From owner-ageing@net.bio.net Mon Jul 01 23:00:00 1996 Path: biosci!bcm.tmc.edu!cs.utexas.edu!swrinde!newsfeed.internetmci.com!news.uoregon.edu!vixen.cso.uiuc.edu!sdd.hp.com!svc.portal.com!portal.com!cup.portal.com!Floyd_-_Meyer From: Floyd_-_Meyer@cup.portal.com Newsgroups: bionet.molbio.ageing Subject: Re: Immortality research Date: 2 Jul 1996 11:00:05 -0700 Organization: The Portal System (TM) Lines: 52 Sender: pccop@unix.portal.com Message-ID: <152614@cup.portal.com> References: <4r5llv$aca@aladdin.rotterdam.luna.net> NNTP-Posting-Host: news1.unix.portal.com About ageing. It may be an ailment like scurvy (vitiman C deficiency), beri-beri (thiamine deficiency),rickets (vitiman D deficiency), pellagra (vitiman B niacin deficiency). The fore mentioned ailments were reolved because "Not every one had them" and we were able to find their cause. Ageing on the other hand is "universal" or so it seems. There are indications that this is not entirely so. Sharks, lobster, alligators and flounder do not age. That is the meat does not get tough. The meat is white and the creature continues to grow throughout its life. One species of flounder has the male stop growing and ages while the female keeps growing and does not age. There are some cows that will sometimes bear a calf that has white tissue in place of red. They usually die young. The old writings that tell of "Golden Ages" where people live 500 to 1,000 years and fossils that are gigantic seems to indicate longer life and continued growth. Taken all together it would seem that from time to time in the past things lived longer and continued to grow throughout their life. MY humble suggestion is that after the earth "REELS" from the crust slipping around like an orange peel, the crust turns slower than the earth for a period of time. This allows the earth's magnetic field to outrun the crust from west to east. This energy should cause the cells evolve better and cause plants to make molecules that they do not make now. These missing molecules could cause our ageing just as if we were missing vitiman C and all got scurvy. Genesis in the Bible would be the history of the Jewish People from the last Reel (extinction) to the last flood (secondary extinction). The flood would be a repeating process that was caused by the moving magnetic field forcing negative water vapor ions high to form a band of ice crystals around the earth and the positive water vapor ions low form the heavy dew wrote of in Genesis. AS the crust was slowly towed up to the speed of the earth the number of days in the year would increace as some old records indicate and the effect of the moving magnetic field would decrease untill it could not support the band of ice crystals and they fall in causing the flood. As we sit here waiting for the next meteor impact to shake the crust loose and cause the crust to reel we are degenerating. We are losing more species than we are gaining. We are living longer through the heroic efforts of the medical profession but not like if we have the missing molecules. Floyd From owner-ageing@net.bio.net Mon Jul 01 23:00:00 1996 Path: biosci!bcm.tmc.edu!cs.utexas.edu!news.sprintlink.net!news-stk-200.sprintlink.net!news.sprintlink.net!new-news.sprintlink.net!EU.net!usenet2.news.uk.psi.net!uknet!usenet1.news.uk.psi.net!uknet!uknet!newsfeed.ed.ac.uk!news From: David Kipling Newsgroups: bionet.molbio.ageing Subject: Re: Update on Negligible Senescence in Long-Lived Fishes Date: Mon, 01 Jul 1996 16:19:54 +0100 Organization: MRC Human Genetics Unit Lines: 16 Message-ID: <31D7EC9A.79BE@hgu.mrc.ac.uk> References: <199606272345.AA27564@lafn.org> <5607588wnr@longevb.demon.co.uk> 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) John de Rivaz wrote: > > I wonder whether life is a complex system of many variable, each one of > which has an undesireable side effect. These can keep the "pin on its > point" only for so long before it falls over. If you can find an > immortal fish, then this theory must be disproved, at least as far as > fishes go. If you define immortality as no age-related increase in mortality rates I gather there are a number of species (e.g. lobsters) which behave in such a fashion. OK, there are no million-year old lobsters, but that's because they suffer accidents, disease and get caught by New England fishermen... :-) But is "no ageing" [which is no increase in mortality rates] the same as "immortality"? Oh dear, I'm confused now. David Kipling Edinburgh From owner-ageing@net.bio.net Tue Jul 02 23:00:00 1996 Path: biosci!agate!spool.mu.edu!uwm.edu!cs.utexas.edu!swrinde!newsfeed.internetmci.com!in2.uu.net!psinntp!psinntp!psinntp!usenet From: yo_doc@usa.pipeline.com(Richard A. Lockshin) Newsgroups: bionet.cellbiol,bionet.immunology,bionet.neuroscience,bionet.molbio.ageing,bionet.drosophila,bionet.general Subject: NYC area cell death club meeting Date: 3 Jul 1996 11:18:42 GMT Organization: Pipeline USA Lines: 35 Message-ID: <4rdkui$qrn@news1.t1.usa.pipeline.com> NNTP-Posting-Host: 38.8.149.7 X-PipeUser: yo_doc X-PipeHub: usa.pipeline.com X-PipeGCOS: (Richard A. Lockshin) X-Newsreader: Pipeline v3.5.0 Xref: biosci bionet.cellbiol:5036 bionet.immunology:9250 bionet.neuroscience:14766 bionet.molbio.ageing:2784 bionet.drosophila:2231 bionet.general:22612 NYC Area Cell Death Club Next meeting: Wednesday, July 17, 1996 6:00-6:30 PM Pizza 6:30-8:00 PM Talks and discussion Rockefeller University, 1230 York Ave., Weiss Research Bldg Room 301 Free Parking after 5PM at 66th St. & York Ave (Please carpool as parking space is limited) Speakers: JULY 17 1. Keith Elkon, Cornell University/N Y Hospital Effects of Fas mutation in immune cell subsets 2. Emanuela Grassili, Univ. Modena, Italy Cell death and the cell cycle To help plan for pizza call lab of Dr. Zahra Zakeri, 718: 997-3429 and let them know the number coming for pizza, talk, and if you need parking. Please RSVP by Tues, July 17, 1996. Otherwise email to me. Organizers: Zahra Zakeri, Fax 718: 997-3445 Phone 718: 997-3417 Raymond Birge: Fax 212 327-7943; Phone 212: 327-7412 Sponsored by: Oncor Appligene and the journal Cell Death and Differentiation We are planning eventually to drop this general world announcement. If you wish to continue receiving these messages, please send an email reply, including your phone & fax numbers and full address as well, along with your research interest. Richard A. Lockshin [also lockshin@sjumusic.stjohns.edu] -- Richard A. Lockshin From owner-ageing@net.bio.net Sat Jul 06 23:00:00 1996 Path: biosci!agate!newsgate.duke.edu!solaris.cc.vt.edu!homer.alpha.net!uwm.edu!news.cse.psu.edu!news.ecn.bgu.edu!vixen.cso.uiuc.edu!cdc2.cdc.net!news.texas.net!nntp.primenet.com!news.primenet.com!news.primenet.com!not-for-mail From: keving@primenet.com (Kevin Goldstein) Newsgroups: bionet.molbio.ageing Subject: Re: Immortality research Date: 7 Jul 1996 11:58:03 -0700 Organization: Primenet Services for the Internet Lines: 12 Message-ID: <4rp1br$rok@nnrp1.news.primenet.com> References: <4r5llv$aca@aladdin.rotterdam.luna.net> <152614@cup.portal.com> X-Posted-By: kg.com X-Newsreader: Forte Free Agent 1.0.82 Floyd_-_Meyer@cup.portal.com wrote: * snip * > The old writings that tell of "Golden Ages" where people live 500 to >1,000 years and fossils that are gigantic seems to indicate longer life and >continued growth. And exactly what writings would that be? -Kevin * snip * From owner-ageing@net.bio.net Sat Jul 06 23:00:00 1996 Path: biosci!ACPUB.DUKE.EDU!smyth From: smyth@ACPUB.DUKE.EDU (Smyth) Newsgroups: bionet.molbio.ageing Subject: Postdoctoral Position Available Date: 7 Jul 1996 14:15:48 -0700 Organization: Duke Lines: 11 Sender: daemon@net.bio.net Distribution: world Message-ID: <31E028F6.62C1@acpub.duke.edu> NNTP-Posting-Host: net.bio.net Postdoctoral position available in laboratory studying signaling pathways involved in the regulation of apoptosis and cell senescence. Appplicants must have experience in molecular and cell biology, and tissue culture. Applicant must be US citizen or permanent resident alien. Send CV and names of three referees to: Dr. M. J. Smyth, Dept. of Medicine, Duke University Medical Center/Durham VA Medical Center, 182 GRECC, 508 Fulton St. Durham, NC 27705-3875 e-mail: smyth @acpub.duke.edu From owner-ageing@net.bio.net Mon Jul 08 23:00:00 1996 Path: biosci!ihnp4.ucsd.edu!munnari.OZ.AU!news.uwa.edu.au!newsman.murdoch.edu.au!vetmac3.murdoch.edu.au!user From: cummins@central.murdoch.edu.au (Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Aging Brown Norway Rat colony Date: Tue, 09 Jul 1996 11:20:04 +0800 Organization: Murdoch University Lines: 5 Message-ID: NNTP-Posting-Host: vetmac3.murdoch.edu.au I've been told that NIH or NICHD maintain an ageing Brown Norway rat colony. Where can I find out more information? -- URL http://numbat.murdoch.edu.au/spermatology/spermhp.html From owner-ageing@net.bio.net Tue Jul 09 23:00:00 1996 Path: biosci!UNIXG.UBC.CA!browley From: browley@UNIXG.UBC.CA (Brian Rowley) Newsgroups: bionet.molbio.ageing Subject: Re: Free radicals and aging Date: 10 Jul 1996 14:36:59 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 137 Sender: daemon@net.bio.net Distribution: world Message-ID: References: <960710151838_573807786@emout13.mail.aol.com> NNTP-Posting-Host: net.bio.net According to Richard Cutler, antioxidant supplementation can suppress production of endogenous antioxidant enzymes like SOD, etc. Darned homeostatic response. The ideal is to find antioxidants that increase the body's NET mop-up of extraneous free radicals; i.e., ones that mop up deleterious free radicals better than they suppress endogenous free radicals. I've heard that different antioxidants act in different compartments (glutatione in water soluble environments, vitamin E in fat soluble environments). If a particular antioxidant is limited to certain compartments of the body but not others, the obvious suggestion is to use a combination of antioxidants. However, evident is required before this can be justified. A good experiment would be to do an experiment with different groups of mice: group 1 is given placebo, group 2 is given antioxidant A, group 3 is given antioxidant B and group 4 is given antioxidant A and antioxidant B. It would be interesting if there was synergy among different antioxidants with regards to longevity benefits. The other thing to think about is that rodents have a greatly inferior antioxidant system to humans. Our blood is almost saturated with uric acid (sometimes it crystalizes in the joints to cause gout). We also do not produce our own vitamin C, unlike most rodents. It turns out that uric acid is a greatly superior antioxidant to vitamin C, or so I've heard. Vitamin C, in really high doses, actually increases free radicals, so I have also heard. So we humans perhaps traded vitamin C for uric acid somewhere along the way for that particular antioxidant niche, giving us greater longevity. And humans produce more SOD per gram of tissue when corrected for metabolic rate. What I'm trying to say is that just because antioxidants increase life expectancy of rodents by 30% does not necessarily imply that they will do the same for people. We have such a good system already, there is less to improve on. Something to consider anyway :-> On 10 Jul 1996 EdKrug@aol.com wrote: > Hello David Cassarino > In answer to your question, presented below, threre are three points I > want to bring up for consideration. > 1. Free radical scavangers may reduce but they do not eliminate totally > free radicals residing outside of tightly coupled reactions. In a lab here > at the Univ. of Colorado Health Sciences Center has been measuring in vitro > free radical damage as evidenced in the accumulation of lipofuscin-like > material. He has been able to reduce the rate of accumulation by no more > than about 30% with all the interventions permitted in vitro. Applying this > concept to the whole organism it becomes relavant to ask "What percentage of > the free radical damage is prevented by antioxidants?" > > 2. Point one above is too simplistic in that even single cell organisms > consist of many compartments from which free radicals can be generated and in > which damage can accumulate. Additionally, the different free radical > scavangers do not necessarly distribute uniformly throughout the whole > organism. The cataloging of all the sources of free radicals and there > relative contribution to the total burden needs to be achieved, first in the > steady state and then the acute conditions with elevated free radical > generation, such as exhaustive exercise. As an aside, would the levels of > antioxidants adequate in steady state life still be adequate in conditions of > elevated free radical generation? I am afraid that there is much yet to be > done before we even know if the whole question has been asked, let alone > answered. > > 3. Free radicals are undoubtedly important but, in the evolution of > increasingly complex organisms the systems which limited life span in one > system may not have been abandoned or resolved as that organism evolved into > a different species. Since Nature is the ultimate concervative it is > probable that some of the limitations of life span in earlier species are > still active in later ones. Add to that the new threats to life span faced > by the later species and you have a many layer problem. Consequently the I > suggest that we are not looking at an "either/or" situation but an "and" > situation. We have: > -accumulation of free radical damage > -loss of cell numbers due to reaching their Hayflick number or > teleomere depletion > -accumulation of simple wear and tear with "not just like new" type > repair > -completion of the growth clock with a subsequent decline in growth > hormones and thymus activity > -completion of the reproductive clock with concomitant loss of > reproductive hormones > -steady and episotic accumulation of nonenzymatic glycosylation of > multiple targets > -gross abuse of the organism with poor choices in present time such as > excesses in food, alcohol, fat, smoking and more > -irreversable "hits" taken from just living, such as intake of heavy > metals, chlorinated organic compounds, uv irridation and probably more. > > That is to say that achieving a fruit fly with ten times normal life > span should provide information useful for humans, humans have additional > life span limiting circumstances not faced by the fruit fly. > > All that said, I contend that the fact that antioxidants can extend mean > life span indicates that they are part of picture. As the free radical > component of senesence gets resolved the mist will lift and the remaining > factors will be seen more clearly. I anticipate that this process will have > to be repeated a number of times. > > I hope this helps. > > "The Devil (or GOD) is in the details" > "Life is what happens while we are getting ready" > > Edward C. Krug, Ph.D. > Dept. of Infectious Diseases > Univ. of Colorado Health Sciences Center > Denver, Colorado > > > ""I have been reading a bit on the putative role of free radicals > in aging, and I'm wondering what others think about the > proposal that free radicals and oxidative damage are a > significant cause of aging?"" > > ""Although it is clear that these factors are involved in such > pathologies as ischemic heart injury, autoimmune diseases, and > neurodegenerative diseases, it is not certain if they just > contribute to aging or are actually causative."" > > ""I think it's very interesting that in calorie-restricted > animals, the levels of free radical scavenging enzymes like SOD > and GPX are elevated, and that mice clones overexpressing SOD > have prolonged life spans. The theory is that these enzymes, > and others like GSH-RD and catalase are protecting the organism > from oxidative damage to DNA, prots, lipids, etc., which > normally => aging and cell death. > Arguing against the free radicals/aging theory are experiments > showing only an increased mean but not MAXIMUM life span in > animals fed antioxidants like Vits A, C, E, Se, etc."" > > ""I would really be interested in hearing others' opinions on > this topic."" > > ""David S. Cassarino "The mind is not a vessel to be filled > MSTP, Neuroscience 2nd Year but a fire to be kindled." > > UVA School of Medicine -Plutarch > dsc9w@virginia.edu "" > > > From owner-ageing@net.bio.net Tue Jul 09 23:00:00 1996 Path: biosci!aol.com!EdKrug From: EdKrug@aol.com Newsgroups: bionet.molbio.ageing Subject: Re: Free radicals and aging Date: 10 Jul 1996 12:19:25 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 101 Sender: daemon@net.bio.net Distribution: world Message-ID: <960710151838_573807786@emout13.mail.aol.com> NNTP-Posting-Host: net.bio.net Hello David Cassarino In answer to your question, presented below, threre are three points I want to bring up for consideration. 1. Free radical scavangers may reduce but they do not eliminate totally free radicals residing outside of tightly coupled reactions. In a lab here at the Univ. of Colorado Health Sciences Center has been measuring in vitro free radical damage as evidenced in the accumulation of lipofuscin-like material. He has been able to reduce the rate of accumulation by no more than about 30% with all the interventions permitted in vitro. Applying this concept to the whole organism it becomes relavant to ask "What percentage of the free radical damage is prevented by antioxidants?" 2. Point one above is too simplistic in that even single cell organisms consist of many compartments from which free radicals can be generated and in which damage can accumulate. Additionally, the different free radical scavangers do not necessarly distribute uniformly throughout the whole organism. The cataloging of all the sources of free radicals and there relative contribution to the total burden needs to be achieved, first in the steady state and then the acute conditions with elevated free radical generation, such as exhaustive exercise. As an aside, would the levels of antioxidants adequate in steady state life still be adequate in conditions of elevated free radical generation? I am afraid that there is much yet to be done before we even know if the whole question has been asked, let alone answered. 3. Free radicals are undoubtedly important but, in the evolution of increasingly complex organisms the systems which limited life span in one system may not have been abandoned or resolved as that organism evolved into a different species. Since Nature is the ultimate concervative it is probable that some of the limitations of life span in earlier species are still active in later ones. Add to that the new threats to life span faced by the later species and you have a many layer problem. Consequently the I suggest that we are not looking at an "either/or" situation but an "and" situation. We have: -accumulation of free radical damage -loss of cell numbers due to reaching their Hayflick number or teleomere depletion -accumulation of simple wear and tear with "not just like new" type repair -completion of the growth clock with a subsequent decline in growth hormones and thymus activity -completion of the reproductive clock with concomitant loss of reproductive hormones -steady and episotic accumulation of nonenzymatic glycosylation of multiple targets -gross abuse of the organism with poor choices in present time such as excesses in food, alcohol, fat, smoking and more -irreversable "hits" taken from just living, such as intake of heavy metals, chlorinated organic compounds, uv irridation and probably more. That is to say that achieving a fruit fly with ten times normal life span should provide information useful for humans, humans have additional life span limiting circumstances not faced by the fruit fly. All that said, I contend that the fact that antioxidants can extend mean life span indicates that they are part of picture. As the free radical component of senesence gets resolved the mist will lift and the remaining factors will be seen more clearly. I anticipate that this process will have to be repeated a number of times. I hope this helps. "The Devil (or GOD) is in the details" "Life is what happens while we are getting ready" Edward C. Krug, Ph.D. Dept. of Infectious Diseases Univ. of Colorado Health Sciences Center Denver, Colorado ""I have been reading a bit on the putative role of free radicals in aging, and I'm wondering what others think about the proposal that free radicals and oxidative damage are a significant cause of aging?"" ""Although it is clear that these factors are involved in such pathologies as ischemic heart injury, autoimmune diseases, and neurodegenerative diseases, it is not certain if they just contribute to aging or are actually causative."" ""I think it's very interesting that in calorie-restricted animals, the levels of free radical scavenging enzymes like SOD and GPX are elevated, and that mice clones overexpressing SOD have prolonged life spans. The theory is that these enzymes, and others like GSH-RD and catalase are protecting the organism from oxidative damage to DNA, prots, lipids, etc., which normally => aging and cell death. Arguing against the free radicals/aging theory are experiments showing only an increased mean but not MAXIMUM life span in animals fed antioxidants like Vits A, C, E, Se, etc."" ""I would really be interested in hearing others' opinions on this topic."" ""David S. Cassarino "The mind is not a vessel to be filled MSTP, Neuroscience 2nd Year but a fire to be kindled." UVA School of Medicine -Plutarch dsc9w@virginia.edu "" From owner-ageing@net.bio.net Tue Jul 09 23:00:00 1996 Newsgroups: bionet.molbio.ageing Path: biosci!bcm.tmc.edu!cs.utexas.edu!chi-news.cic.net!newsfeeder.sdsu.edu!newspump.sol.net!homer.alpha.net!uwm.edu!newsfeed.internetmci.com!news.fibr.net!nntp.primenet.com!uunet!inXS.uu.net!hearst.acc.Virginia.EDU!murdoch!avery.med.Virginia.EDU!dsc9w From: dsc9w@avery.med.Virginia.EDU (David Cassarino) Subject: Free radicals and aging X-Nntp-Posting-Host: avery.med.virginia.edu Message-ID: Sender: usenet@murdoch.acc.Virginia.EDU Organization: uva Date: Wed, 10 Jul 1996 16:14:23 GMT Lines: 44 I've noticed that this newsgroup seems rather random and have seen very few good discussions on the molecular causes of aging. I would like to start a discussion on the role of free radicals in aging. I have been reading a bit on the putative role of free radicals in aging, and I'm wondering what others think about the proposal that free radicals and oxidative damage are a significant cause of aging? Although it is clear that these factors are involved in such pathologies as ischemic heart injury, autoimmune diseases, and neurodegenerative diseases, it is not certain if they just contribute to aging or are actually causative. I think it's very interesting that in calorie-restricted animals, the levels of free radical scavenging enzymes like SOD and GPX are elevated, and that mice clones overexpressing SOD have prolonged life spans. The theory is that these enzymes, and others like GSH-RD and catalase are protecting the organism from oxidative damage to DNA, prots, lipids, etc., which normally => aging and cell death. Arguing against the free radicals/aging theory are experiments showing only an increased mean but not MAXIMUM life span in animals fed antioxidants like Vits A, C, E, Se, etc. I would really be interested in hearing others' opinions on this topic. -- David S. Cassarino "The mind is not a vessel to be filled MSTP, Neuroscience 2nd Year but a fire to be kindled." UVA School of Medicine -Plutarch dsc9w@virginia.edu From owner-ageing@net.bio.net Tue Jul 09 23:00:00 1996 Path: biosci!UNIXG.UBC.CA!browley From: browley@UNIXG.UBC.CA (Brian Rowley) Newsgroups: bionet.molbio.ageing Subject: Free radicals and Aging (antioxidants) Date: 10 Jul 1996 14:59:48 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 143 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net According to Richard Cutler, antioxidant supplementation can suppress production of endogenous antioxidant enzymes like SOD, etc. Darned homeostatic response. The ideal is to find antioxidants that increase the body's NET mop-up of extraneous free radicals; i.e., ones that mop up deleterious free radicals better than they suppress endogenous free radicals. I've heard that different antioxidants act in different compartments (glutatione in water soluble environments, vitamin E in fat soluble environments). If a particular antioxidant is limited to certain compartments of the body but not others, the obvious suggestion is to use a combination of antioxidants. However, evident is required before this can be justified. A good experiment would be to do an experiment with different groups of mice: group 1 is given placebo, group 2 is given antioxidant A, group 3 is given antioxidant B and group 4 is given antioxidant A and antioxidant B. It would be interesting if there was synergy among different antioxidants with regards to longevity benefits. The other thing to think about is that rodents have a greatly inferior antioxidant system to humans. Our blood is almost saturated with uric acid (sometimes it crystalizes in the joints to cause gout). We also do not produce our own vitamin C, unlike most rodents. It turns out that uric acid is a greatly superior antioxidant to vitamin C, or so I've heard. Vitamin C, in really high doses, actually increases free radicals, so I have also heard. So we humans perhaps traded vitamin C for uric acid somewhere along the way for that particular antioxidant niche, giving us greater longevity. And humans produce more SOD per gram of tissue when corrected for metabolic rate. What I'm trying to say is that just because antioxidants increase life expectancy of rodents by 30% does not necessarily imply that they will do the same for people. We have such a good system already, there is less to improve on. Something to consider anyway :-> On 10 Jul 1996 EdKrug@aol.com wrote: > Hello David Cassarino > In answer to your question, presented below, threre are three points I > want to bring up for consideration. > 1. Free radical scavangers may reduce but they do not eliminate totally > free radicals residing outside of tightly coupled reactions. In a lab here > at the Univ. of Colorado Health Sciences Center has been measuring in vitro > free radical damage as evidenced in the accumulation of lipofuscin-like > material. He has been able to reduce the rate of accumulation by no more > than about 30% with all the interventions permitted in vitro. Applying this > concept to the whole organism it becomes relavant to ask "What percentage of > the free radical damage is prevented by antioxidants?" > > 2. Point one above is too simplistic in that even single cell organisms > consist of many compartments from which free radicals can be generated and in > which damage can accumulate. Additionally, the different free radical > scavangers do not necessarly distribute uniformly throughout the whole > organism. The cataloging of all the sources of free radicals and there > relative contribution to the total burden needs to be achieved, first in the > steady state and then the acute conditions with elevated free radical > generation, such as exhaustive exercise. As an aside, would the levels of > antioxidants adequate in steady state life still be adequate in conditions of > elevated free radical generation? I am afraid that there is much yet to be > done before we even know if the whole question has been asked, let alone > answered. > > 3. Free radicals are undoubtedly important but, in the evolution of > increasingly complex organisms the systems which limited life span in one > system may not have been abandoned or resolved as that organism evolved into > a different species. Since Nature is the ultimate concervative it is > probable that some of the limitations of life span in earlier species are > still active in later ones. Add to that the new threats to life span faced > by the later species and you have a many layer problem. Consequently the I > suggest that we are not looking at an "either/or" situation but an "and" > situation. We have: > -accumulation of free radical damage > -loss of cell numbers due to reaching their Hayflick number or > teleomere depletion > -accumulation of simple wear and tear with "not just like new" type > repair > -completion of the growth clock with a subsequent decline in growth > hormones and thymus activity > -completion of the reproductive clock with concomitant loss of > reproductive hormones > -steady and episotic accumulation of nonenzymatic glycosylation of > multiple targets > -gross abuse of the organism with poor choices in present time such as > excesses in food, alcohol, fat, smoking and more > -irreversable "hits" taken from just living, such as intake of heavy > metals, chlorinated organic compounds, uv irridation and probably more. > > That is to say that achieving a fruit fly with ten times normal life > span should provide information useful for humans, humans have additional > life span limiting circumstances not faced by the fruit fly. > > All that said, I contend that the fact that antioxidants can extend mean > life span indicates that they are part of picture. As the free radical > component of senesence gets resolved the mist will lift and the remaining > factors will be seen more clearly. I anticipate that this process will have > to be repeated a number of times. > > I hope this helps. > > "The Devil (or GOD) is in the details" > "Life is what happens while we are getting ready" > > Edward C. Krug, Ph.D. > Dept. of Infectious Diseases > Univ. of Colorado Health Sciences Center > Denver, Colorado > > > ""I have been reading a bit on the putative role of free radicals > in aging, and I'm wondering what others think about the > proposal that free radicals and oxidative damage are a > significant cause of aging?"" > > ""Although it is clear that these factors are involved in such > pathologies as ischemic heart injury, autoimmune diseases, and > neurodegenerative diseases, it is not certain if they just > contribute to aging or are actually causative."" > > ""I think it's very interesting that in calorie-restricted > animals, the levels of free radical scavenging enzymes like SOD > and GPX are elevated, and that mice clones overexpressing SOD > have prolonged life spans. The theory is that these enzymes, > and others like GSH-RD and catalase are protecting the organism > from oxidative damage to DNA, prots, lipids, etc., which > normally => aging and cell death. > Arguing against the free radicals/aging theory are experiments > showing only an increased mean but not MAXIMUM life span in > animals fed antioxidants like Vits A, C, E, Se, etc."" > > ""I would really be interested in hearing others' opinions on > this topic."" > > ""David S. Cassarino "The mind is not a vessel to be filled > MSTP, Neuroscience 2nd Year but a fire to be kindled." > > UVA School of Medicine -Plutarch > dsc9w@virginia.edu "" > > > From owner-ageing@net.bio.net Wed Jul 10 23:00:00 1996 Path: biosci!bcm.tmc.edu!cs.utexas.edu!swrinde!newsfeed.internetmci.com!news.sprintlink.net!news-stk-200.sprintlink.net!coopnews.coop.net!boulder.earthnet.net!usenet From: "Phillip E. Schwartz" Newsgroups: bionet.molbio.ageing Subject: New FDA Regs Date: Thu, 11 Jul 1996 12:44:16 -0700 Organization: Affinity BioReagents, Inc. Lines: 42 Message-ID: <31E55990.380F@bioreagents.com> NNTP-Posting-Host: slip12.earthnet.net Mime-Version: 1.0 Content-Type: text/plain; charset=iso-8859-1 Content-Transfer-Encoding: 8bit X-Mailer: Mozilla 2.0 (Win16; I) Please help! Will the individual at your organization who is in charge of regulatory affairs or who is concerned about the negative effects new FDA regulations may have on basic scientific and medical research in addition to health care in general please contact me regarding this matter. I am trying to get as many people to comment on and become involved in a grass-roots effort to keep the FDA from including all antibody research reagents as ‘in vitro diagnostic devices’. Granted, some are but most are not. Please review the information at: http:/www.earthnet.net/~affinity/fda/ It would be optimal if this website could be hotlinked to yours to gain the maximum amount of exposure prior to August 30, 1996 public comment deadline. I would appreciate any comments, questions, referred contacts, etc. that may be useful in changing the language of this pending FDA regulation. FDA Regulation: The Immunohistochemistry Reagents and Kits Regulation: 21/CFR 864 Docket Number: 94P-0342 Sincerely, Phillip E. Schwartz Antibody Partnership Project Manager Affinity BioReagents, Inc. 14818 W. 6th Ave., Suite 13A Golden, CO 80401 TEL: 800-527-4535 FAX: 303-278-2424 email: schwartz@bioreagents.com website: http://www.bioreagents.com/affinity From owner-ageing@net.bio.net Wed Jul 10 23:00:00 1996 Path: biosci!daresbury!not-for-mail From: samuelc@max.roehampton.ac.uk (Samuel Cronin) Newsgroups: bionet.molbio.ageing Subject: Living longer - Living better Date: 11 Jul 1996 14:08:49 +0100 Lines: 197 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <4s2ud1$hok@mserv1.dl.ac.uk> Fcc: outgoing Security: None Original-To: ageing@dl.ac.uk Type: External Classification: Certified Having just returned from the three day 'Living Longer - Living Better' conference in Manchester this last week I thought some of the members of this group may be interested in the highlights. Admittedly, the short review below hardly gives a feel for all of what was discussed at the conference as I have purposefully biased my choice of speakers to those I am personally interested in and who I think will be of most interest to the readers of this group. The conference itself was very well attended by over 200 delegates with 124 poster presentations and 85 speakers whose talks were divided into parallel symposiums of either biological, clinical or social gerontology. The first two speaker summaries I have prepared are primarily concerned with the 'glycation theory of ageing' and possible interventions whereas the last two consider the antiageing effects of the only 'proven' method of extending lifespan - dietary restriction. I would also have liked to included a summary of the several discussions that took place concerning Werner's Syndrome and related topics such as the telomere hypothesis but I know there are far better qualified researchers in these areas than me on this list who were also at the conference, such as Richard Faragher and David Kipling, who may perhaps wish to comment. Antony Cerami - Sugar-derived advanced glycation end products (AGEs) in circulation and tissues promote the adverse sequelae of ageing. ====================================================================== Antony Cerami began by summarising the historical evidence for the accumulation of advanced glycation end products (AGEs) derived from the reaction of reducing sugars such as glucose with proteins, lipids or nucleic acids (the glycation theory of ageing). He also provided some evidence for the role of AGEs in disease, including experiments where AGE peptides injected into rodents or rabbits caused many of the complications of diabetes (accelerated atherosclerosis etc.) as well as the generation of B-amyloid plaques in the brain. Antony explained that although the structure of several AGEs have been proposed there was no agreement which ones were most important in the adverse effects of ageing. Nevertheless, he proposed that a new AGE molecule called an ene-dione discovered in his lab had the potential to be the most common AGE produced in ageing, and hence perhaps the most important. Prevention of AGE formation in rat models has long been achieved by the use of aminoguanidine, however, Antony's group had discovered that the B vitamin thymine can react with the specific AGE protein- crosslink associated with the ene-dione structure and actually separate the proteins, essentially reversing cross-linkage. Tests showed that thymine uncrosslinked 80% of all AGE-linked Ig and red blood cells, suggesting that the other known AGE structures (eg. FFI, pyraline etc) may be less important. Experiments testing the effectiveness of thymine at reversing crosslinking are continuing (presumably also crosslinkage between lipids and nucleic acids), and the latest results indicate thymine is also effective at disaggregating the amyloid plaques associated with Alzheimer's disease. JE Preston - B-Amyloid and AGE-protein toxicity in endothelial cell culture of the rat blood-brain barrier ====================================================================== Continuing the theme of Alzheimer's disease, Preston described the B- amyloid toxicity on the blood-brain-barrier following accumulation of these plaques in the endothelial cells lining the blood vasculature of the brain. The transfer of nutrients to the brain is hindered and have reduced glucose uptake and lactate production In addition Preston found endothelial cells cultured with B-amyloid have only about 40% survival which is thought to be due to a generation of a hyperoxic state leading to massive lipid peroxidation. Preston decided to investigate whether the naturally occurring dipeptide carnosine (B-alanyl-L-histadine), which has been reported as having both antioxidant and antiglycosylation effects, could protect against amyloid toxicity. He found carnosine allowed 100% survival of endothelial cells when exposed to B-amyloid, as well as improving glucose uptake and lactate production. In addition, the metabolites of carnosine, B-alanine and L-histadine also improved survival (in particular B-alanine). He also found that carnosine provided a greater protective effect than SOD or glutathione. The concentrations used in his experiments found a protective effect from carnosine concentrations of 20mM and above in neuronal tissue. Ed Masoro - A biological evaluation of dietary energy intake and the ageing of laboratory rodents ====================================================================== Ed Masoro (University of Texas) began his presentation by first asking the question "what is the specific item which when restricted slows ageing?". Restricting only fat in rats in his lab led to no difference in life span compared to isocaloricaly fed controls, and protein restricted rats fed in the same way also exhibited no change in life span. In fact he found no particular item led to improvements in life span except the absolute caloric (energy) intake, leading to his first conclusion that reduced energy intake is the dietary factor involved in the life extending effects of dietary restriction (DR). The next question he had set out to answer was whether the effect of DR was to actually slow ageing or just to postpone the onset of sexual maturity which would only give the impression of a slowed rate of ageing. He fed four groups of rats either (1) ad libitum, (2) DR all through life, (3) DR from birth to sexual maturity and (4) DR from sexual maturity to death and compared their maximum life spans (MLS). Groups 2 and 4 were the longer lived with MLS of 1295 and 1298 days respectively while groups 3 and 1 came a distant second, leading Masoro to rule out any effect of DR working via slowing fertility onset. He also compared the life extending effect of DR on lean and obese mice and although no statistically significant difference was found he did note that if anything the obese rats lived longer! Another unexpected discovery was that metabolic rate/unit of lean body mass of DR and normal rats was the same as was O2 consumption. However, their was much lower 24 hour plasma glucose levels in DR rats as well as lower maximum levels of insulin compared to ad libitum fed rats which suggested DR rats could utilise glucose with less insulin by either increasing "insulin sensitivity" or "glucose utilization effectiveness" or both. Comparing the response of DR and normally fed rats to several stressors found DR rats to be far more resistant. Recovery after surgery was faster (and the amount of weight loss less) in DR rats, and they also showed a much quicker immune response to antigens. Survival following heat shock was 16% in ad libitum fed rats compared to 70% in DR rats which were also showed to have a greater expression of heat shock protein hsp70. Ed Masoro concluded that the changes that occur during DR have evolved to cope with increased stressors and not to slow ageing, although the antistressing effect directly leads to an antiageing effect. Axel Kowald - Life extension through diet: evolutionary implications ==================================================================== Axel's mathematical model for the observed antiageing effects of dietary restriction appeared surprisingly simpler than some of his previous models (his last paper on the Network Theory of Ageing contained literally hundreds of variables), however, most of the predictions of the model fitted experimental observations quite well. The theoretical basis for the model derived from evolutionary biology (Disposable Soma Theory: Kirkwood) which in a nutshell and highly simplified states that the energy (food) entering the organism is shared between somatic maintenance (repair processes etc), growth and reproduction in such a way that maximises the number of surviving offspring. Growth Energy ----> Maintenance ----> progeny Reproduction The optimal allocation of resources depends on the environment (ie. food availability) and can be calculated using the 'Lotka equation' which describes the ideal input into maintenance and reproduction for maximising progeny in a given environment. The Lotka equation also contains an expression 'r' which relates to the mortality rate doubling time (MRDT) or the rate of ageing and thus by altering the environment the equation predicts changes in the pace at which ageing occurs. In humans the MRDT is about 8 years after sexual maturity (ie. every 8 years your risk of dying from any particular intrinsic cause of death doubles), however, by simulating famine conditions using an extended version of the Lotka equation the model predicts an increase in the MRDT which is dependant on the severity of starvation. As far as I could tell the model didn't predict the optimum degree of starvation to obtain the highest MRDT, although it did predict greater improvements in longevity the earlier DR is started with diminishing benefits in later life. Even brief periods of 10 days of severe DR was predicted by the model to have marginally beneficial effects on MRDT which may be relevant in terms of the effects of fasting. Overall the model agreed well with experimental observations with both average life span and maximum life span being increased during DR and the extent of this effect depending on the length and severity of dietary restriction. *** Considering this was the first British congress of gerontology ever the organisers saw it as a quite a landmark in British gerontological research. Speaking to Tom Kirkwood, one of main the organisers of this congress, he said that judging by the interest and success of this first congress we can expect another next year in what may become an annual event taking place in different locations throughout the UK. Newcastle is strongly tipped to be next years location and as soon as I know more information I could post the registration details to this group if anyone is interested in attending. All the best, Sam Cronin ***I will be away from my terminal for two weeks after July 16 and only intermittently thereafter during the summer*** ~ From owner-ageing@net.bio.net Wed Jul 10 23:00:00 1996 Path: biosci!aol.com!EdKrug From: EdKrug@aol.com Newsgroups: bionet.molbio.ageing Subject: Re: Free radicals and aging Date: 11 Jul 1996 05:01:20 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 18 Sender: daemon@net.bio.net Distribution: world Message-ID: <960711080208_153555196@emout14.mail.aol.com> NNTP-Posting-Host: net.bio.net Hello Brian Rowley I had feared that raising dietary antioxidants might reduce production of endogenous antioxidants and you said that Richard Cutler suggested that it does. I will have to find out what has been published on that. However, the observation that increased intake of antioxidants can produce increases in mean life span suggests that you can produce an effect, that the down regulation of antioxidant systems is less overall or in some important compartments than the increase in dietary antioxidants added to the system. A related question, I am beginning to wonder how much of the accumulated free radical damage is from steady state production and how much is from acute high levels from metabolic free radical storms. Related, from your e-mail addres are you at the British Columbia Cancer Research Center? If so, can you e-mail me direct the phone number of Dr. Olive's lab? I have a techniques question. Thanks, Ed Krug From owner-ageing@net.bio.net Thu Jul 11 23:00:00 1996 Path: biosci!bcm.tmc.edu!cs.utexas.edu!howland.reston.ans.net!nntp.coast.net!netnews.worldnet.att.net!cbgw2.att.com!nntphub.cb.lucent.com!not-for-mail From: norm@mthost2.mt.att.com (nl7010b00-Norman Andrews(MT0000)NOBIN) Newsgroups: bionet.molbio.ageing Subject: Re: Free radicals and aging Date: 12 Jul 1996 17:16:22 GMT Organization: AT&T Lines: 11 Message-ID: <4s6196$r1s@nntpa.cb.lucent.com> References: <960710151838_573807786@emout13.mail.aol.com> NNTP-Posting-Host: mthost2.mt.lucent.com For tests on synergistic effects of antioxidant vitamins, see the paper by Roger Williams (et al?) in The Physicians' Handbook of Orthomolecular Medicine. Rats predisposed to cataracts were the test subjects. Not only did the development of cataracts prevented or slowed, in some cases the damage was reversed. Based on my memory after a couple of decades. The work was done in San Antonio. Roger J. Williams was a discoverer/codiscoverer of some of the B vitamins. I believe he died at UT-Austin area in his 90's a few years ago. Norm Andrews. From owner-ageing@net.bio.net Fri Jul 12 23:00:00 1996 Path: biosci!rutgers!csn!nntp-xfer-1.csn.net!magnus.acs.ohio-state.edu!lerc.nasa.gov!purdue!mozo.cc.purdue.edu!not-for-mail From: barani@deft.cc.purdue.edu (Raman) Newsgroups: bionet.molbio.ageing Subject: Re: Beyond MEDLINE Abstracts?? Date: 13 Jul 1996 11:52:55 -0500 Organization: Purdue University Computing Center Lines: 45 Distribution: world Message-ID: <4s8k97$i26@deft.cc.purdue.edu> NNTP-Posting-Host: deft.cc.purdue.edu Keywords: library, journals, public access, ageing >Article: 2732 of bionet.molbio.ageing >From: Peter Ezzell >Subject: Beyond MEDLINE Abstracts?? >Date: Sat, 13 Jul 1996 09:26:34 -0700 >Organization: Crystal Wind Communications > >How do you get "free" access to scientific papers? I've found quite a >few that, based on their abstracts, appear worth reading in full. > >If they're not available free, is there an inexpensive service which >provides the full text? I have always felt that public must be given access to university library collections on a membership basis. Unfortunately that is not the case. If you are working in an industry or company, you may be able to obtain a corporate membership at a nearby University. Before you do that, confirm that they subscribe to relevant journals. If you are simply looking for a few articles, an easier thing to do would be to befriend a research student :-) You may directly write to the author of the papers and request reprints of their publications. Usually they authors are more than happy to bring their works to the others notice. Among other useful ideas, you may explore registering for a single easy course in a nearby school and obtain a student id - and get full access to journals and computers. Journals have copyrights on their papers; however, they do not oppose photocopying for personal or educational use and object only to commercial reproductions. | | | ----- ----- ----- | | | ------------------------------------------------------------------- | This box is dedicated to the memory of those who spent their | | lifetimes working on the age-old problem of the old-age problem.| ------------------------------------------------------------------- From owner-ageing@net.bio.net Fri Jul 12 23:00:00 1996 Path: biosci!ns1.faseb.org!lamarck.sura.net!ra.nrl.navy.mil!news.math.psu.edu!chi-news.cic.net!nntp.coast.net!news.sprintlink.net!news-stk-200.sprintlink.net!newsfeed.internetmci.com!uuneo.neosoft.com!winnie-ppp-h4.NeoSoft.com!pproctor From: pproctor@neosoft.com (Peter H. Proctor) Newsgroups: bionet.molbio.ageing Subject: Re: Free radicals and Aging (antioxidants) Date: Sat, 13 Jul 1996 11:00:10 UNDEFINED Organization: NeoSoft, Inc. Lines: 35 Distribution: world Message-ID: References: NNTP-Posting-Host: 206.109.10.170 X-Newsreader: Trumpet for Windows [Version 1.0 Rev B final beta #1] In article browley@UNIXG.UBC.CA (Brian Rowley) writes: >From: browley@UNIXG.UBC.CA (Brian Rowley) >Subject: Free radicals and Aging (antioxidants) >Date: 10 Jul 1996 14:59:48 -0700 >The other thing to think about is that rodents have a greatly inferior >antioxidant system to humans. Our blood is almost saturated with uric acid >(sometimes it crystalizes in the joints to cause gout). We also do not >produce our own vitamin C, unlike most rodents. It turns out that uric >acid is a greatly superior antioxidant to vitamin C, or so I've heard. >Vitamin C, in really high doses, actually increases free radicals, so I >have also heard. So we humans perhaps traded vitamin C for uric acid >somewhere along the way for that particular antioxidant niche, giving us >greater longevity. And humans produce more SOD per gram of tissue when >corrected for metabolic rate. What I'm trying to say is that just because >antioxidants increase life expectancy of rodents by 30% does not >necessarily imply that they will do the same for people. We have such a >good system already, there is less to improve on. Something to consider >anyway :-> It gets even worse. Uric acid is a good example. Yes, it is a good antioxidant and probably substtitutes for ascorbate in Human evolution. ( BTW, I originally suggested this, he says modestly ). OTOH, like ascorbate and other strong reducing substances , uric acid can actually mediate radical oxidations by reducing oxygen to it radical forms. In fact, this may account for the pathogensis of hyperuricemic diseases such as the lesch-Nyhan syndrome. Same with a lot of other so-called "antioxidants". Such processes may actually contribute to some human diseases. See P. Proctor, Free Radicals and Human Disease, in CRC Handbook of Free Radicals and Antioxidants, Vol. 1 (1989 ) p211. Peter H. Proctor, PhD, MD From owner-ageing@net.bio.net Fri Jul 12 23:00:00 1996 Path: biosci!rutgers!news.iag.net!newsboy.utelfla.com!opal.xtalwind.net!usenet From: Peter Ezzell Newsgroups: bionet.molbio.ageing Subject: Beyond MEDLINE Abstracts?? Date: Sat, 13 Jul 1996 09:26:34 -0700 Organization: Crystal Wind Communications Lines: 5 Message-ID: <31E7CE3A.336A@xtalwind.net> NNTP-Posting-Host: slipper22b.xtalwind.net Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.0 (Win16; I) How do you get "free" access to scientific papers? I've found quite a few that, based on their abstracts, appear worth reading in full. If they're not available free, is there an inexpensive service which provides the full text? From owner-ageing@net.bio.net Sat Jul 13 23:00:00 1996 Path: biosci!agate!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!in2.uu.net!news2.digex.net!news1.digex.net!haven.umd.edu!cville-srv.wam.umd.edu!rac4.wam.umd.edu!theoblit From: theoblit@wam.umd.edu (Jason Taylor) Newsgroups: bionet.molbio.ageing Subject: Mini Book Review#3: Fountains of Youth, eds. Everone, Dean, & Mann Date: 14 Jul 1996 02:51:51 GMT Organization: University of Maryland College Park Lines: 38 Distribution: world Message-ID: <4s9nc7$he4@cville-srv.wam.umd.edu> NNTP-Posting-Host: rac4.wam.umd.edu Summary: Mini Book Review: Fountains of Youth, eds. Everone, Dean, & Mann Keywords: Mini Book Review: Fountains of Youth, eds. Everone, Dean, & Mann X-Newsreader: TIN [version 1.2 PL2] If you have a really good memory and have been reading this newsgroup regularly you might recall that I ordered _Fountains of Youth: How to Live Longer and Healthier_ a YEAR ago. Well it finally came in --- last week! Talk about delays! Oh well. I figured that since John Mann and Ward Dean were editors (when I ordered the book I had thought that Mann was sole author actually) that this book would be worth the wait. With wide-open eyes I did what I am generally guilty of under these circumstances: I peaked straight away at the reference section. My eyes turned to half-squinted as I realized that most of the references in the book were other pop books (in a section entitled "Suggested Reading" that I'd of entitled "Slightly Better Buys"). Now don't get me wrong: it's not that I expect a good life extension book to be collection of abstracts down-loaded off Medline. However, I like to see the claims a book makes referenced so that I can question them and go directly to the horse's mouth so to speak. For instance, there is no source mentioned to support the statement (picked almost at random --- page 93), "Beta carotene seems to have a substantial protective effect against lung cancer in smokers." This book is weak as a politician's promise in that respect: few original sources are cited and only "well-accepted" life extension knowledge is discussed (i.e., calories restriction). On the whole, I'd guess that some marketing majors at Ronin Publishing decided that a book on life extension would sell and that they would turn a profit by paying some names to put something together. But like a suit-conceptualized movie sequel, this work lacks personality and does little more for me than take up money and time. On the upside, this book is easy to read and would serve as a very general overview of life extension to those with a mild curiosity about it. But if you are the type who doesn't bother reading the health section of periodicals like _Time_, then I would suggest saving yourself about $20 and passing over this book as well. -- Jason Taylor, Greenbelt, MD USA|"Doctor, don't cut so deep! That's the third http://www.wam.umd.edu/~theoblit| operating table you've ruined this week!" From owner-ageing@net.bio.net Sat Jul 13 23:00:00 1996 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!swrinde!newsfeed.internetmci.com!news-feed.iguide.com!news.delphi.com!usenet From: Lou Pagnucco Newsgroups: bionet.molbio.ageing Subject: Re: Living longer - Living better Date: Sun, 14 Jul 96 09:44:00 -0500 Organization: Delphi (info@delphi.com email, 800-695-4005 voice) Lines: 32 Message-ID: References: <4s2ud1$hok@mserv1.dl.ac.uk> NNTP-Posting-Host: bos1b.delphi.com X-To: Samuel Cronin Samuel Cronin writes: >Antony Cerami began by summarising the historical evidence for the >accumulation of advanced glycation end products (AGEs) derived from >the reaction of reducing sugars such as glucose with proteins, lipids >or nucleic acids (the glycation theory of ageing). He also provided >some evidence for the role of AGEs in disease, including experiments >where AGE peptides injected into rodents or rabbits caused many of the >complications of diabetes (accelerated atherosclerosis etc.) as well >as the generation of B-amyloid plaques in the brain. > : > : > : >Prevention of AGE formation in rat models has long been achieved by >the use of aminoguanidine, however, Antony's group had discovered that >the B vitamin thymine can react with the specific AGE protein- >crosslink associated with the ene-dione structure and actually >separate the proteins, essentially reversing cross-linkage. Tests >showed that thymine uncrosslinked 80% of all AGE-linked Ig and red >blood cells, suggesting that the other known AGE structures (eg. FFI, >pyraline etc) may be less important. Experiments testing the > This is a very interesting note, but please clarify it. Thymine is not a B-vitamin. Perhaps, you meant thiamine? Or possibly you did mean "thymine" in which case you should not have refered to it as a vitamin. Thanks for the information, Lou Pagnucco (lpagnucco@delphi.com) From owner-ageing@net.bio.net Sun Jul 14 23:00:00 1996 Path: biosci!bcm.tmc.edu!pendragon!news.msfc.nasa.gov!newsfeed.internetmci.com!uunet!inXS.uu.net!psinntp!psinntp!psinntp!usenet From: jmsdean@pipeline.com Newsgroups: bionet.molbio.ageing Subject: lobsters Date: 15 Jul 1996 01:51:14 GMT Organization: PSINet/Pipeline USA Lines: 6 Message-ID: <4sc86i$9m1@news2.h1.usa.pipeline.com> NNTP-Posting-Host: 38.8.61.2 i'm a lurker here because i am not a doctor, but i saw something that was very curious. it was said that a lobster which is kept free of disease and away from fisherman will not age. is that right? will the lobster live for ever? luke From owner-ageing@net.bio.net Sun Jul 14 23:00:00 1996 Path: biosci!rutgers!uwm.edu!cs.utexas.edu!swrinde!news-res.gsl.net!news.gsl.net!hunter.premier.net!news2.cais.net!news.cais.net!nntp.primenet.com!uunet!in2.uu.net!news.sprintlink.net!new-news.sprintlink.net!gol2!user From: joel@pac.co.jp (Joel Sassone) Newsgroups: bionet.molbio.ageing Subject: Re: Update on Negligible Senescence in Long-Lived Fishes Date: Tue, 16 Jul 1996 00:12:55 +0900 Organization: Himself Lines: 16 Message-ID: References: <199606272345.AA27564@lafn.org> <5607588wnr@longevb.demon.co.uk> <31D7EC9A.79BE@hgu.mrc.ac.uk> NNTP-Posting-Host: yok2-71.gol.com >If you define immortality as no age-related increase in mortality rates I gather >there are a >number of species (e.g. lobsters) which behave in such a fashion. OK, there are >no million-year >old lobsters, but that's because they suffer accidents, disease and get caught >by New England >fishermen... :-) But is "no ageing" [which is no increase in mortality rates] >the same as >"immortality"? Oh dear, I'm confused now. An interesting experiment would be to capture some such lobsters, and try to keep them alive indefinitely (this experiment may take multiple human generations). Has anyone heard of such an experiment being performed? From owner-ageing@net.bio.net Sun Jul 14 23:00:00 1996 Path: biosci!daresbury!not-for-mail From: jcoward@mail.islandnet.com (Jim Coward) Newsgroups: bionet.molbio.ageing Subject: ITCH'96 UPDATE Date: 15 Jul 1996 22:53:56 +0100 Lines: 24 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <4seelk$dom@mserv1.dl.ac.uk> X-Sender: jcoward@mail.islandnet.com (Unverified) Original-To: itch@hsd.uvic.ca ITCH'96 is building up to an exciting event. Its working theme of "APPROPRIATE SYSTEMS/APPROPRIATE DECISIONS" has attracted a lot of interest and enthusiasm world-wide. 73 Papers have been accepted for presentation and publication from people in eleven different countries. These include; England, Australia, New Caledonia, France, South Africa, Sweden, Germany, Nigeria and Austria. There will be presenters from almost every province and territory in Canada. Plus, papers from 12 different states in the U.S. All of the abstracts are now on ITCH'96's world wide website. Please take the time to have a close look at it. There is a lot of other information there as well. It's URL is "http://www.hsd.uvic.ca/HIS/ITCH/ITCH'96" This is the seventh time the conference has been held in the last ten years. It will be attended by health professionals, physicians, information and computer systems experts, academics and researchers, hospital administrator, and public health providers. This is a continuously growing, very high-quality conference that you don't want to miss. Jim Coward, CHE (Coordinator, BC Health Information Standards Council) Organizing Committee - ITCH'96 Information Technology in Community Health ITCH'96 WEBPAGE: http://www.hsd.uvic.ca/HIS/ITCH/ITCH.htm Phone (604)952-1838 FAX (604) 658-6394 Cell Phone (604) 881-2537 Jim's Website: http://www.islandnet.com/~jcoward/homepage.htm From owner-ageing@net.bio.net Sun Jul 14 23:00:00 1996 Path: biosci!daresbury!not-for-mail From: jcoward@mail.islandnet.com (Jim Coward) Newsgroups: bionet.molbio.ageing Subject: URL ADDRESS CORRECTIONS - ITCH'96 Date: 15 Jul 1996 23:07:35 +0100 Lines: 10 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <4seff7$en7@mserv1.dl.ac.uk> X-Sender: jcoward@mail.islandnet.com Original-To: itch@hsd.uvic.ca URL ADDRESS CORRECTION FOR ITCH'96 (apologies for the double mailing) "http://www.hsd.uvic.ca/HIS/ITCH/ITCH.htm" Jim Coward, CHE (Coordinator, BC Health Information Standards Council) Organizing Committee - ITCH'96 Information Technology in Community Health ITCH'96 WEBPAGE: http://www.hsd.uvic.ca/HIS/ITCH/ITCH.htm Phone (604)952-1838 FAX (604) 658-6394 Cell Phone (604) 881-2537 Jim's Website: http://www.islandnet.com/~jcoward/homepage.htm From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!GNN.COM!DSchwa1234 From: DSchwa1234@GNN.COM (Douglas Schwartz) Newsgroups: bionet.molbio.ageing Subject: Re: Update on Negligible Senescence in Long-Lived Fishes Date: 15 Jul 1996 19:09:05 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 103 Sender: daemon@net.bio.net Distribution: world Message-ID: <199607160208.WAA29424@mail-e2b-service.gnn.com> NNTP-Posting-Host: net.bio.net 0 >From: joel@pac.co.jp (Joel Sassone) >An interesting experiment would be to capture some such > lobsters, and try >to keep them alive indefinitely (this experiment may take > multiple human >generations). Has anyone heard of such an experiment being > performed? > In a way, I think you could say that Nature has already done this. Old Colonial-era accounts spoke of 5-6 foot long lobsters in NY=20 harbor, which permanently left as a result of the noise from the=20 incessant shelling during the Revolution. Nobody really believed=20 these accounts until the 1960s when Rhode Island lobstermen kept=20 going further & further offshore & finding more & more huge=20 lobsters. They found huge stocks of monster lobsters in the canyons=20 at the edge of the shelf. (They seek out a steady 50=B0F temp.=20 gradient out at the margin of the Gulf Stream.) These have been=20 greatly reduced by intensive fishing since then. In the early days=20 there were so many that dragging was the easiest way to get them,=20 now pots are the most-efficient method with the reduced stocks. I=20 believe the record is 44 lbs., but I think most in the industry=20 would agree that far-larger specimens are out there. I suspect that=20 the biggest ones move about little, if at all. Their preferred=20 habitat is wedged under the underside of a boulder where nothing can=20 yank them out. I think that potting & dragging miss these big ones,=20 as they are not mobile. There is evidence that they can survive on=20 plankton & algae, so there is no need to move about. They are the largest of the arthropods, and can be said to have been=20 extraordinarily successful in their range. Old accounts speak of=20 masses of lobsters a few feet thick washed up on New England beaches=20 after storms. The contracts of indentured servants of that era=20 often had clauses that the servant was not to be fed lobster more=20 than so many times as week (they used to boil them for extended=20 periods, which kills the taste). Apparently, there was no aging=20 mechanism to control populations, just attrition from violent=20 deaths. =20 They exhibit indeterminate growth. They only grow when molting, and=20 the interesting thing is that the claws grow disproportionately to=20 the body. When they are young, smaller than legal size, the claws=20 are similar to crawfish, but swell in the big specimens. I mention=20 this as it may provide clues to the age of the monsters. Don't=20 quote this, but I believe that intervals between molts probably=20 increase exponentially with age, in other words they molt several=20 times a year when very young, but many years transpire between molts=20 when they get up around 5 lbs., if memory is correct. If you are=20 talking about a 6-foot lobster I would not think that an age in=20 centuries is out of the question.=20 Another important thing is that there are 2 distinct populations of=20 the same species, those above Cape Cod, and those below. Above the=20 Cape they migrate seasonally only for rather short distances, mostly=20 under 5 miles in and out to follow the 50=B0 temp. gradient with the=20 seasons. Below the Cape they will make the long trek in from the=20 canyons on the edge of the shelf where they winter over. [This is=20 not to imply that there are not monster specimens above the Cape. =20 They is no doubt that there are huge ones up there also, it is just=20 that they are found in much greater concentrations south of the=20 Cape.] They go into the coastal estuaries to molt at the 50=B0 line=20 as it moves into the coast in early summer. After molting they=20 burrow into the estuarine mud to escape predators while in their=20 defenseless state until the new shell hardens. This is also when=20 the young are hatched to mature in the estuarine nursuries. I=20 forget, but believe the only time the females can be mated with is=20 when they have just molted. Then as the inshore water temps. get=20 too hot during the late summer, the stocks will pull back out into=20 deeper water, to return around late Nov. when the temp. is back to=20 optimum. They will begin the migration back to the canyons near the=20 end of the year. You can get some very big lobsters (25+ lbs.=20 anyway) which come inshore during these summer & fall runs, but my=20 sense of it is that real monsters stay out in the canyons on the=20 edge of the shelf. I don't think anybody knows if the whole stock=20 of younger lobsters participates each year in these migrations, or=20 if only some do. By the way, this species, Homarus Americanus, is=20 essentially identical to the lobsters found on the W. coast of=20 Europe, Homarus Vulgarus, with the two just having a slightly=20 different rostrum, the little beak between the eyes. The heavier=20 fishing pressure there and the lack of the ideal temp. conditions=20 combine to keep their stocks a lot lower, but I have no doubt that=20 these lobsters also have the same potential for reaching extended=20 ages. I went into all this detail not because I think this is the proper=20 forum to discuss the natural history of lobsters, but to alert=20 people to a subject which needs a lot more study. I seem to recall=20 something about a stoney structure found in their heads which=20 exhibits growth rings, but may be confusing this with some other=20 species. I am fully convinced that there are lobsters out there now=20 aged well into the centuries, anyhow. The fact that they live at=20 such cool temps. has something to do with this, but there is a lot=20 more going on here which needs intensive study. =20 --Doug Schwartz dschwa1234@gnn.com From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!UNIXG.UBC.CA!browley From: browley@UNIXG.UBC.CA (Brian Rowley) Newsgroups: bionet.molbio.ageing Subject: (none) Date: 15 Jul 1996 21:12:44 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 11 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net This message is in MIME format. The first part should be readable text, while the remaining parts are likely unreadable without MIME-aware tools. Send mail to mime@docserver.cac.washington.edu for more info. --OAA27754.837464862/unixg.ubc.ca Content-Type: TEXT/PLAIN; CHARSET=US-ASCII Content-ID: --OAA27754.837464862/unixg.ubc.ca-- From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!UNIXG.UBC.CA!browley From: browley@UNIXG.UBC.CA (Brian Rowley) Newsgroups: bionet.molbio.ageing Subject: Re: Update on Negligible Senescence in Long-Lived Fishes Date: 15 Jul 1996 21:31:16 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 132 Sender: daemon@net.bio.net Distribution: world Message-ID: References: <199607160208.WAA29424@mail-e2b-service.gnn.com> NNTP-Posting-Host: net.bio.net Wonderfully interesting review, thank you. I might add that if anyone is interested, there is a series of reviews in the Journal Gerontology--big, comprehensive, all you ever wanted to know type reviews. One of the reviews is called, "Ageing in Amphibians", one is called "AGeing in Reptiles", etc. Here's a specific reference to one of the articles: Patnaik, B.K., Mahapatro, N., and Jena, B.S. Ageing in Fishes. Gerontology 1994;40:113-132. Anyway, I flipped through the article on ageing in reptiles to find out whether or not tortoises age--I've always heard that tortoises exhibit "negligible senescence"--this is what Caleb Finch, Alex Comfort and Hayflick say. However, the authors of "Ageing in Fishes", and the authors of "Ageing in Reptiles" both state that it is a myth that tortoises and sturgeons (e.g.) don't age. Apparently their growth slows as the years go by and they get lipofuscin deposits eventually. I might also add that tortoises have a Hayflick limit of over 100, but a Hayflick limit nonetheless. Still, apparently there are some specimens about 180 years and still laying eggs! No menopause there. Anyway, if anyone is interested in further reading on reptile, amphibian or fish ageing, do flip through recent Gerontology journals. As I say, there is a recent series of major reviews :-> On 15 Jul 1996, Douglas Schwartz wrote: > 0 > > >From: joel@pac.co.jp (Joel Sassone) > > > >An interesting experiment would be to capture some such > > lobsters, and try > >to keep them alive indefinitely (this experiment may take > > multiple human > >generations). Has anyone heard of such an experiment being > > performed? > > > > In a way, I think you could say that Nature has already done this. > > Old Colonial-era accounts spoke of 5-6 foot long lobsters in NY=20 > harbor, which permanently left as a result of the noise from the=20 > incessant shelling during the Revolution. Nobody really believed=20 > these accounts until the 1960s when Rhode Island lobstermen kept=20 > going further & further offshore & finding more & more huge=20 > lobsters. They found huge stocks of monster lobsters in the canyons=20 > at the edge of the shelf. (They seek out a steady 50=B0F temp.=20 > gradient out at the margin of the Gulf Stream.) These have been=20 > greatly reduced by intensive fishing since then. In the early days=20 > there were so many that dragging was the easiest way to get them,=20 > now pots are the most-efficient method with the reduced stocks. I=20 > believe the record is 44 lbs., but I think most in the industry=20 > would agree that far-larger specimens are out there. I suspect that=20 > the biggest ones move about little, if at all. Their preferred=20 > habitat is wedged under the underside of a boulder where nothing can=20 > yank them out. I think that potting & dragging miss these big ones,=20 > as they are not mobile. There is evidence that they can survive on=20 > plankton & algae, so there is no need to move about. > > They are the largest of the arthropods, and can be said to have been=20 > extraordinarily successful in their range. Old accounts speak of=20 > masses of lobsters a few feet thick washed up on New England beaches=20 > after storms. The contracts of indentured servants of that era=20 > often had clauses that the servant was not to be fed lobster more=20 > than so many times as week (they used to boil them for extended=20 > periods, which kills the taste). Apparently, there was no aging=20 > mechanism to control populations, just attrition from violent=20 > deaths. =20 > > They exhibit indeterminate growth. They only grow when molting, and=20 > the interesting thing is that the claws grow disproportionately to=20 > the body. When they are young, smaller than legal size, the claws=20 > are similar to crawfish, but swell in the big specimens. I mention=20 > this as it may provide clues to the age of the monsters. Don't=20 > quote this, but I believe that intervals between molts probably=20 > increase exponentially with age, in other words they molt several=20 > times a year when very young, but many years transpire between molts=20 > when they get up around 5 lbs., if memory is correct. If you are=20 > talking about a 6-foot lobster I would not think that an age in=20 > centuries is out of the question.=20 > > Another important thing is that there are 2 distinct populations of=20 > the same species, those above Cape Cod, and those below. Above the=20 > Cape they migrate seasonally only for rather short distances, mostly=20 > under 5 miles in and out to follow the 50=B0 temp. gradient with the=20 > seasons. Below the Cape they will make the long trek in from the=20 > canyons on the edge of the shelf where they winter over. [This is=20 > not to imply that there are not monster specimens above the Cape. =20 > They is no doubt that there are huge ones up there also, it is just=20 > that they are found in much greater concentrations south of the=20 > Cape.] They go into the coastal estuaries to molt at the 50=B0 line=20 > as it moves into the coast in early summer. After molting they=20 > burrow into the estuarine mud to escape predators while in their=20 > defenseless state until the new shell hardens. This is also when=20 > the young are hatched to mature in the estuarine nursuries. I=20 > forget, but believe the only time the females can be mated with is=20 > when they have just molted. Then as the inshore water temps. get=20 > too hot during the late summer, the stocks will pull back out into=20 > deeper water, to return around late Nov. when the temp. is back to=20 > optimum. They will begin the migration back to the canyons near the=20 > end of the year. You can get some very big lobsters (25+ lbs.=20 > anyway) which come inshore during these summer & fall runs, but my=20 > sense of it is that real monsters stay out in the canyons on the=20 > edge of the shelf. I don't think anybody knows if the whole stock=20 > of younger lobsters participates each year in these migrations, or=20 > if only some do. By the way, this species, Homarus Americanus, is=20 > essentially identical to the lobsters found on the W. coast of=20 > Europe, Homarus Vulgarus, with the two just having a slightly=20 > different rostrum, the little beak between the eyes. The heavier=20 > fishing pressure there and the lack of the ideal temp. conditions=20 > combine to keep their stocks a lot lower, but I have no doubt that=20 > these lobsters also have the same potential for reaching extended=20 > ages. > > I went into all this detail not because I think this is the proper=20 > forum to discuss the natural history of lobsters, but to alert=20 > people to a subject which needs a lot more study. I seem to recall=20 > something about a stoney structure found in their heads which=20 > exhibits growth rings, but may be confusing this with some other=20 > species. I am fully convinced that there are lobsters out there now=20 > aged well into the centuries, anyhow. The fact that they live at=20 > such cool temps. has something to do with this, but there is a lot=20 > more going on here which needs intensive study. =20 > > > --Doug Schwartz > dschwa1234@gnn.com > > > From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!UNIXG.UBC.CA!browley From: browley@UNIXG.UBC.CA (Brian Rowley) Newsgroups: bionet.molbio.ageing Subject: Future Date: 15 Jul 1996 21:43:46 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 55 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net There are two plausible outcomes of research geared towards extending longevity: (1) We will never, ever break the species life span of humans. Our biological limits have been reached, and medical tinkering with the underlying rate of aging itself, or reversing it, will not be successful--or at least not in our life times. (2) Perhaps within the next 20 years, we will come up with a combination of treatments that can influence the fundamental aging clock powerfully enough to make a big dent in human aging. It is practical and non-toxic enough to use on humans to successfully retard or reverse aging in a fundamental, not merely symptomatic way. Both of the above ideas are PLAUSIBLE. Looking back over this last century, stranger things have happened. We are not talking about pink aliens landing on earth within the next 5 years. Both of the above scenarios fall under the plausible category. Which of the above you choose does not depend on your wisdom, intelligence or credentials. Roy L. Walford, Smith-Sonneborne, Cutler and I pick #2. However, there are great biogerontologists who prefer #1. It depends on attitude more than knowledge--some have a guarded attitude about the future, some have an optimistic attitude towards the future. Yet neither position #1 nor position #2 can be refuted, as they are only opinions, currently untestable hypotheses. A lot of people will tell you that their crystal ball is better than anyone else's, but one has to keep in mind that crystal balls in general are pretty cloudy when it comes to science. A lot of people would argue with me by saying, "Yes, but we are only scratching the surface of aging; we do not understand enough about the aging process to come up with anything that will slow it." Well, I would argue back that discovery leads to understanding a lot more often than understanding leads to discovery. The man who discovered a vaccine for small pox did not even have a clear idea about what bacteria or viruses were. He had no understanding, but he was able to recognize something which works. Milk maids with cow pox (a minor skin affliction) never got small pox. So, if we expose people to cow pox, maybe they won't get small pox either. No complicated viral attenuation, no selected viral antigens, no pathology. Just a needle, a milk maid, a bunch of uninfected test subjects and time. Voila, the first vaccine. You don't need understanding to tell when something works. Caloric restriction has longevity benefits for rodents--that observation was made before we found out that it improves immune system function, antioxidant enzymes, lowers body temperature, lowers blood sugar and sugar cross-linkages... The point is that something was discovered without any understanding of underlying mechanism. Along the same lines, it wouldn't take understanding of the aging process to see that drug A slows aging, when all mice receiving it are still alive after 5 years. From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!bcm.tmc.edu!pendragon!news.msfc.nasa.gov!newsfeed.internetmci.com!news.compuserve.com!news.production.compuserve.com!news From: JAN CZEKAJEWSKI <75144.2413@CompuServe.COM> Newsgroups: bionet.microbiology,bionet.molbio.ageing,bionet.molbio.methds-reagnts,bionet.neuroscience,bionet.neuroscience.amyloid Subject: LAB-ANIMAL RES.EQUIP.CATALOG ON WEB Date: 16 Jul 1996 12:36:07 GMT Organization: Columbus Instruments Lines: 18 Message-ID: <4sg2bn$nl8$2@mhadf.production.compuserve.com> Xref: biosci bionet.microbiology:6605 bionet.molbio.ageing:2814 bionet.molbio.methds-reagnts:46935 bionet.neuroscience:14895 bionet.neuroscience.amyloid:524 NEW COLUMBUS INSTRUMENTS LAB-ANIMAL RESEARCH INSTRUMENTATION CATALOG IS NOW ON THE WEB. It describes over 60 instruments for physiology, pharmacology, toxicology and behavioral research. For example, you will find description of Cardiac output computers for rats and mice, Treadmill for rats and mice, End-tidal CO2/N2O computer with very small air sample (5ml/min) applicable for small rodents, Oxygen consumption computer for rats, mice, dogs, horses and humns, pyrogenic activity meters, oxygen and CO2 gas analyzers, Bacteria respirometers and more. You may view this catalog accessing: http://www.colinst.com If you need hard copy, we will send it to you at free of charge. Please e-mail your street address to 75144.2413@compuserve.com Jan Czekajewski Columbus Instruments. From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!rutgers!uwm.edu!lll-winken.llnl.gov!nntp.coast.net!howland.reston.ans.net!newsfeed.internetmci.com!news.texas.net!nntp.primenet.com!uunet!inXS.uu.net!nntp.crl.com!news.PBI.net!usenet From: mlmack@SoCA.com Newsgroups: bionet.molbio.ageing Subject: Cataracts and dairy products. Date: Tue, 16 Jul 1996 16:08:06 -0700 Organization: Pacific Bell Internet Services Lines: 26 Message-ID: <31EC20D6.23EA@SoCA.com> NNTP-Posting-Host: ppp-66-5.nhwd02.pacbell.net Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.01E-LAXE (Win16; I) As a lacto-vegetarian for sometime, I was recently motivated to check out the myth/rumor that yogurt and other dairy products can contribute or cause cataracts. The motivation arose from my increasing sensitiviy to glare such as a lighted window shining into a darkened room or even the TV screen. I have read that this can be symtomatic of the formation of cataracts. So I did a little research and this is what I found: 1. The USDA did some tests on rats fed with a 10-30% solution of galactose (milk sugar) and they developed cataracts. 2. In those countries that maintain livestock and consume the dairy products, the incidence of cataracts/blindness are at epidemic proportions. These include India, Bangledesh, Nepal, Pakistan.(Some of this is attributed to malnutrition and UV ). In the US 25% of those 65 or older will develop cataracts but no one will go blind from them. 3. In those countries/populations with little or no dairy livestock, blindness from cataracts is unheard of. These include Palau, Wallis/Futuna, The Federal States of Micronesia and the Marshall Islands. 4. The World Health Organization; "global data on blindness" indicates that in economic regions that maintain livestock and consume dairy products, cataracts are the major cause of blindness. 5. The Physicians Committee for Responsible Medicine group favors the elimination of dairy products from the american diet. What is the opinion of the scientific community about this? M. L. Mack From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!rutgers!uwm.edu!vixen.cso.uiuc.edu!newsfeed.internetmci.com!news.compuserve.com!news.production.compuserve.com!news From: JAN CZEKAJEWSKI <75144.2413@CompuServe.COM> Newsgroups: bionet.molbio.ageing Subject: Biology Research Equip-catalog Date: 16 Jul 1996 17:03:44 GMT Organization: Columbus Instruments Lines: 18 Message-ID: <4sgi1g$g9u$2@mhade.production.compuserve.com> NEW COLUMBUS INSTRUMENTS LAB-ANIMAL RESEARCH INSTRUMENTATION CATALOG IS NOW ON THE WEB. It describes over 60 instruments for physiology, pharmacology, toxicology and behavioral research. For example, you will find description of Cardiac output computers for rats and mice, Treadmills for rats and mice, End-tidal CO2/N2O computer with very small air sample 5ml/min applicable for small rodents, Oxygen consumption computer for rats, mice, dogs, horses and humans, pyrogenic activity meters, oxygen and CO2 gas analyzers, Bacteria respirometers and more. You may view this catalog accessing: http://www.colinst.com If you need hard copy, I will send it to you at free of charge. Please e-mail your street address to 75144.2413@compuserve.com Jan Czekajewski Columbus Instruments. From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!bloom-beacon.mit.edu!spool.mu.edu!usenet.eel.ufl.edu!warwick!lyra.csx.cam.ac.uk!hgmp.mrc.ac.uk!gmorley From: gmorley@hgmp.mrc.ac.uk (Mr. G. Morley) Newsgroups: bionet.molbio.ageing Subject: Mitochondria oxidative damage? Date: 16 Jul 1996 13:11:50 GMT Organization: MRC Human Genome Resource Centre Lines: 25 Message-ID: <4sg4em$lnt@mercury.hgmp.mrc.ac.uk> NNTP-Posting-Host: tin.hgmp.mrc.ac.uk One theory I heard about the role of free radicals in the aging process mentioned that they can cause oxidative damage to the mitochondria.The argument went like this: All mitochondria in humans are of maternal origin - being passed down via the egg. New mitochondria are made only by other mitochondria - they are not encoded in the genome - and over time a higher proportion of dysfunctional ones are produced. I am not sure but I believe that like plasmids mitochondria have a copy number per cell.. thus eventually a large proportion of a cells resident mito. become defective. The resultant loss in energy output leads to general cellular damage, loss of skin elasticity and fatigue - aging in other words. This is not really my field so I was wondering about what other peoples reaction to this theory was? Personally I preffer telomeric shortening but I supose the two are not mutually exclusive. It might be interesting to translate the mitochondrial code into the genomic code (I believe there are differences) and engineer a mouse egg with the mitochondrail code intergrated into the genome.. it may be likely that the "error level correction" apparatus finds it more difficult to correct DNA mutations in mito than in the genome.(??) Does anyone have any ideas on this? Thanks (and be kind :)) Gary Morley gmorley@rpms.ac.uk From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!UNIXG.UBC.CA!browley From: browley@UNIXG.UBC.CA (Brian Rowley) Newsgroups: bionet.molbio.ageing Subject: Re: Update on Negligible Senescence in Long-Lived Fishes Date: 15 Jul 1996 21:45:20 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 136 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Re: Douglas Schwartz, ageing in lobsters Wonderfully interesting review, thank you. I might add that if anyone is interested, there is a series of reviews in the Journal Gerontology--big, comprehensive, all you ever wanted to know type reviews. One of the reviews is called, "Ageing in Amphibians", one is called "AGeing in Reptiles", etc. Here's a specific reference to one of the articles: Patnaik, B.K., Mahapatro, N., and Jena, B.S. Ageing in Fishes. Gerontology 1994;40:113-132. Anyway, I flipped through the article on ageing in reptiles to find out whether or not tortoises age--I've always heard that tortoises exhibit "negligible senescence"--this is what Caleb Finch, Alex Comfort and Hayflick say. However, the authors of "Ageing in Fishes", and the authors of "Ageing in Reptiles" both state that it is a myth that tortoises and sturgeons (e.g.) don't age. Apparently their growth slows as the years go by and they get lipofuscin deposits eventually. I might also add that tortoises have a Hayflick limit of over 100, but a Hayflick limit nonetheless. Still, apparently there are some specimens about 180 years and still laying eggs! No menopause there. Anyway, if anyone is interested in further reading on reptile, amphibian or fish ageing, do flip through recent Gerontology journals. As I say, there is a recent series of major reviews :-> On 15 Jul 1996, Douglas Schwartz wrote: > 0 > > >From: joel@pac.co.jp (Joel Sassone) > > > >An interesting experiment would be to capture some such > > lobsters, and try > >to keep them alive indefinitely (this experiment may take > > multiple human > >generations). Has anyone heard of such an experiment being > > performed? > > > > In a way, I think you could say that Nature has already done this. > > Old Colonial-era accounts spoke of 5-6 foot long lobsters in NY=20 > harbor, which permanently left as a result of the noise from the=20 > incessant shelling during the Revolution. Nobody really believed=20 > these accounts until the 1960s when Rhode Island lobstermen kept=20 > going further & further offshore & finding more & more huge=20 > lobsters. They found huge stocks of monster lobsters in the canyons=20 > at the edge of the shelf. (They seek out a steady 50=B0F temp.=20 > gradient out at the margin of the Gulf Stream.) These have been=20 > greatly reduced by intensive fishing since then. In the early days=20 > there were so many that dragging was the easiest way to get them,=20 > now pots are the most-efficient method with the reduced stocks. I=20 > believe the record is 44 lbs., but I think most in the industry=20 > would agree that far-larger specimens are out there. I suspect that=20 > the biggest ones move about little, if at all. Their preferred=20 > habitat is wedged under the underside of a boulder where nothing can=20 > yank them out. I think that potting & dragging miss these big ones,=20 > as they are not mobile. There is evidence that they can survive on=20 > plankton & algae, so there is no need to move about. > > They are the largest of the arthropods, and can be said to have been=20 > extraordinarily successful in their range. Old accounts speak of=20 > masses of lobsters a few feet thick washed up on New England beaches=20 > after storms. The contracts of indentured servants of that era=20 > often had clauses that the servant was not to be fed lobster more=20 > than so many times as week (they used to boil them for extended=20 > periods, which kills the taste). Apparently, there was no aging=20 > mechanism to control populations, just attrition from violent=20 > deaths. =20 > > They exhibit indeterminate growth. They only grow when molting, and=20 > the interesting thing is that the claws grow disproportionately to=20 > the body. When they are young, smaller than legal size, the claws=20 > are similar to crawfish, but swell in the big specimens. I mention=20 > this as it may provide clues to the age of the monsters. Don't=20 > quote this, but I believe that intervals between molts probably=20 > increase exponentially with age, in other words they molt several=20 > times a year when very young, but many years transpire between molts=20 > when they get up around 5 lbs., if memory is correct. If you are=20 > talking about a 6-foot lobster I would not think that an age in=20 > centuries is out of the question.=20 > > Another important thing is that there are 2 distinct populations of=20 > the same species, those above Cape Cod, and those below. Above the=20 > Cape they migrate seasonally only for rather short distances, mostly=20 > under 5 miles in and out to follow the 50=B0 temp. gradient with the=20 > seasons. Below the Cape they will make the long trek in from the=20 > canyons on the edge of the shelf where they winter over. [This is=20 > not to imply that there are not monster specimens above the Cape. =20 > They is no doubt that there are huge ones up there also, it is just=20 > that they are found in much greater concentrations south of the=20 > Cape.] They go into the coastal estuaries to molt at the 50=B0 line=20 > as it moves into the coast in early summer. After molting they=20 > burrow into the estuarine mud to escape predators while in their=20 > defenseless state until the new shell hardens. This is also when=20 > the young are hatched to mature in the estuarine nursuries. I=20 > forget, but believe the only time the females can be mated with is=20 > when they have just molted. Then as the inshore water temps. get=20 > too hot during the late summer, the stocks will pull back out into=20 > deeper water, to return around late Nov. when the temp. is back to=20 > optimum. They will begin the migration back to the canyons near the=20 > end of the year. You can get some very big lobsters (25+ lbs.=20 > anyway) which come inshore during these summer & fall runs, but my=20 > sense of it is that real monsters stay out in the canyons on the=20 > edge of the shelf. I don't think anybody knows if the whole stock=20 > of younger lobsters participates each year in these migrations, or=20 > if only some do. By the way, this species, Homarus Americanus, is=20 > essentially identical to the lobsters found on the W. coast of=20 > Europe, Homarus Vulgarus, with the two just having a slightly=20 > different rostrum, the little beak between the eyes. The heavier=20 > fishing pressure there and the lack of the ideal temp. conditions=20 > combine to keep their stocks a lot lower, but I have no doubt that=20 > these lobsters also have the same potential for reaching extended=20 > ages. > > I went into all this detail not because I think this is the proper=20 > forum to discuss the natural history of lobsters, but to alert=20 > people to a subject which needs a lot more study. I seem to recall=20 > something about a stoney structure found in their heads which=20 > exhibits growth rings, but may be confusing this with some other=20 > species. I am fully convinced that there are lobsters out there now=20 > aged well into the centuries, anyhow. The fact that they live at=20 > such cool temps. has something to do with this, but there is a lot=20 > more going on here which needs intensive study. =20 > > > --Doug Schwartz > dschwa1234@gnn.com > > > From owner-ageing@net.bio.net Mon Jul 15 23:00:00 1996 Path: biosci!daresbury!not-for-mail From: samuelc@max.roehampton.ac.uk (Samuel Cronin) Newsgroups: bionet.molbio.ageing Subject: Re: Living longer - Living bett Date: 15 Jul 1996 11:21:31 +0100 Lines: 50 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <4sd63b$48b@mserv1.dl.ac.uk> Fcc: outgoing Security: None Original-To: ageing@dl.ac.uk Type: External Classification: Certified On Sun, 14 Jul, Lou Pagnucco wrote: > Samuel Cronin writes: > > >Antony Cerami began by summarising the historical evidence for the > >accumulation of advanced glycation end products (AGEs) derived from > >the reaction of reducing sugars such as glucose with proteins, lipids > >or nucleic acids (the glycation theory of ageing). He also provided > >some evidence for the role of AGEs in disease, including experiments > >where AGE peptides injected into rodents or rabbits caused many of the > >complications of diabetes (accelerated atherosclerosis etc.) as well > >as the generation of B-amyloid plaques in the brain. > > > : > > : > > : > > >Prevention of AGE formation in rat models has long been achieved by > >the use of aminoguanidine, however, Antony's group had discovered that > >the B vitamin thymine can react with the specific AGE protein- > >crosslink associated with the ene-dione structure and actually > >separate the proteins, essentially reversing cross-linkage. Tests > >showed that thymine uncrosslinked 80% of all AGE-linked Ig and red > >blood cells, suggesting that the other known AGE structures (eg. FFI, > >pyraline etc) may be less important. Experiments testing the > > > > This is a very interesting note, but please clarify it. > Thymine is not a B-vitamin. Perhaps, you meant thiamine? > Or possibly you did mean "thymine" in which case you should not > have refered to it as a vitamin. > > Thanks for the information, > Lou Pagnucco (lpagnucco@delphi.com) > > Lou, well spotted, you were right to point that out. In the notes I made I wrote thiamine but a quick check of Antony's abstract showes it to be in fact thymine (the nucleotide). However, one additional point I'll add is that he used an analog version of thymine which he didn't elaborate on. I'd guess thats probably not that significant but I'd have to look up the paper from which the results he discussed came from (if its published yet, I'll have to check) to get more details. Sam ***I will be away from my terminal for two weeks from July 17 and only present intermittently thereafter during the summer*** ~ From owner-ageing@net.bio.net Tue Jul 16 23:00:00 1996 Path: biosci!rutgers!uwm.edu!spool.mu.edu!daily-planet.execpc.com!newspump.sol.net!news.mindspring.com!psinntp!psinntp!psinntp!usenet From: jmsdean@pipeline.com Newsgroups: bionet.molbio.ageing Subject: Re: Future Date: 17 Jul 1996 14:43:17 GMT Organization: PSINet/Pipeline USA Lines: 6 Message-ID: <4siu65$3vp@news2.h1.usa.pipeline.com> References: NNTP-Posting-Host: 38.8.61.2 can someone help me with the calorie restriction theory. i thought if you restrict calories your body gets weak and your immune system is not at maximum performance. luke From owner-ageing@net.bio.net Tue Jul 16 23:00:00 1996 Newsgroups: bionet.molbio.ageing Path: biosci!bloom-beacon.mit.edu!spool.mu.edu!uwm.edu!vixen.cso.uiuc.edu!newsfeed.internetmci.com!hunter.premier.net!netnews.worldnet.att.net!uunet!in2.uu.net!hearst.acc.Virginia.EDU!murdoch!avery.med.Virginia.EDU!dsc9w From: dsc9w@avery.med.Virginia.EDU (David Cassarino) Subject: Re: Mitochondria oxidative damage? X-Nntp-Posting-Host: avery.med.virginia.edu Message-ID: Sender: usenet@murdoch.acc.Virginia.EDU Organization: uva References: <4sg4em$lnt@mercury.hgmp.mrc.ac.uk> Date: Wed, 17 Jul 1996 16:27:21 GMT Lines: 61 gmorley@hgmp.mrc.ac.uk writes: > One theory I heard about the role of free radicals > in the aging process mentioned that they can cause oxidative damage > to the mitochondria.The argument went like this: > All mitochondria in humans are of maternal origin - > being passed down via the egg. New mitochondria are made > only by other mitochondria - they are not encoded in the genome - > and over time a higher proportion of dysfunctional ones are produced. > I am not sure but I believe that like plasmids mitochondria have > a copy number per cell.. thus eventually a large proportion of a cells > resident mito. become defective. The resultant loss in energy output > leads to general cellular damage, loss of skin elasticity and fatigue - > aging in other words. This is not really my field so I was wondering > about what other peoples reaction to this theory was? > Personally I preffer telomeric shortening but I supose the two are > not mutually exclusive. It might be interesting to translate the > mitochondrial code into the genomic code (I believe there are differences) > and engineer a mouse egg with the mitochondrail code intergrated > into the genome.. it may be likely that the "error level correction" > apparatus finds it more difficult to correct DNA mutations in mito > than in the genome.(??) Does anyone have any ideas on this? > Thanks (and be kind :)) > > Gary Morley > gmorley@rpms.ac.uk > Although I am not an expert on this, I do believe that mitochondrial damage is integral to aging. Most neurodegenerative diseases s involve damage to mitochondria and increased free radical production. There is evidence that mitochodrial mutations in the genes for the electron transport chain are involved in the cell death in Alzheimer's and Parkinson's disease (see recent papers by W.D. Parker and M.F. Beal), which are not of course always a part of aging, although clearly age-related. As neurons are teminally differentiated, their aging and death must involve mechanisms other than telomere loss. As the brain is highly sensitive to oxidative damage and has relatively lower levels of free-radical scavenging enzymes than other tissues, mitochondrial dysfunction producing high amounts of free radicals and hence damage and aging in the brain is very plausible. It has already been demonstrated conclusively that many rare neurodegenerative diseases are due to mitochondrial mutations (MERRF, MELAS, Hereditary Optic Neuropathy or Leber's Disease, Leigh's Disease, etc), and now the evidence that the most common ND diseases like Alzheimer's and Parkinson's are due to (or at least prominently involve) mitochondrial pathology convinces me that mitochondria are clearly involved somewhere in aging. I think it's also interesting to note that Coenz Q, which improves mitochondrial electron trans chain functioning (and hence lessens free radical production) has been shown to extend the life span of lab animals. -- David S. Cassarino "The mind is not a vessel to be filled MSTP, Neuroscience 2nd Year but a fire to be kindled." UVA School of Medicine -Plutarch dsc9w@virginia.edu From owner-ageing@net.bio.net Wed Jul 17 23:00:00 1996 Path: biosci!bloom-beacon.mit.edu!spool.mu.edu!daily-planet.execpc.com!newspump.sol.net!news.mindspring.com!psinntp!psinntp!psinntp!usenet From: jmsdean@pipeline.com Newsgroups: bionet.molbio.ageing Subject: hayflick numbers Date: 18 Jul 1996 03:06:28 GMT Organization: PSINet/Pipeline USA Lines: 12 Message-ID: <4sk9nk$a89@news2.h1.usa.pipeline.com> NNTP-Posting-Host: 38.8.61.2 some of you have seen my posts. i'm just a lay person with a large degree of curiosity in cellular ageing. i'm also just getting started. i went through a lot of Medline abstracts today so i'm learning. my question is: is the Hayflick number always 50 +/- 10 ? or is it different for each type of cell? what happens when a cell reaches its hayflick number? any replies are much appreciated. luke From owner-ageing@net.bio.net Wed Jul 17 23:00:00 1996 Path: biosci!LAFN.ORG!ba182 From: ba182@LAFN.ORG (John Guerin) Newsgroups: bionet.molbio.ageing Subject: Mitochondria ageing Date: 17 Jul 1996 19:48:12 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 36 Sender: daemon@net.bio.net Distribution: world Message-ID: <199607180248.AA03838@lafn.org> Reply-To: ba182@lafn.org NNTP-Posting-Host: net.bio.net There have been several references lately to mitochondria aging. The authors might be interested in an article that appeared this year in Mechanisms of Ageing and Development entitled "Low fatty acid unsaturation protects against lipid peroxidation in liver mitochondria from long-lived species: the pigeon and human case" by R. Pamplona et al (V86 (1996) 53-66). Following is the abstract: Birds have a much higher maximum longevity (MLSP) than mammals of similar metabolic rate. Recent data showed that pigeon mitochondria produce oxygen at a rate much slower than rat mitochondria, in spite of showing similar levels of oxygen consumption (Free Rad. Res., 21 (1994) 317-328). Since oxidative damage from and to mitochondria seems important in relation to aging and longevity, and mitochondrial membranes are situated at the place where oxygen radicals are generated, we studied protein and lipid peroxidation and fatty acid composition of the three main membrane phospholipids of liver mitochondria from rats (MLSP = 4 years) and pigeons (MLSP = 35 years). It was found that pigeon mitochondria show lower levels of fatty acid unsaturation than rat mitochondria in the three lipid fractions, mainly due to a substitution of highly unsaturated fatty acids (20:4 and 22:6) by linoleic acid (18:2), and that these mitochondria are more resistant to lipid peroxidation. Previous research has also obtained exactly the same major difference in fatty acid composition in human mitochondria when compared to those of rat. Thus, present information suggests that the liver mitochondrial membranes of especially long-lived species show both a low level of free radical production and a low degree of fatty acid unsaturation as important constitutive protective traits to slow down aging. For further information, see the article. Sincerely, John C. Guerin -- John C. Guerin From owner-ageing@net.bio.net Wed Jul 17 23:00:00 1996 Path: biosci!ihnp4.ucsd.edu!munnari.OZ.AU!news.mel.connect.com.au!news.uwa.edu.au!newsman.murdoch.edu.au!vetmac3.murdoch.edu.au!user From: cummins@central.murdoch.edu.au (Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Re: Mitochondria oxidative damage? Date: Thu, 18 Jul 1996 09:02:24 +0800 Organization: Murdoch University Lines: 26 Message-ID: References: <4sg4em$lnt@mercury.hgmp.mrc.ac.uk> NNTP-Posting-Host: vetmac3.murdoch.edu.au In article <4sg4em$lnt@mercury.hgmp.mrc.ac.uk>, gmorley@hgmp.mrc.ac.uk (Mr. G. Morley) wrote: > One theory I heard about the role of free radicals > in the aging process mentioned that they can cause oxidative damage > to the mitochondria. There's extensive information now on the role of mitochondria in ageing and degenerative diseases. I suggest you have a look at the excellent Emory University MitoMap page on http://www.gen.emory.edu/mitomap.html As to inheritance - well the jury's still out on that. Despite the African Eve protagonists, there is good evidence that (in humans, at any rate) sperm mitochondria enter the egg and can be identified as such for several days (see my page on http://numbat.murdoch.edu.au/spermatology/sath01.html). The simplest explanation for "maternal inheritance" is dilution - the sperm contains 75-100 copies of mtDNA compared to the 10,000 or so in the egg. One interesting point for thought is that the egg's mitochondria derive from a very few precursor copies - between 1 and 10. The term "genetic filter" has been proposed, as ovulatory processes may act to select against defective or heteroplasmic mtDNA. -- URL http://numbat.murdoch.edu.au/spermatology/spermhp.html From owner-ageing@net.bio.net Wed Jul 17 23:00:00 1996 Path: biosci!ihnp4.ucsd.edu!news1.ucsd.edu!usenet From: Oliver Bogler Newsgroups: bionet.molbio.ageing Subject: Re: Mitochondria oxidative damage? Date: Thu, 18 Jul 1996 11:58:56 -0700 Organization: The Avant-Garde of the Now, Ltd. Lines: 11 Message-ID: <31EE8970.621B@ucsd.edu> References: <4sg4em$lnt@mercury.hgmp.mrc.ac.uk> 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 2.01 (Macintosh; I; 68K) > New mitochondria are made > > only by other mitochondria - they are not encoded in the genome - > Mitochondria consist of proteins (which perform the functions of the mitochondria) and other types of molecules made by proteins (lipids, carbohydrate, nucleic acid) - these proteins are of course encoded by genes. Some genes are in the nuclear genome and some are in a seperate mitochondrial genome. Therefore, mitochondrial damage, like cellular damage in general can be repaired by replacement of proteins. From owner-ageing@net.bio.net Sat Jul 20 23:00:00 1996 Path: biosci!agate!spool.mu.edu!uwm.edu!news.cse.psu.edu!news.ecn.bgu.edu!vixen.cso.uiuc.edu!news.uoregon.edu!news-feed.iguide.com!news.delphi.com!usenet From: Lou Pagnucco Newsgroups: bionet.molbio.ageing Subject: Re: Mitochondria oxidative damage? Date: Sat, 20 Jul 96 23:59:23 -0500 Organization: Delphi (info@delphi.com email, 800-695-4005 voice) Lines: 18 Message-ID: References: <4sg4em$lnt@mercury.hgmp.mrc.ac.uk> NNTP-Posting-Host: bos1d.delphi.com X-To: David Cassarino David Cassarino writes: >As neurons are teminally differentiated, their aging and death >must involve mechanisms other than telomere loss. As the brain >is highly sensitive to oxidative damage and has relatively >lower levels of free-radical scavenging enzymes than other >tissues, mitochondrial dysfunction producing high amounts of >free radicals and hence damage and aging in the brain is very >plausible. It has already been demonstrated conclusively that Given the large body of research implicating mitochondrial free- radicals in the aging process, it seems reasonable to try to slow these damaging effects with anti-oxidants. Several papers accessible thru Medline contend that tocotrienols appear to retard the aging of the brain in lab animals. If these results are valid, then toco- trienols must have some affinity for mitochondrial membranes. Does anyone know which anti-oxidants are most likely to actually quench mitochondrial free-radicals within the mitochondrion? From owner-ageing@net.bio.net Sat Jul 20 23:00:00 1996 Newsgroups: bionet.molbio.ageing Path: biosci!bcm.tmc.edu!pendragon!news.msfc.nasa.gov!newsfeed.internetmci.com!in2.uu.net!hearst.acc.Virginia.EDU!murdoch!avery.med.Virginia.EDU!dsc9w From: dsc9w@avery.med.Virginia.EDU (David Cassarino) Subject: Re: Future X-Nntp-Posting-Host: avery.med.virginia.edu Message-ID: Sender: usenet@murdoch.acc.Virginia.EDU Organization: uva References: <4siu65$3vp@news2.h1.usa.pipeline.com> Date: Sun, 21 Jul 1996 16:47:22 GMT Lines: 19 jmsdean@pipeline.com writes: > can someone help me with the calorie restriction theory. > > i thought if you restrict calories your body gets weak and your immune > system is not at maximum performance. > > luke Luke, I think you're confusing calorie restriction with starvation. Consuming a diet with low total calories but sufficient vitamins and minerals should not weaken you, and should actually stimulate the IS. -- David S. Cassarino "The mind is not a vessel to be filled MSTP, Neuroscience 2nd Year but a fire to be kindled." UVA School of Medicine -Plutarch dsc9w@virginia.edu From owner-ageing@net.bio.net Sun Jul 21 23:00:00 1996 Path: biosci!ihnp4.ucsd.edu!swrinde!cs.utexas.edu!howland.reston.ans.net!spool.mu.edu!uwm.edu!news-res.gsl.net!news.gsl.net!hunter.premier.net!newsfeed.internetmci.com!newsxfer2.itd.umich.edu!portc01.blue.aol.com!newstf01.news.aol.com!newsbf02.news.aol.com!not-for-mail From: ofields@aol.com (OFields) Newsgroups: bionet.molbio.ageing Subject: DHEA Date: 21 Jul 1996 21:07:39 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 6 Sender: root@newsbf02.news.aol.com Message-ID: <4suk8r$fpu@newsbf02.news.aol.com> Reply-To: ofields@aol.com (OFields) NNTP-Posting-Host: newsbf02.mail.aol.com I have been doing a bit of reading on DHEA. Does anyone out there have any thoughts concerning the usefulness of hormone replacement therapay with DHEA (that is, trying to maintain 20-year-old levels of DHEA via supplementation)? Thanks From owner-ageing@net.bio.net Mon Jul 22 23:00:00 1996 Newsgroups: bionet.molbio.ageing Path: biosci!rutgers!uwm.edu!vixen.cso.uiuc.edu!uchinews!news From: Hong Qin Subject: (no subject) X-Nntp-Posting-Host: fuchs-mac-16.bsd.uchicago.edu Content-Type: text/plain; charset=us-ascii Message-ID: Sender: news@midway.uchicago.edu (News Administrator) Content-Transfer-Encoding: 7bit Organization: University of Chicago Mime-Version: 1.0 Date: Tue, 23 Jul 1996 00:01:09 GMT X-Mailer: Mozilla 1.1N (Macintosh; I; PPC) X-Url: news:bionet.molbio.ageing Lines: 14 Hi there, I would like to know how many methods now we have to check the apoptosis in vivo? I will summarize the answers after a while. Thanks, Hong Qin Biochem and Mol Biol Univ of Chicago From owner-ageing@net.bio.net Mon Jul 22 23:00:00 1996 Path: biosci!bloom-beacon.mit.edu!spool.mu.edu!uwm.edu!vixen.cso.uiuc.edu!cdc2.cdc.net!news.texas.net!nntp.primenet.com!news.goodnet.com!xroads!news.sprintlink.net!news-fw-12.sprintlink.net!moonbeam.aecom.yu.edu!post!skrao From: Sreenivasa Rao Newsgroups: bionet.molbio.ageing Subject: Postdoctoral feloowship available. Date: Tue, 23 Jul 1996 16:25:10 -0400 Organization: Albert Einstein College of Medicine Lines: 10 Message-ID: References: <4sg4em$lnt@mercury.hgmp.mrc.ac.uk> NNTP-Posting-Host: post.aecom.yu.edu Mime-Version: 1.0 Content-Type: TEXT/PLAIN; charset=US-ASCII X-Sender: skrao@post In-Reply-To: A postdoctoral fellowship for 1-2 years is available to work in my lab on Molecular biological aspects of Telomeres and aging. Interested candiadtes can send send C.V. by fax 718 343 3429 or email . ( rao@lij.edu ) The lab is located in LIJMC ( long Island Campus of Albert Einsteine college of Medicine, New Hyde Park, New York) From owner-ageing@net.bio.net Tue Jul 23 23:00:00 1996 Path: biosci!bcm.tmc.edu!pendragon!news.msfc.nasa.gov!newsfeed.internetmci.com!news.sprintlink.net!news-stk-200.sprintlink.net!news.sprintlink.net!news-stk-11.sprintlink.net!news.gate.net!stpfl1-38.gate.net!dhealth From: dhealth@gate.net (diane hein) Newsgroups: bionet.molbio.ageing Subject: ANYONE TAKING OXANDRIN FOR MUSCLE WASTING/LOSS OF STRENGTH?---please email me! Date: Wed, 24 Jul 1996 16:52:25 Organization: CyberGate, Inc. Lines: 11 Message-ID: NNTP-Posting-Host: stpfl1-38.gate.net X-Newsreader: Trumpet for Windows [Version 1.0 Rev A] If anyone is taking the anabolic steroid Oxandrin for muscle wasting or loss of strength (someone who is in a catabolic state and out of nitrogen balance) would you kindly email me. (Continued muscle wasting leads to early death) I would like to discuss diet, supplements, and the medication etc. Thank you. Diane Hein From owner-ageing@net.bio.net Wed Jul 24 23:00:00 1996 Path: biosci!CHOLLIAN.DACOM.CO.KR!iam From: iam@CHOLLIAN.DACOM.CO.KR (Hangjun Chang) Newsgroups: bionet.molbio.ageing Subject: "Disposable Soma" Theory of Aging Date: 25 Jul 1996 02:05:29 -0700 Organization: Dansan Public Health Care Center Lines: 77 Sender: daemon@net.bio.net Distribution: world Message-ID: <3014B3E5.3F3D@chollian.dacom.co.kr> NNTP-Posting-Host: net.bio.net Hi! Dear Friends who are interested in aging mechanism all around world. Today, I want to talk about the *disposable soma * theory. I have though over the connection between aging process and reproduction for a long time. In virtue of the *diposable soma* theory, I*ve got many insights into aging process. Many aging researches are focused on the cellular or molecular level of aging process. I want to see aging process in the level of organism. In that point, the theories of evolution of aging are helpful to me. According to the *disposable soma theory* because of the requirement for reproduction, natural selection favors a strategy that invests fewer resources in maintenance of somatic cells and tissues than are necessary for indefinite survival. This beautiful hypothesis are based on the fact that both somatic maintenance and reproduction require energy. This theory predicts that aging is due to the accumulation of unrepaired somatic defects and the primary genetic control of longevity operates through selection to raise or lower the investment in basic cellular maintenance systems in relation to the level of environment hazard. This theory also proposes that a high level of accuracy is maintained in immortal germ line cells, or alternatively, that any defective germ cells are eliminated. More interestingly, some taoists in ancient China avoided their reproductive activities in order to save energy, in their terms, 'Ki', turning it into making their body young as long as possible. I have several questions on the *disposable soma * theory 1. If this theory is true, early castrated animals must live more longer period than do non-castrated animals because early castration abolishes the energy demands for reproduction, turning some extra- energy back into the use for the body maintenance. I think it is the most simplest way to test this hypothesis. Is there any evidence to support the early castration effect on life extension in animals or even in humans? 2. How much energy do the gametogenesis require over the entire life of that organism? How does reproductive demands for energy compete with that of body maintenance and repair? In other words, for what life resources is such a competition made? 3. Is there any aging control gene that might be a coordinate regulator of a range of stress response genes that shift cellular physiology toward maintenance? In a recent issue .of Science, Gordon J. Lithgow et al. suggest that age-1 may be such a candidate because age-1 mutant strains of C. elegans are better equipped than their wild type counterparts to overcome the effects of extrinsic stress, such as better resistance to oxidative stress and fewer deletions of the mitochodrial genomes. I am thinking over the epigenetic control of such a gene to stop aging process. I am eager to know what signals or factors in blood can activate longevity assuring pathways in metabolism. 4. Is it true that higher accuracy is maintained in immortal germ line cells than do somatic cells? 5. Is there any evidence or opinion that sex hormones have some effects on aging process? I am looking forward to people who are very kind enough to answer my questions :) Thanks for reading my post. Hangjun Chang M.D. iam@chollian.dacom.co.kr 1. From owner-ageing@net.bio.net Thu Jul 25 23:00:00 1996 Path: biosci!utoronto.ca!sherry.nouraini From: sherry.nouraini@utoronto.ca (sherry nouraini) Newsgroups: bionet.molbio.ageing Subject: (none) Date: 26 Jul 1996 09:38:36 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 7 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Hi folks, I heared that there is supposed to be a cell-death meeting some time in October. Anybody knows about the specifics of this? Thanks in advance for your reply. Sherry Nouraini From owner-ageing@net.bio.net Fri Jul 26 23:00:00 1996 Path: biosci!agate!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!newsxfer2.itd.umich.edu!portc01.blue.aol.com!newstf01.news.aol.com!newsbf02.news.aol.com!not-for-mail From: mfossel@aol.com (MFossel) Newsgroups: bionet.molbio.ageing Subject: Reversing Human Aging Date: 27 Jul 1996 09:05:34 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 68 Sender: root@newsbf02.news.aol.com Message-ID: <4td46u$lb1@newsbf02.news.aol.com> Reply-To: mfossel@aol.com (MFossel) NNTP-Posting-Host: newsbf02.mail.aol.com As the author, I thought you might like a few generic comments. First: telomere shortening does not (even theoretically) "cause" aging. Rather it times the onset and progression of aging in cells, ultimately resulting in the myriad of disease that we collectively associate with (and sometimes define as) aging. The "causes" of aging are the usual suspects: free radicals, spontaneous isomerization, and so forth, as well as the subsequent damage they cause. Telomere shortening alters gene expression ("SGE" or senescent gene expression) by limiting a cell's ability to maintain homeostasis and fulfill its normal physiologic role vis a vis other cells. Second: many normal cells do not divide (postnatally) and therefore do not show telomere shortening, senescent gene expression, or direct cell senescence. Typical cells in this category include neurons (but not the glia cells which make up 90% of the nervous system by cell numbers) and muscle cells (but not the fibroblasts in the muscle, nor the endothelial cells lining the vessels which supply such muscle cells). The upshot is that many cells do not directly senescence, but show pathology which is (only theoretically in the case of dementia; with excellent evidence in the case of atherosclerosis and secondary heart attacks and strokes) secondary to senescent changes in cells which DO divide and whose telomeres shorten. Neurons depend on glial cells; cardiac muscle cells depend on endothelial cells that line the vessels. In both cases, non-aging cells are the "innocent bystanders" to the pathology of cells which do age. It is hard to believe how people STILL confuse cell division with aging pathology and try to cite neurons and muscle cells as evidence against the telomere theory of aging when their very lack of *direct* aging changes supports the theory. It seems to come up in every posted note I read. Aging pathology in non-dividing somatic cells is secondary. Aging pathology in non-dividing cells is secondary. Aging pathology in non-dividing cells is secondary. I'll bet I am still explaining this to people in a hundred years... Third: we can *probably* find a therapeutic window between aging and cancer. The approach would be to first use a TI (telomerase inhibitor) to force senescence (and death) of cancer cells, THEN proceed to telomerase activation in remaining cells. If we reconstitute youthful immune function (aged lymphocytes have shorter telomeres), we may enable the immune system to more effectively recognize and more efficiently kill remaining early clonal populations of cancer cells whose telomeres were still sufficiently long to survive initial TI therapy. Theory... Fourth: is it too early to speculate? Not in my mind: clearly others disagree, stating that the book should be banned (seriously) or was irresponsible. My own feeling is that: 1) the general public is capable (on the average) of drawing its own conclusions, and that 2) the social implications of altering the healthy human lifespan will be so profound that early discussion is imperative. Fifth: telomere shortening does NOT merely correlate with cell aging, but is causal. This was true until three years ago and the data was published only this spring (March 15, 1996 in EMB0 by Jerry Shay, Woody Wright, et al) when we found that lengthening the telomere pushed back the Hayflick limit correspondingly. Causing telomere shortening the "cause" of cellular senescence is still sloppy: see point one above. Sixth: yes, insects somatic cells are post-mitotic. The cells are "terminally differentiated". Telomere length has -- as far as I know -- no particular relevance to insect aging. Insects are probably the classic case of "wear and tear" as the cause of aging. Humans are not insects. In humans, cells continue to divide and telomeres play a role in altering gene expression, undercutting cell defences (eg against free radical damage) and cell function, and timing aging and its defining pathology. Michael Fossel, MD, PhD Author, "Reversing Human Aging" From owner-ageing@net.bio.net Sat Jul 27 23:00:00 1996 Path: biosci!agate!newsgate.duke.edu!news-feed-1.peachnet.edu!usenet.eel.ufl.edu!news-res.gsl.net!news.gsl.net!uwm.edu!news.cse.psu.edu!news.math.psu.edu!news.iag.net!newsfeeder.sdsu.edu!nntp04.primenet.com!news.shkoo.com!nntp.primenet.com!news.cais.net!van-bc!unixg.ubc.ca!info.ucla.edu!newsfeed.internetmci.com!newsxfer2.itd.umich.edu!portc01.blue.aol.com!newstf01.news.aol.com!newsbf02.news.aol.com!not-for-mail From: mfossel@aol.com (MFossel) Newsgroups: bionet.molbio.ageing Subject: Re: Future Date: 28 Jul 1996 12:31:05 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 13 Sender: root@newsbf02.news.aol.com Message-ID: <4tg4k9$q9d@newsbf02.news.aol.com> References: Reply-To: mfossel@aol.com (MFossel) NNTP-Posting-Host: newsbf02.mail.aol.com Luke: Dave Cassarino is correct. The usual figures for dietary restriction (with careful attention to vitamin and mineral requirements) is about 30-40% of a "standard diet". The best references are from Richard Weindruch at the University of Wisconsin. See especially either his book (with Roy Walford) "The retardation of aging and disease with dietary restriction" or his recent article (last few months) in Scientific American. Best wishes, Michael Fossel, MD, PhD Author, Reversing Human Aging From owner-ageing@net.bio.net Sat Jul 27 23:00:00 1996 Path: biosci!agate!newsgate.duke.edu!news-feed-1.peachnet.edu!usenet.eel.ufl.edu!news-res.gsl.net!news.gsl.net!portc01.blue.aol.com!newstf01.news.aol.com!newsbf02.news.aol.com!not-for-mail From: mfossel@aol.com (MFossel) Newsgroups: bionet.molbio.ageing Subject: Re: Mitochondria oxidative damage? Date: 28 Jul 1996 12:06:03 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 24 Sender: root@newsbf02.news.aol.com Message-ID: <4tg35b$pp6@newsbf02.news.aol.com> References: <4sg4em$lnt@mercury.hgmp.mrc.ac.uk> Reply-To: mfossel@aol.com (MFossel) NNTP-Posting-Host: newsbf02.mail.aol.com Hello Gary. Mitochondria are one of the driving sources of aging damage within cells: they produce about 95% of the free radicals and as the cell "ages", they leak. You are, of course, right about the maternal source of mitchondria. Remember, however that the maternal *germ cell* line of mitochondria has not shown and sign of aging in the past 1-2 billion years since this particular organelle first took up permanent residence within eukaryotic cells. Although (retrospectively in surviving germ cell line mitochondria) they have not age, they show oxidative degradation within a few decades in human somatic cells. This implies that non-mitochondrial (eg, nuclear genes, etc) factors determine mitochondrial "aging", not merely mitochondrial damage *per se*. Telomere theory of aging suggests that homeostatic defences against (among other things) mitochondrial oxidative damage are "down-regulated" as the telomere shortens. Far from being mutually exclusive, mitochondrial damage plays a pivotal role in the intracellular aging process in telomere aging theory. The same in true of cumulative DNA damage (and down-regulation of DNA repair), protein turnover rates, etc. Thanks for your thoughts: you are pretty close to hitting the nail on the head Best wishes, Michael Fossel, MD, PhD Author, Reversing Human Aging From owner-ageing@net.bio.net Sat Jul 27 23:00:00 1996 Path: biosci!GNN.COM!DSchwa1234 From: DSchwa1234@GNN.COM (Douglas Schwartz) Newsgroups: bionet.molbio.ageing Subject: Re: Reversing Human Aging Date: 27 Jul 1996 17:10:49 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 42 Sender: daemon@net.bio.net Distribution: world Message-ID: <199607280010.UAA28926@mail-e2b-service.gnn.com> NNTP-Posting-Host: net.bio.net mfossel@aol.com (MFossel) wrote: >Sixth: yes, insects somatic cells are post-mitotic. The > cells are >"terminally differentiated". Telomere length has -- as far > as I know -- >no particular relevance to insect aging. Insects are > probably the classic >case of "wear and tear" as the cause of aging. Humans are > not insects. >In humans, cells continue to divide and telomeres play a role > in altering >gene expression, undercutting cell defences (eg against free > radical >damage) and cell function, and timing aging and its defining > pathology. Lobsters & insects are all arthropods, with the former being the largest of them all. I don't know if their anomalously large size has some relevance to the great ages lobsters can attain, but I think the above statement of Fossel points out important anomalies which are derserving of intensive investigation. The fact that lobsters exhibit indeterminate growth (in contrast to all the other arthropods I am aware of) is probably central to all this. Albert Szent-Gyorgyi argued