fossil and say: "Hey, this fellow was 200 years old when he died!" How would we tell? Are there no instances of other species, where there are two distinct strains, differing only in their average lifespans? Which strain would win out in an evolutionary contest? >In general, in the wild, animals never >reach their maximum possible age because they get eaten first! Probably true, animals always get eaten before 'maximum' age. But humans (even prehistoric ones) have social structures that tend to distort such purely ecological models. >So I guess, most scientists who work on telomeres do so to learn more about tumors, than >for the sake of living forever. Also the connection between cellular ageing and telomere >length is so far only correlative: no direct evidence of causation has been provided. And the way to prove it, is to switch on the teleomere patch-up system in a cell line, and see what happens. You know that, right? Anyone trying to do it? Then of course, if a multicellular organism was 'tellomere patched' it would have the problem that every cell that went feral would result in a full-on cancer, rather than just a bunch of cells that multipled out of control for 40 or so generations then died off. Problems, problems... But its a start. Certainly, I'm aware there is no direct proven link yet. But then, I'm not writing research papers, I'm just speculating. So I don't have to stick to discussion of proven facts. Nor am I engaged in the field, and so constrained to be careful of what I say for reasons of professional standing. I'm just a computer programmer who reads NewScientist & Sci-Amer. with interest, particularly noting the parallels between computer science and genetics. And in this case, my speculation is that as the telomeres shorten (at differing rates) in the various populations of cells in the body, and the statistical spread (of cells in each line that have exhausted their telomeres and begun to suffer loss of whatever genes were nearest the fraying ends) alters, then that seems likely to me to result in the wide range of effects that are involved in aging. After all, there are _lots_ of variables. Telomere exhaustion will doubtless occur at different rates in different:- - individuals (hence the spread of rates of aging between people) - cell lines (so different organs and metabolic systems will 'age' differently in any individual) - individual chromosomes (and hence 'hit' different genes first - so the mechanisms of failure will be many and varied.) In a given individual, with so many different modes of failure coming into play, all of them in statistical fashion among cell populations (rather than all or nothing effects), then its no wonder that aging looks like a general systemic decline in effectiveness. Then again, I'd be surprised if other age related problems (such as mechanical and structural wear and alteration) don't show up in the first experimental subjects to have their 'telomere aging' fixed. For instance, there's also the mitochondria functionality problem. But I just have a gut feeling that telomere loss is the major cause of the 'cellular death' clock. (Hope its not just wishful thinking.) Incidentally, while I'm talking to someone who no doubt knows, are there any listservers that carry more detailed information about this topic? I'd very much like to subscribe to them. Your advice would be greatly appreciated. If you do, could you please email to me, my server here in Sydney seems to miss a lot of US posts. Regards, GuyD guyd@world.net Sydney, Australia. From owner-ageing@net.bio.net Fri Mar 29 22:00:00 1996 Path: biosci!rutgers!gatech!newsfeed.internetmci.com!howland.reston.ans.net!torn!newshost.uwo.ca!usenet From: Charles Carter Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: 30 Mar 1996 05:06:04 GMT Organization: (UWO, London, Canada) Lines: 9 Message-ID: <4jiffs$3er@falcon.ccs.uwo.ca> References: <4i13j9$go6@bisance.citi2.fr> <4jgjp5$2u9@sydney1.world.net> <315C29EC.7220@ucsd.edu> NNTP-Posting-Host: ts4-2.slip.uwo.ca Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Authenticated: ccarter2@ts4-2.slip.uwo.ca X-Mailer: Mozilla 1.22 (Windows; I; 16bit) Hi Dr. Bogler, I would be interested in hearing your theories on the mechanism of aging (senescence, rather). It's refreshing to hear from someone other than a melatonin junkie. C. Carter From owner-ageing@net.bio.net Sat Mar 30 22:00:00 1996 Path: biosci!agate!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!panix!news.columbia.edu!chalfie-mac.bio.columbia.edu!user From: schwarz@cubsps.bio.columbia.edu (Erich Schwarz) Newsgroups: bionet.molbio.ageing Subject: Re: Taboo Subjects Date: Sat, 30 Mar 1996 21:12:35 -0500 Organization: Dept. of Biol. Sci., Columbia Univ. Lines: 29 Message-ID: References: <4j49bc$1vok@news.doit.wisc.edu> NNTP-Posting-Host: chalfie-mac.bio.columbia.edu X-Newsreader: Yet Another NewsWatcher 2.1.8 Joseph asked, about curing aging: > ... Is it a selfish egotistical endeavor and > would we cause global havoc ... Maybe, but what's the alternative? What are we here for, to get killed off like herd animals by stuff that we might in fact control? I think how you feel about this aspect of the problem depends a lot on deep-rooted attitudes that really aren't open to much free argument. Some people like myself will see refusal to push advances as monstrous. Others will see it the reverse way. About the one thing I can suggest is that, if aging's cured, people born 50-100 years after the cure won't see it as "unnatural": they'll look at old people today the way most of us view goiter victims 100 years ago. > ... or would it really benefit mankind and remove > that "the one who dies with the most toys wins" attitude. Probably both. Human beings have been radically innovating ever since we harnessed fire. We haven't been destroyed or turned into angels yet, and probably won't be. OTOH, few people I know really want to go back to 1496 A.D.-level technology, so I suspect that on *average* innovation is experienced as beneficial even by its avowed critics. --Erich Schwarz From owner-ageing@net.bio.net Sat Mar 30 22:00:00 1996 Path: biosci!agate!howland.reston.ans.net!news.starnet.net!waikato!kcbbs!planet!chambers!steve From: steve@chambers.ak.planet.co.nz (Steve Chambers) Newsgroups: bionet.molbio.ageing,sci.life-extension Subject: Re: Premature Ageing Message-ID: Date: Sun, 31 Mar 96 21:50:11 +1200 References: <4jjfbj$bsp@sydney1.world.net> Organization: PlaNet (Auckland New Zealand) Lines: 39 Xref: biosci bionet.molbio.ageing:2597 sci.life-extension:11627 In <4jjfbj$bsp@sydney1.world.net> GuyD@world.net (Guy Dunphy) writes: >Then again, I'd be surprised if other age related problems (such as mechanical >and structural wear and alteration) don't show up in the first experimental >subjects to have their 'telomere aging' fixed. >For instance, there's also the mitochondria functionality problem. And the AGEs + other crosslinking problems, the free radical problems, the lipofuscin and other garbage accumulation problems, the autoimmune problems, the telomere-unrelated neoplasm problems, the protracted development problems, atherosclerosis and other blood supply problems, a multitude of homeostasis and "wear & tear" related problems, slow acting pathogens, and a truckload of others. And let's not forget the progressive loss of cells that can't divide in the first place. Evolutionary theory predicts that there will be literally hundreds of processes that contribute to what we call aging - and experimental observation has done nothing but support such a prediction. No observations that I'm aware of have shown telomere shortening to be a significant factor in aging, and it's statistically unlikely that, with all these other observed and predicted "aging" processes to compete with, it ever will. >But I just have a gut feeling that telomere loss is the major cause of the >'cellular death' clock. (Hope its not just wishful thinking.) Maybe it is the major cause of cell death, but it remains to be seen just what influence controlled "immortalised" cells would have on the aging of an organism. Remember that your average 90-year-old human cell population still has plenty of doubling potential in vitro, and we have no reason to assume that it doesn't have even more in vivo (check out the effects of cortisol etc.) But you're right, it would make for an interesting experiment. Steve -- ________________________ (I_lurk,_therefore_I_am!_\ ,,, Steve Chambers (o o) steve@chambers.ak.planet.co.nz -----------------------oOO--(_)--OOo------------------------------------ From owner-ageing@net.bio.net Sat Mar 30 22:00:00 1996 Path: biosci!rutgers!gatech!newsfeed.internetmci.com!news.fibr.net!nntp.news.primenet.com!news.primenet.com!melsmi From: Melvin W. Smith Newsgroups: bionet.molbio.ageing Subject: Re: How old should you be before start eating Melatonin? Date: 31 Mar 1996 08:21:01 -0700 Organization: Primenet (602)395-1010 Lines: 24 Sender: root@primenet.com Distribution: world Message-ID: <4jm7st$poe@nnrp1.news.primenet.com> References: <4je7dr$cie@nyheter.chalmers.se> X-Posted-By: melsmi@usr3.primenet.com Niclas Johansson wrote: : Well the subject says it all: : How old should you be before start eating Melatonin? : I am 24, is it to early??? : Niclas. Niclas, Somewhere I read that no one under the age of 40 needs to have Melatonin. I'm nearly 64, and have been taking Melatonin for two months. I don't feel any younger or better than I did before, but its probably better than buying lottery tickets. (Anyway, I don't think my 6mg a day is going to hurt me - I hope) -Mel -- ------------------------------------------------------------------------------- Mel Smith (in the Valley of the Sun) Fax: (602) 832-7672 melsmi@primenet.com /__)/__) / / / / /_ /\ / /_ / / / \ / / / / /__ / \/ /___ /------------------------------------------------------------------------------- From owner-ageing@net.bio.net Sun Mar 31 23:00:00 1996 Path: biosci!rutgers!gatech!newsfeed.internetmci.com!babylon.fcl.net!usenet From: Justin Lindemann Newsgroups: bionet.molbio.ageing Subject: Re: Telomerase Trouble Date: Mon, 01 Apr 1996 19:27:17 +0000 Organization: FCI TheNet - Global Internet Access Lines: 3 Message-ID: <31602E15.287E@thenet.co.uk> References: <315DE2DF.520F@novell2.bham.ac.uk> <4jovpj$61m@mother.usf.edu> NNTP-Posting-Host: dip-28-28.thenet.co.uk Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.01 (Win95; I) I didn't see the original branch in this discussion but Greider and Blackburn have written a fine and very accessible review of the subject. ref = Scientific American, 1996, 274, 2, p. P 80. Justin Lindemann B.Sc. (Phys) From owner-ageing@net.bio.net Sun Mar 31 23:00:00 1996 Path: biosci!CS.Arizona.EDU!news.Arizona.EDU!hamblin.math.byu.edu!sol.ctr.columbia.edu!news.msfc.nasa.gov!newsfeed.internetmci.com!panix!news.columbia.edu!vanakam.cc.columbia.edu!tac2 From: tac2@vanakam.cc.columbia.edu (Todd A Carter) Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: 1 Apr 1996 14:16:16 GMT Organization: Columbia University Lines: 15 Message-ID: <4joofg$qhq@apakabar.cc.columbia.edu> References: <4i13j9$go6@bisance.citi2.fr> <4jgjp5$2u9@sydney1.world.net> <315C29EC.7220@ucsd.edu> NNTP-Posting-Host: vanakam.cc.columbia.edu In article <315C29EC.7220@ucsd.edu>, Oliver Bogler wrote: > >This is all very interesting, but you seem to unaware that there is no evidence of a >connection between telomere length/cellular ageing and organismal ageing. Organismal Except for the fact that cell cultures from Werner Syndrome patients can go throught significantly fewer passes than those taken from "normal" individuals of the same age. This is also true in "normal ageing," where a cell culture from an infant can be passed more times than one from an elderky individual. Of course, this doesn't prove anything, it's just a correlation, and no cause and effect can be defined here. --Todd Carter --Dept. Genetics --Columbia University From owner-ageing@net.bio.net Sun Mar 31 23:00:00 1996 Path: biosci!rutgers!gatech!newsfeed.internetmci.com!in2.uu.net!svc.portal.com!portal.com!cup.portal.com!Floyd_-_Meyer From: Floyd_-_Meyer@cup.portal.com Newsgroups: bionet.molbio.ageing Subject: Re: Premature Ageing Date: 31 Mar 1996 08:40:03 -0800 Organization: The Portal System (TM) Lines: 5 Sender: pccop@unix.portal.com Message-ID: <151304@cup.portal.com> References: <4i13j9$go6@bisance.citi2.fr> <4jgjp5$2u9@sydney1.world.net> NNTP-Posting-Host: news1.unix.portal.com Ageing may be a vitamin problem like scurvy,rickets and beri beri. If nothing on earth made vitamin C we would all get scurvy and think it was normal. Floyd From owner-ageing@net.bio.net Sun Mar 31 23:00:00 1996 Path: biosci!ns1.faseb.org!lamarck.sura.net!mother.usf.edu!chuma!mmunoz1 From: mmunoz1@chuma.cas.usf.edu (Mauricio Munoz (BIO)) Newsgroups: bionet.molbio.ageing Subject: Re: Telomerase Trouble Date: 1 Apr 1996 16:21:07 GMT Organization: Univ of South Florida, College of Arts and Sciences Lines: 5 Distribution: world Message-ID: <4jovpj$61m@mother.usf.edu> References: <315DE2DF.520F@novell2.bham.ac.uk> NNTP-Posting-Host: chuma.cas.usf.edu X-Newsreader: TIN [version 1.2 PL2]