From owner-ageing@net.bio.net Mon Oct 03 23:00:00 1994 Path: biosci!daresbury!bioftp.unibas.ch!rc1.vub.ac.be!idefix.CS.kuleuven.ac.be!ub4b!EU.net!howland.reston.ans.net!swrinde!sgiblab!sgigate.sgi.com!enews.sgi.com!decwrl!netcomsv!ix.netcom.com!netnews From: Bhupi@ix.netcom.com (Bhupinder Singh) Newsgroups: bionet.molbio.ageing Subject: Need help: Plague vaccine, save hundreds of lives S.O.S. Date: 4 Oct 1994 05:33:55 GMT Organization: Netcom Lines: 6 Distribution: world Message-ID: <36qpg3$l57@ixnews1.ix.netcom.com> NNTP-Posting-Host: ix-sj9-28.ix.netcom.com Due to sudden break in of the plague epidamic in India, there are lot of anxities for demand of vaccine for human plague. Any information regading such vaccine from any agency would help save hundreds of thousands lives. Please get in touch with me as soon as possible. Bhupi Ph.(408) 383-0800 From owner-ageing@net.bio.net Tue Oct 04 23:00:00 1994 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!usc!howland.reston.ans.net!pipex!lyra.csx.cam.ac.uk!warwick!unicorn.nott.ac.uk!macfd.biochem.nottingham.ac.uk!user From: mbxfd@unicorn.nott.ac.uk (Fergus Doherty) Newsgroups: bionet.molbio.ageing Subject: Antibodies to oxidized proteins Followup-To: bionet.molbio.ageing Date: 5 Oct 1994 09:46:08 GMT Organization: Nottingham University, UK. Lines: 12 Distribution: world Message-ID: NNTP-Posting-Host: macfd.biochem.nottingham.ac.uk Anybody out there got abs to malonyldialdehyde-modified proteins or 4-HNE-modified proteins eg. like the autoantibodies that some people raise to oxidized LDL? If they have any chance I could have some for investigations into protein oxidation and intracellular protein degradation? Fergus Doherty, dept. Biochemistry, University Medical School, Queen's Medical Centre, Nottingham NG7 2UH Tel: 602 709366 FAX 602 422225 Internet: mbxfd@unicorn.nott.ac.uk From owner-ageing@net.bio.net Tue Oct 04 23:00:00 1994 Path: biosci!rutgers!gatech!howland.reston.ans.net!europa.eng.gtefsd.com!news.umbc.edu!haven.umd.edu!cville-srv.wam.umd.edu!mag From: mag@wam.umd.edu (Michael) Newsgroups: bionet.molbio.ageing,um.housing Subject: test - please ignoreignore Date: 5 Oct 1994 20:46:34 GMT Organization: University of Maryland, College Park Lines: 2 Message-ID: <36v3ba$frr@cville-srv.wam.umd.edu> NNTP-Posting-Host: rac5.wam.umd.edu test From owner-ageing@net.bio.net Wed Oct 05 23:00:00 1994 Path: biosci!agate!soda.CSUA.Berkeley.EDU!tjyeh From: tjyeh@soda.CSUA.Berkeley.EDU (Tsung-Jui Yeh) Newsgroups: bionet.molbio.ageing Subject: Hayflick limit for rapid dividing cells Date: 6 Oct 1994 03:26:04 GMT Organization: University of California, Berkeley Lines: 8 Message-ID: <36vqoc$dme@agate.berkeley.edu> NNTP-Posting-Host: soda.csua.berkeley.edu X-Newsreader: TIN [version 1.2 PL2] I was wondering about the Hayflick limit for rapid dividing cells like ones that line the stomach and also cells of the cornea. Do these cells have the same Hayflick limit as fibroblasts? If so, why can these cells afford to divide so fast? Thanks From owner-ageing@net.bio.net Wed Oct 05 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!agate!howland.reston.ans.net!usc!elroy.jpl.nasa.gov!lll-winken.llnl.gov!fnnews.fnal.gov!gw1.att.com!nntpa!not-for-mail From: norm@chico.uucp (Norman E. Andrews [ MT 2C-402 9089575786 NC6241000 ]) Subject: Re: Hayflick limit for rapid dividing cells Message-ID: Sender: news@nntpa.cb.att.com (Netnews Administration) Nntp-Posting-Host: chico.wh.att.com Organization: AT&T, Whippany, NJ References: <36vqoc$dme@agate.berkeley.edu> Date: Thu, 6 Oct 1994 14:04:41 GMT Lines: 5 I thought the Hayflick Limit turned out to be spurious, that it was due to improper culture techniques (poor nutrition or contamination). Anyone know about this? Norm Andrews, AT&T, norm@chico.wh.att.com From owner-ageing@net.bio.net Wed Oct 05 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!rutgers!umdnj!soma!pgrandon From: pgrandon@soma.UMDNJ.EDU (Patricia Grandoni) Subject: WWW site for ageing? Message-ID: Keywords: WWW Sender: news@umdnj.edu () Organization: Univ. of Medicine and Dentistry of NJ Date: Thu, 6 Oct 1994 15:55:25 GMT Lines: 9 Hi, We are looking for a WWW site (or gopher) based on the subject of ageing or geriatrics. In advance, thank you, Patti Grandoni-- Patricia Grandoni internet pgrandon@umdnj.edu UMDNJ/ACS User Support Camden (609)757-7875 Camden/Stratford Stratford (609)566-6805 From owner-ageing@net.bio.net Sun Oct 09 23:00:00 1994 Path: biosci!ilr.uucp.free.net!gavrilov From: gavrilov@ilr.uucp.free.net ("Leonid Gavrilov") Newsgroups: bionet.molbio.ageing Subject: INVITATION FOR DEBATES !!! Date: 10 Oct 1994 12:27:17 -0700 Organization: A.N.Belozersky Institute, Moscow State University Lines: 342 Sender: daemon@net.bio.net Distribution: world Message-ID: <2e99a92f.ilr@ilr.uucp.free.net> NNTP-Posting-Host: net.bio.net TO: FROM: Dr. Leonid A.Gavrilov, Ph.D. A.N.Belozersky Institute Moscow State University 119899 Moscow, RUSSIA FAX: 7 (095) 939-0338 7 (095) 939-3181 October 10, 1994 Dear Sirs, Recently BioEssays (16/8 AUG 1994, p.591-593) has published very hot scientific debates between Dr.Leonard Hayflick and us on the so-called 'in vitro ageing'. Since the Journal space was restricted, only 2 opposite views were published in a very short form without detailed discussion. For this reason we kindly invite all the interested persons to continue these debates here, at AGEING list ! We would be most grateful for any comments on our debates published in BioEssays and we would be also very happy to answer any questions. PLEASE WRITE !!! Thank you in advance for your kindness. Sincerely yours, Dr.Leonid A.Gavrilov, Ph.D. and Dr.Natalia S.Gavrilova, Ph.D. P.S.: CV is printed below for introduction and additional information. ************************************************************************* C U R R I C U L U M V I T A E Dr. Leonid A. Gavrilov, Ph.D. Phone: 7 (095) 427 0047 Principal Research Scientist FAX: 7 (095) 939 0338 or A.N.Belozersky Institute 7 (095) 939 3181 Moscow State University E-mail addresses: Moscow 119899 aeiveos@glas.apc.org Russia Date of Birth: August 28, 1954 Place of Birth: USSR (Russia), town of Sverdlovsk (now Ekaterinburg) Research interests: Mechanisms of ageing, age-related mortality, longevity. Education: Ph.D. - Moscow State University (1980) in mortality kinetics in human populations and animal models, with emphasis on mathematical models of mortality. M.Sc. - Moscow State University (1976) in mechanisms of aging with emphasis on mathematical models of aging Professional Experience: 1991-Present Principal Research Scientist, A.N.Belozersky Institute, Moscow State University. 1987-1991 Senior Research Scientist, A.N.Belozersky Institute, Moscow State University. 1980-1987 Research Scientist, A.N.Belozersky Institute, Moscow State University. Professional Activities and Other Positions: - Member of the New York Academy of Science - Principal Investigator of the International Science Foundation Research Grant # M7E000. - Chairman of the Subsection of the Biology of Life Span at Moscow Society of Naturalists (1981-1992). - Expert (book reviewer) for journals AGE AND AGEING, AGEING AND SOCIETY, J.GENERAL BIOLOGY and Publishers "MIR". - Expert (peer reviewer) for journals MATHEMATICAL POPULATION STUDIES, J.GENERAL BIOLOGY. - Chairperson of the Biological Session at the II European Congress of Gerontology (Madrid, 1991). Certificate signed by F.Guillen Llera, General Secretary of the Congress. - Expert (book editor) for Institute of Scientific Information (VINITI, Moscow). - Fellow of Moscow Society of Naturalists. - Senior Research Scientist at the Russian Academy of Sciences Institute for System Analysis. - Scientific Secretary of Demographic Section of Moscow House of Scientists (1984-1991). - Fellow of the Moscow House of Scientists. Awards: - International Science Foundation (ISF) 1994 Research Grant #M7E000. - International Science Foundation (ISF) 1993 Emergency Grant Award. - International Science Foundation (ISF) 1994 Emergency Grant for Russian Scientists of the Top Category. - The Certificate from the International Association of Gerontology (1993) signed by the President and the Secretary General of the International Association of Gerontology. - A.N.Belozersky Institute 1991 Award for the best scientific research in the Institute in 1990-1991. - Moscow Society of Naturalists 1989 Award for the best scientific research in natural science in 1986-1988. - Grant Award with invitation to European Population Conference (Paris, October 1991). - Financial Award with invitation of giving a lectures to Trinity College, Cambridge University (December, 1991). - Financial Award with invitation to the Annual Meeting of British Biochemical Society (Southampton, April, 1992). Publications: 65 publications, including 5 books. Selected publications in the most prestigeous scientific peer reviewed journals are: - "Sex and Longevity", Nature, 1994, vol.367, No.6463, p.520. - "Fruit Fly Aging and Mortality", Science, 1993, vol.260, No.5114, p.1565. - "When Your Time's Up", British Medical Journal, 1993, vol.306, No.6880, p.796. - "Human Life Span Stopped Increasing: Why?", Gerontology, 1983, vol.29, pp.176-180. - "Life Span is Determined by Resting Metabolic Rate of Parents Only!", Age, 1989, vol.12, p.113. - "Human Species-Specific Life-Span: Its Estimation and Interpretation", Age, 1985, vol.8, p.94. - "A New Trend in Human Mortality Decline: Derectangularization of the Survival Curve", Age, 1985, vol.8, p.93. - "Biology of Aging (Book Review)", Age and Ageing, 1993, vol.22, pp.233-234. - "Evolutionary Biology of Aging (Book Review)", Ageing and Society, 1992, vol.12, No.4, pp.539-541. - "How Many Cell Divisions in 'Old' Cells?", International Journal of Geriatric Psychiatry, 1993, vol.8, No.6, p.528. - "Common Sense and the Limits to Life", International Journal of Geriatric Psychiatry, 1993, vol.8, No.8, p.695. - "Historically Stable Indices of Mortality and their Use for Medical Geography", Geographia Medica, 1984, vol.14, pp.305-306. - "Epidemiologic Approach to the Biology of Human Life Span", Geographia Medica, 1985, vol.15, pp.40-64. The key publication where the main results of the previous studies are summarised is: THE BIOLOGY OF LIFE SPAN: A QUANTITATIVE APPROACH. By Leonid A.Gavrilov and Natalia S.Gavrilova. Harwood Academic Publishers: 1991. Pp. 385, $ 120, ISBN 3-7186-4983-7. Positive reviews of this book were published by the following journals: 1. AGE AND AGEING, 1992, vol.21, No.5, pp.386-387. 2. AGEING AND SOCIETY, 1991, vol.11, No.4, pp.509-510. 3. ARCHIVES OF GERONTOLOGY AND GERIATRICS, 1992, vol.15, No.2, pp.192-194. 4. ARGOMENTI DI GERONTOLOGIA, 1993, vol.5, No.2, p.91. 5. BIOESSAYS, 1993, vol.15, No.5, pp.359-362. 6. BOLLETTINO DELLA SOCIETA ITALIANA DI GERONTOLOGIA E GERIATRIA, 1992, No.7, p.1. 7. BRITISH MEDICAL JOURNAL, 1992, vol.305, No.6850, p.431. 8. EDUCATIONAL GERONTOLOGY, 1993, vol.19, No.1, pp.92-93. 9. EXPERIMENTAL GERONTOLOGY, 1992, vol.27, pp.251-253. 10. FREE RADICAL BIOLOGY & MEDICINE, 1992, vol.12, pp.331-332. 11. GERONTOLOGIST, 1991, vol.31, No.5, p.707. 12. HUMAN BIOLOGY, 1992, vol.64, No.4, pp.630-632. 13. INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, 1992, vol.7, No.8, p.614. 14. JOURNAL OF CROSS-CULTURAL GERONTOLOGY, 1993, vol.8, No.3, pp.281-290. 15. JOURNAL OF EPIDEMIOLOGY & COMMUNITY HEALTH, 1992, vol.46, No.6, p.630. 16. JOURNAL OF THE INSTITUTE OF ACTUARIES, 1992, vol.119, Part II, pp.379-381. 17. JOURNAL OF ORTHOMOLECULAR MEDICINE, 1993, vol.8, No.1, pp.59-60. 18. NATURE, 1991, vol.352, 29 August, pp.767-768. 19. POPULATION AND DEVELOPMENT REVIEW, 1992, vol.18, No.3, pp.555-558. 20. POPULATION STUDIES, 1992, vol.46, No.2, pp.366-367. 21. QUARTERLY REVIEW OF BIOLOGY, 1993, vol.68, p.92. 22. STATISZTIKAI SZEMLE (STATISTICAL REVIEW, In Hungarian), 1992,vol.70,No.6,pp.546-547. Response of the Leading Scientists to the Scientific Research and the Book by L.A.Gavrilov: "HIGHLY RECOMMENDED FOR STIMULATING FRESH APPROACHES ... " - Professor Roy L.Walford, M.D., UCLA School of Medicine, USA. THE GERONTOLOGIST, 1991, vol.31, No.5, p.707. "CLEARLY, THIS IS A VERY INTERESTING, PROVOCATIVE AND THOUGHT-PROVOKING BOOK" - Dr. Ward Dean, M.D., The Center for Bio-Gerontology, Pencasola, Florida, USA. EXPERIMENTAL GERONTOLOGY, 1992, vol.27, No.2, pp.251-253. "THIS IS AN INTERESTING BOOK, FULL OF TABLES AND DATA AND POLEMICAL IN ITS APPROACH." - Professor William A.Pryor, Director of Biodynamic Institute, Louisiana State University, Baton Rouge, LA,USA. FREE RADICAL BIOLOGY & MEDICINE, 1992, vol.12, pp.331-332. "IT BRINGS TO BEAR A FRESH APPROACH WHOSE IDEAS ARE LOGICALLY PRESENTED AND DEVELOPED". - Dr. Brian Merry, Ph.D., Institute of Human Aging, University of Liverpool, United Kingdom. AGEING AND SOCIETY, 1991, vol.11, No.4, pp.509-510. "GOOD NEW BOOK ON AGEING". - Dr. Thomas B.L.Kirkwood, Ph.D. Head of the Laboratory of Mathematical Biology, National Institute for Medical Research, London, United Kingdom. NATURE, 1991, vol.352, 29 August, pp.767-768. "... SHOULD BE READ BY ANYONE SERIOUSLY INTERESTED IN AGEING. ... YOU WILL FIND THIS A SURPRISINGLY GOOD 'READ', AND A MUST FOR EVERY LIBRARY". - Dr. D.Sebastian Fairweather, Physician, Department of Geriatric Medicine, Oxford, United Kingdom. AGE AND AGEING, 1992, vol.21, No.5, pp.386-387. "THE BOOK FEATURES QUITE A BIT OF DEMOGRAPHIC THEORY AND ANALYSIS. ... IT IS REFRESHING" - Professor Michael R.Rose, University of California, Irvine, USA. ANNALS OF HUMAN BIOLOGY, 1992, vol.19, No.3, pp.320-321. "THE GAVRILOVS HAVE MADE A VALUABLE CONTRIBUTION TO THE STUDY OF LIFE SPAN, AND ANY FUTURE WORK ON THE SUBJECT WILL HAVE TO TAKE ACCOUNT OF THE RICH CONTENTS OF THIS BOOK". - Dr. Vaino Kannisto, Former United Nations Adviser on Demography POPULATION STUDIES, 1992, vol.46, No.2, pp. 366-367. "EIN AKTUELLES BUCH, DAS SICHERLICH DIE INTERNATIONALE DISKUSSION DES PROBLEMS BEFORDERN KANN." - Prof. Dr. Ingeborg Falck, Berlin, Germany. ZEITSCHRIFT FUR GERONTOLOGIE, 1991, Band 25, Heft 1, S.56. "THE BOOK IS WELL WRITTEN, EASY TO READ, AND SHOULD BE OF INTEREST TO A WIDE SPECTRUM OF READERS INCLUDING PHYSICIANS, BIOLOGISTS, BIOCHEMISTS, GERONTOLOGISTS..." - Prof. Robert W.Gracy, University of North Texas, USA. EDUCATIONAL GERONTOLOGY, 1993, vol.19, No.1, pp.92-93. "... THIS BOOK IS A HIGHLY VALUABLE CONTRIBUTION TO THE DISCIPLINE. ...THIS BOOK SHOULD MAKE SCIENTISTS TAKE NOTICE OF RESEARCH ON AGING AND LONGEVITY ... IN THE FORMER SOVIET UNION" - Dr. S.Jay Olshansky, Ph.D., University of Chicago, USA POPULATION AND DEVELOPMENT REVIEW, 1992, vol.18, No.3, pp.555-558. "... MANY WILL FIND AN EXCURSION INTO IT STIMULATING". - Dr. Emily Grundy, Lecturer in Gerontology, Age Concern Institute of Gerontology, King's College, London, UK. BRITISH MEDICAL JOURNAL, 1992, vol.305, No.6850, p.431. "GAVRILOV MAKES THE BEST ATTEMPT I KNOW OF TO DISTINGUISH HOW LONG PEOPLE COULD LIVE FROM HOW LONG THEY ACTUALLY LIVE - ONE OF THE MORE DIFFICULT TASKS FOR BOTH BIOLOGY AND STATISTICS... GAVRILOV'S SCHOLARSHIP IS IMPRESSIVE". - Professor Nathan Keyfitz, International Institute for Applied Systems Analysis, Laxenburg, Austria. MATHEMATICAL POPULATION STUDIES, 1991, vol.3, No.2, p.161. "LEONID GAVRILOV IS A TOP-FLIGHT STATISTICAL POPULATION BIOLOGIST... THE AREA IS IMPORTANT WELL BEYOND THE CONFINES OF BIOLOGICAL GERONTOLOGY AND EXTENDS INTO POLITICS AND SOCIAL PLANNING. GAVRILOV IS VERY GOOD ON JUST THIS SORT OF THING. HE HAS A FRESH APPROACH, NEW IDEAS, A GREAT DEAL OF DATA NOT READILY AVAILABLE ELSEWHERE." - Roy. L. Walford, Professor of Pathology, UCLA School of Medicine, USA. MATHEMATICAL POPULATION STUDIES, 1991, vol.3, No.2, p.161. "THIS BOOK IS DIRECTED TOWARD RESEARCHERS INTERESTED IN STATISTICAL PATTERNS AND MATHEMATICAL MODELS OF HUMAN LIFE SPAN. FOR STUDENTS WITHIN THIS DEFINED AREA OF RESEARCH, THIS TEXT OFFERS A GOOD HISTORICAL PERSPECTIVE, INSIGHT INTO THE RUSSIAN LITERATURE, AND INSIGHT INTO THE QUANTITATIVE ANALYSIS OF LIFE SPAN" - Dr. Deborah A.Roach, Department of Zoology, Duke University, Durham, USA. ECOLOGY, 1992, vol.73, No.1, pp.379-381. "THIS BOOK IS IN ESSENCE A BIOSTATISTICAL ANALYSIS OF THE PROBLEMS OF LIFESPAN, HUMAN AND ANIMAL. ... THE LITERATURE IN MANY LANGUAGES HAD CLEARLY BEEN WELL COVERED, AND MUCH HAS BEEN MADE OF NATIONAL AND OTHER MORTALITY STATISTICS IN THIS CENTURY. ... A USEFUL SOURCE BOOK." - Dr. F.I.Caird, D.M., F.R.C.P., Professor of Geriatric Medicine, Southern General Hospital, Glasgow, UK. J. OF CLINICAL AND EXPERIMENTAL GERONTOLOGY, 1992, vol.14, No. 3 & 4, p.309. "... THE READER WILL BENEFIT ENORMOUSLY FROM THE BROADENING OF PERSPECTIVE AS A RESULT OF EXPOSURE TO THE GAVRILOVS' THEORIES ON THE BIOLOGY OF LIFE SPAN" - Dr. M. Michael Akiyama, University of Michigan, Dearborn, USA. HUMAN BIOLOGY, 1992, vol.64, No.4, pp.630-632. "THIS IS A PROVOCATIVE AND REFRESHING BOOK" - Dr.Alan R.Hipkiss, Age Concern Institute of Gerontology, King's College London, UK. INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, 1992, vol.7,No.8,p.614. "THIS BOOK SHOULD BE READ BY ALL MEMBERS OF THE PROFESSION INTERESTED IN MORTALITY - WHICH SHOULD BE ALL MEMBERS OF THE PROFESSION" - Dr. H.A.R.Barnett, Institute of Actuaries, UK. J.OF THE INSTITUTE OF ACTUARIES, 1992, vol.119, Part II, pp.379-381. "TO SUM UP, THE BOOK IS SUBSTANTIAL, INTERESTING AND BRINGS FRESH AIR. WE CAN CONFIDENTLY COMMEND ITS STUDY TO ALL SCIENTISTS ... " - Dr. Janos Izsak, Department of Zoology, Berzsenyi Teachers' College, Szombathely, Hungary. ARCHIVES OF GERONTOLOGY AND GERIATRICS, 1992, vol.15, No.2,pp.192-194. "A GENERAL THEORY OF LIFESPAN IS THUS CREATED." - - Dr. Norman Vetter, University Hospital of Wales, Cardiff, UK. J.OF EPIDEMIOLOGY & COMMUNITY HEALTH, 1992, vol.46, No.6, p.630. "I FOUND IT TO BE HIGHLY REWARDING READING." - Dr. Edward J.Masoro, University of Texas Health Science Center. QUARTERLY REVIEW OF BIOLOGY, 1993, vol.68, p.92. "THIS ... IS AN EXCELLENT BOOK. ... NOBODY INTERESTED IN AGING SHOULD FAIL TO READ". - Dr. C.S.Downes, Department of Zoology, University of Cambridge, UK. BIOESSAYS, 1993, vol.15, No.5, pp.359-362. "...PROVOCATIVE AND ENTERTAINING READING AND CAN BE RECOMMENDED TO ANYONE WITH AN INTEREST IN BIOLOGICAL AGING." - Dr. Douglas E.Crews, Department of Anthropology, Ohio State University, USA JOURNAL OF CROSS-CULTURAL GERONTOLOGY, 1993, vol.8, No.3, pp.281-290. "IT DESERVES TO BE READ WIDELY. SCIENTISTS AND PHYSICIANS WHO ARE INTERESTED IN THE AGING OF POPULATIONS OR OF INDIVIDUALS WILL BE MUCH MORE EFFECTIVE IN THEIR WORK IF THEY BECOME FAMILIAR WITH THE SUBJECT MATTER OF THIS BOOK." - JOURNAL OF ORTHOMOLECULAR MEDICINE, 1993, vol.8, No.1, pp.59-60. *********************************THE END****************************** From owner-ageing@net.bio.net Mon Oct 10 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!lyra.csx.cam.ac.uk!doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Date: 11 Oct 1994 10:12:59 GMT Organization: University of Sussex Lines: 28 Message-ID: <37dofb$3ln@infa.central.susx.ac.uk> References: <36vqoc$dme@agate.berkeley.edu> NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] Tsung-Jui Yeh (tjyeh@soda.CSUA.Berkeley.EDU) wrote: : I was wondering about the Hayflick limit for rapid dividing cells like : ones that line the stomach and also cells of the cornea. Do these cells : have the same Hayflick limit as fibroblasts? If so, why can these cells : afford to divide so fast? : Thanks Cells from different tissues display different Hayflick limits. This means that some cells like fibroblasts may go through about 50 to 70 population doublings, in about 150 cell generations. On the other hand, adult dermal fibroblasts, chondrocytes experience many fewer generations. Lymphocytes seem in most growth media, to experience only about 23 population doublings. So, at the moment we do not really know whether there is one fixed Hayflick limit; the evidence available so far would suggest that there are specific Hayflick limits for different tissues. This clearly has important implications for the homeostasis of each individual tissue. Moreover, it is very well established that the same cell type from different animal species show a species-specific Hayflick limit; this is part of the evidence for the notion that the Hayflick limit is genetically controlled. -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Telephone: +44.273.67.83.03 FAX: +44.273.67.84.33 From owner-ageing@net.bio.net Mon Oct 10 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!lyra.csx.cam.ac.uk!doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Date: 11 Oct 1994 10:21:18 GMT Organization: University of Sussex Lines: 32 Message-ID: <37douu$3r5@infa.central.susx.ac.uk> References: <36vqoc$dme@agate.berkeley.edu> NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] Norman E. Andrews [ MT 2C-402 9089575786 NC6241000 ] (norm@chico.uucp) wrote: : I thought the Hayflick Limit turned out to be spurious, that it was due : to improper culture techniques (poor nutrition or contamination). Anyone : know about this? : Norm Andrews, AT&T, norm@chico.wh.att.com No, the hayflick limit is NOT due to culture techniques. The best experimental evidence for this statement is the well established observation that when the same cell types, from different species are grown under identical conditions with the identical solutions in the same incubator, quite different Hayflick limits are observed. The observation is quite good evidence that the Hayflick limit is due to the cells and not to the medium. The second line of evidence is the existence of human genetic disorders like Werner's syndrome, which is a premature ageing disease, in which the identical cells to a normal control, in the same mediium in the same incubator, do in fact grow as much as 1000 times less than the control cells. This again makes it clear that the hayflick limit is due the cells and not the medium. Finally, one can grow normal cells and observe an Hayflick limit and tumour cells and not observe any limit; in the same medium and incubator. In general therefore, the hayflick limit is a biological phenomenon, and not a culture artifact. This evidence given above does not prove that the culture conditions are totally irrelevant to the way normal cells grow in culture; the culture conditions very clearly do modulate the growth rate and the Hayflick limit, but only within narrow boundaries. -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Telephone: +44.273.67.83.03 FAX: +44.273.67.84.33 From owner-ageing@net.bio.net Mon Oct 10 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!rutgers!att-out!nntpa!not-for-mail From: norm@chico.uucp (Norman E. Andrews [ MT 2C-402 9089575786 NC6241000 ]) Subject: Re: Hayflick limit for rapid dividing cells Message-ID: Sender: news@nntpa.cb.att.com (Netnews Administration) Nntp-Posting-Host: chico.wh.att.com Organization: AT&T, Whippany, NJ References: <36vqoc$dme@agate.berkeley.edu> <37dofb$3ln@infa.central.susx.ac.uk> Date: Tue, 11 Oct 1994 17:11:02 GMT Lines: 92 Hello, Sidney Shall, Thank you for your reply about the Hayflick limit. My thought was that the Hayflick limit turned out to spurious due to improper culture techniques (poor nutrition or contamination). While _some_ of the evidence you mentioned (which I abstracted from your posts for presentation and comment below) does imply the existence of a Hayflick limit, it is not yet clear in my mind that _all_ of the evidence you advanced implies a genetically determined limit that would also exist in vivo. Perhaps you would be kind enough to post further explanations to aid my understanding. I don't think you mentioned in vivo tests, but I'll bring that subject up. One can still interpret the aging differences between in vivo and in vitro as an artifact of inadequate culture technique, if the nutrition delivery and waste/immune system disposal systems??? of in vivo differ from and are probably better than what scientists are now able to provide in vitro. So what I am suggesting is that there may indeed be a genetically related Hayflick limit that occurs with in vitro testing, but that such a limit may not exist in vivo, or if it does, perhaps not to an extent that explains the sensescence of man. I am ignorant of whatever in vivo testing may have been done to explore this. In 2 replies to 2 persons' queries on Hayflick limits you wrote (I have deleted what I think is not essential to this my current post, and added numbers): | | From: bafa1@central.susx.ac.uk (Sydney Shall) | Organization: University of Sussex | | [1] | No, the hayflick limit is NOT due to culture techniques. | ...when the same cell types, from different species are | grown under identical conditions with the identical solutions in the | same incubator, quite different Hayflick limits are observed. The | observation is quite good evidence that the Hayflick limit is due to the | cells and not to the medium. ... I fail to see your conclusion in [1]. One simple and perhaps wrong explanation will serve to illustrate: Suppose the metabolism of the different cell types proceeds at different rates, but that they all require something that is inadequately provided by the culture technique, perhaps nutrition or waste disposal. There would be a genetic link, expressed thropugh different rates of metabolism, but the inadequate culture technique could be the cause of existence of the (different) Hayflick limits. The magnitude of the differences would be genetically related, but the _existence_ of the limit would be because of the culture technique. | | [2] | The second line of evidence is the | existence of human genetic disorders like Werner's syndrome, which is a | premature ageing disease, in which the identical cells to a normal | control, in the same mediium in the same incubator, do in fact grow as | much as 1000 times less than the control cells. This again makes it | clear that the hayflick limit is due the cells and not the medium. ... Again , by similar reasoning, I fail to see your conclusion in [2]. | | [3] | Finally, one can grow normal cells and observe an Hayflick limit and | tumour cells and not observe any limit; in the same medium and | incubator. ... Now this seems to me to be the most solid evidence, except I still wonder: could tumor cells have requirements for metabolism that are in _some_ respects less demanding than normal cells? | | [4] | Cells from different tissues display different Hayflick | limits. ... ... the evidence available so far would suggest | that there are specific Hayflick limits for different tissues. Again, my objection is the same as for [1]. | | [5] | In general therefore, the hayflick limit is a biological | phenomenon, and not a culture artifact. ... | This evidence given above does not prove that the culture conditions are | totally irrelevant to the way normal cells grow in culture; the culture | conditions very clearly do modulate the growth rate and the Hayflick | limit, but only within narrow boundaries. | | -- | Sydney SHALL, | Laboratory of Cell and Molecular Biology, | Biology Building, Univ. of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND | Telephone: +44.273.67.83.03 FAX: +44.273.67.84.33 | So I hope you can lay to rest my uneasiness with your previous explanations, and also shed some light on whatever testing may have been done in vivo for establishing Hayflick limits. I am sure the topic is a good one for this bulletin board. Thank you for your time.... Norm Andrews, AT&T, norm@chico.wh.att.com From owner-ageing@net.bio.net Tue Oct 11 23:00:00 1994 Path: biosci!sjubiol.stjohns.edu!rick From: rick@sjubiol.stjohns.edu (Richard Lockshin) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Date: 11 Oct 1994 20:26:29 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 4 Sender: daemon@net.bio.net Distribution: world Message-ID: <9410111359.AA05563@sjubiol.stjohns.edu> NNTP-Posting-Host: net.bio.net Different cell types have different limits - for instance, see work by David Harrison and others on the limits of hematopoetic cells - but I don't know of a reported limit for intestinal epithelial cells. Try Hayflick's books or Handbook of Aging. From owner-ageing@net.bio.net Tue Oct 11 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!swrinde!pipex!uknet!daresbury!not-for-mail From: Newsgroups: bionet.molbio.ageing Subject: Limited lifespan of cells Date: 12 Oct 1994 10:16:22 +0100 Lines: 9 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <37g9h6$ir5@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk With reference to the ongoing discussion about the limited lifespan of normal cells, can one say: Limited lifespan of any organism is also merely an artifact of its living conditions. If we can find "ideal" culture/living conditions, we will never die.....? Of course, this cannot be said. Therefore.... from: Suresh Rattan/Aarhus/Denmark From owner-ageing@net.bio.net Tue Oct 11 23:00:00 1994 Path: biosci!agate!auxin.hip.berkeley.edu!user From: tjyeh@soda.CSUA.berkeley.edu (Raymond Yeh) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Date: Wed, 12 Oct 1994 02:10:17 -0800 Organization: UC Berkeley Lines: 46 Message-ID: References: <36vqoc$dme@agate.berkeley.edu> <37dofb$3ln@infa.central.susx.ac.uk> NNTP-Posting-Host: auxin.hip.berkeley.edu In article , norm@chico.uucp (Norman E. Andrews [ MT 2C-402 9089575786 NC6241000 ]) wrote: > I don't think you mentioned in vivo tests, but I'll bring that subject up. > One can still interpret the aging differences between in vivo and > in vitro as an artifact of inadequate culture technique, if the nutrition > delivery and waste/immune system disposal systems??? of in vivo differ from > and are probably better than what scientists are now able to provide in vitro. > So what I am suggesting is that there may indeed be a genetically related > Hayflick limit that occurs with in vitro testing, but that such a limit > may not exist in vivo, or if it does, perhaps not to an extent that explains > the sensescence of man. I am ignorant of whatever in vivo testing may have > been done to explore this. I don't know if this helps, but there also seems to be a relationship between the telomeric length of cells and its age. With each division, the telomeres on each chromosome shorten. However, in cancer cells this does not happen. Their telomores are kept at a constant length. It is my understanding that normal cells do have telomerases that keep up their telomores, but I guess they just don't do it at as an efficient rate as the cancerous cells. > I fail to see your conclusion in [1]. One simple and perhaps wrong > explanation will serve to illustrate: Suppose the metabolism of the > different cell types proceeds at different rates, but that they all > require something that is inadequately provided by the culture > technique, perhaps nutrition or waste disposal. There would be > a genetic link, expressed thropugh different rates of metabolism, but > the inadequate culture technique could be the cause of existence > of the (different) Hayflick limits. The magnitude of the differences > would be genetically related, but the _existence_ of the limit would be > because of the culture technique. I think the difference in metabolism would show up as a difference in how long the cells live and not the number of population doublings. > Now this seems to me to be the most solid evidence, except I still > wonder: could tumor cells have requirements for metabolism that > are in _some_ respects less demanding than normal cells? To me, cancerous cell would be more demanding in terms of metabolism than normal cells. Raymond Yeh From owner-ageing@net.bio.net Tue Oct 11 23:00:00 1994 Path: biosci!agate!auxin.hip.berkeley.edu!user From: tjyeh@soda.CSUA.berkeley.edu (Raymond Yeh) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Date: Wed, 12 Oct 1994 01:56:34 -0800 Organization: UC Berkeley Lines: 9 Message-ID: References: <36vqoc$dme@agate.berkeley.edu> <37douu$3r5@infa.central.susx.ac.uk> NNTP-Posting-Host: auxin.hip.berkeley.edu In article <37douu$3r5@infa.central.susx.ac.uk>, bafa1@central.susx.ac.uk (Sydney Shall) wrote: > In general therefore, the hayflick limit is a biological > phenomenon, and not a culture artifact. Also, when you take one cell's cytoplasm and another nucleus and put them together, the Hayflick limit seems to be controlled by the nucleus and not the cytoplasm. From owner-ageing@net.bio.net Tue Oct 11 23:00:00 1994 Path: biosci!bcm!cs.utexas.edu!howland.reston.ans.net!spool.mu.edu!sgiblab!nbn!news.hh.sbay.org!not-for-mail From: kingsley@hh.sbay.org (Kingsley G. Morse Jr.) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Date: 12 Oct 1994 12:03:10 -0700 Organization: Hip-Hop BBS Lines: 9 Message-ID: <37hbte$35j@hip-hop.hh.sbay.org> References: <36vqoc$dme@agate.berkeley.edu> <37dofb$3ln@infa.central.susx.ac.uk> NNTP-Posting-Host: hip-hop.hh.sbay.org Dr. Bob Becker says that small electric currents cause fibroblast cells to dedifferentiate into all other types of cells, as one sees in regenerating limbs of amphibians and normal mammal development. My point is that the Hayflick "limit" may not be insurmountable as long as one has fibroblast cells. Dr. Becker has done some really cool experiments with limb regeneration in mammals. He used (uses?) small electric currents. Watch this spot. From owner-ageing@net.bio.net Thu Oct 13 23:00:00 1994 Path: biosci!bcm!cs.utexas.edu!swrinde!sgiblab!nbn!news.hh.sbay.org!not-for-mail From: kingsley@hh.sbay.org (Kingsley G. Morse Jr.) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells (fwd) Date: 13 Oct 1994 22:48:17 -0700 Organization: Hip-Hop BBS Lines: 12 Message-ID: <37l631$f31@hip-hop.hh.sbay.org> References: NNTP-Posting-Host: hip-hop.hh.sbay.org In kruged@ESSEX.HSC.COLORADO.EDU (Edward Krug) writes: > I currently grow human foreskin fibroblasts in culture as host for >an intracellular parasite. I find that with high passage numbers the ^^^^^^^^^^^^^^^ What are "passage numbers"? >fibroblasts become poor hosts for the parasite long before there is a >noticable decrease in fibroblasts growth rate. I study different media >formulations and I have yet to find anything which overcomes sheer passage >number. From owner-ageing@net.bio.net Thu Oct 13 23:00:00 1994 Path: biosci!ESSEX.HSC.COLORADO.EDU!kruged From: kruged@ESSEX.HSC.COLORADO.EDU (Edward Krug) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells (fwd) Date: 13 Oct 1994 17:36:13 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 44 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net This is my first contribution, I hope it works. Assuming the cell replication score keeper does ultimately prove to be telomeric length as you suggested, what is the process which resets the length with every new egg/sperm pairing? At a Gordon conference on ageing in 1983 Joan Smith-Sonneborn described the limited number of doublings paramecium could undergo (somewhere near 200 doublings) without sexual conjugation before it stopped dividing and died. If it was permitted to exchange DNA during sexual conjugation the counter was reset to 1 again. Unfortunately, the paramecium had to be visually separated after each division to prevent conjugation, so it is practically impossible to get enough material to do any experiments with. The point is that the counter can be reset in some systems. I suspect that this processess is quite different from the release from terminal differentiation seen in some amphibians when they regenerate amputated limbs. There are several amphibians which are capable of limb regeneration at an early age but after undergoing a thyroid hormone pulse they loose that ability. The number of doublings consumed doesn't jump, the cells have just passed a developmental switch. There are some major issues in ageing involved with thyroid hormones, but I will ask for input on this later. I currently grow human foreskin fibroblasts in culture as host for an intracellular parasite. I find that with high passage numbers the fibroblasts become poor hosts for the parasite long before there is a noticable decrease in fibroblasts growth rate. I study different media formulations and I have yet to find anything which overcomes sheer passage number. Also, fibroblasts kept in a low serum medium to stop replication and just stored in stasis also seem to accumulate some indicator of the passage of time. They loose some of their maximum replication potential even though they are not replicating. The Hayflick number given for cells assumes rapid division, but non-dividing cells clearly show the effects of passage of time. Is this type of senesence different from that produced by exhaustion of replicative potential? I don't know. Lastly, the Hayflick number for most cells doesn't apply to the human condition since it is based on rapidly replicating cells, and in most animal bodies they only rapidly replicating cells are some form of lining cells or cancers. Oh, I would that it were simple. Edward C. Krug Instructor Uni. of Colorado Med. Sch. From owner-ageing@net.bio.net Thu Oct 13 23:00:00 1994 Path: biosci!bcm!cs.utexas.edu!not-for-mail From: david_small@muwayf.unimelb.edu.au (David Small) Newsgroups: bionet.jobs,bionet.molbio.ageing,bionet.molbio.proteins,bionet.neuroscience Subject: Positions available Date: 13 Oct 1994 19:26:31 -0500 Organization: UTexas Mail-to-News Gateway Lines: 22 Sender: nobody@cs.utexas.edu Message-ID: <01HI9HKRX1ZM001VAZ@muwayb.ucs.unimelb.edu.au> NNTP-Posting-Host: news.cs.utexas.edu Xref: biosci bionet.jobs:5972 bionet.molbio.ageing:943 bionet.molbio.proteins:2871 bionet.neuroscience:4596 Positions available#000# ALZHEIMER'S DISEASE RESEARCH GROUP Several positions at the post-doctoral, research assistant and graduate student (PhD scholarship) level are now available. The research and therapeutic target is the amyloid precursor protein, a cell-surface receptor. Persons with an interest or experience in the wider areas of cell biology and molecular biochemistry, or in the specialized areas of protein structure-function analysis, proteases, immunoassay development, and neuronal tissue culture are invited to apply. Conditions of employment will be very competitive. Further details from Professor Colin L. Masters Tel. 61-3-344-5968, FAX 61-3-344-4004. E-mail: pathology.pathology@muwayf.unimelb.edu.au The first round of applications will close on 7th November, and should be sent to Helene Marszalek, Pathology Department, The University of Melbourne, Parkville, Victoria 3052, Australia. From owner-ageing@net.bio.net Thu Oct 13 23:00:00 1994 Path: biosci!bcm!cs.utexas.edu!howland.reston.ans.net!pipex!doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Date: 14 Oct 1994 09:58:58 GMT Organization: University of Sussex Lines: 72 Message-ID: <37lkp2$63m@infa.central.susx.ac.uk> References: <36vqoc$dme@agate.berkeley.edu> <37dofb$3ln@infa.central.susx.ac.uk> NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] Sydney Shall (bafa1@central.susx.ac.uk) wrote: : Tsung-Jui Yeh (tjyeh@soda.CSUA.Berkeley.EDU) wrote: : : I was wondering about the Hayflick limit for rapid dividing cells like : : ones that line the stomach and also cells of the cornea. Do these cells : : have the same Hayflick limit as fibroblasts? If so, why can these cells : : afford to divide so fast? : : Thanks : Cells from different tissues display different Hayflick limits. This : means that some cells like fibroblasts may go through about 50 to 70 : population doublings, in about 150 cell generations. On the other hand, : adult dermal fibroblasts, chondrocytes experience many fewer : generations. Lymphocytes seem in most growth media, to experience only : about 23 population doublings. So, at the moment we do not really know : whether there is one fixed Hayflick limit; the evidence available so far : would suggest that there are specific Hayflick limits for different : tissues. This clearly has important implications for the homeostasis of : each individual tissue. : Moreover, it is very well established that the same cell type from : different animal species show a species-specific Hayflick limit; this is : part of the evidence for the notion that the Hayflick limit is : genetically controlled. : -- : Sydney SHALL, : Laboratory of Cell and Molecular Biology, : Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. : Telephone: +44.273.67.83.03 FAX: +44.273.67.84.33 RESPONSE: I think the major question to arise from this discussion is whether a Hayflick limit exists in vivo, that is in intact bodies. Regrettably, there is very little published evidence on this question. The only evidence that I can adduce is (1) Werner's syndrome, where a very evident premature ageing is correlated with a changed Hayflick limit in vitro, and (2) secondly a paper by Rohme in which he convincingly shows a correlation between both average and maximum lifespans of different animals and the life-span of there cells in vitro (their Haflick limit number). Both of these items of evidence are correlations; so although they are persuasive to me, I would say the question as to whether there is an in vivo Hayflick limit is completely open and unresolved. The second question raised abou whether the Hayflick limit has an COMPONENT of culture conditions in it is different. I think that the question being asked is whether the hayflick limit is an artifact; this means, is it TOTALLY due to the way we grow the cells. There is no doubt that the way we grow cells influences the value of the Hayflick limit. But the direct question is: can we grow cells in such a way that there is NO Hayflick limit. This question has been directly addressed by one author, who has given the answer that for mice one can grow cells in the absence of serum and then they are immortal. But I understand that the same author says that this does NOT work for human cells. Furthermore, I observe that so far there is no published confirmation of this one report. So, I think that this must be viewed with some caution. Again, I would say that culture conditions modulate the value of the Hayflick limit, but the existence of such a limit is abiological property of the cells. The real issue in my view is whether this limit is a biological property, at least in part, or SOLELY,a consequence of the culture conditions. If the latter, then one should not look for genes which are important in this process. If the former is true, then one is probably justified in searching for genes which are relevant to the phenomenon. -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Tel:+44.273.67.83.03 FAX:+44.273.67.84.33; E-Mail:Janet:S.Shall@uk.ac.sussex Elsewhere:S.Shall@sussex.ac.uk EARN/BITNET:S.Shall%sussex@ukacrl From owner-ageing@net.bio.net Thu Oct 13 23:00:00 1994 Path: biosci!daresbury!not-for-mail From: Newsgroups: bionet.molbio.ageing Subject: Ageing humour again Date: 14 Oct 1994 11:52:04 +0100 Lines: 13 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <37lnsk$8kq@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk I thought that you may like to smile a little bit over the weekend: As soon as an elderly person entered a doctor's office the doctor said:"Sir, you need high power glasses". The grand old man was very much impressed, and wanted to know from the doctor how could she tell without checking what he needed. The clever doctor said: "Oh, that was easy. As soon as you entered my office through that window, I understood that you needed good glasses...." Moral of the story: Distinction between a door and a window disppears with age... Suresh Rattan/Aarhus/Denmark From owner-ageing@net.bio.net Thu Oct 13 23:00:00 1994 Path: biosci!rutgers!uwm.edu!cs.utexas.edu!howland.reston.ans.net!pipex!uunet!psinntp!sjuvm!yprlbio Nntp-Posting-Host: 149.68.2.20 Date: Fri, 14 Oct 1994 16:14:08 -0400 From: "LOCKSHIN, RICHARD A" Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Message-ID: <14OCT94.17530788.0032@sjumusic.stjohns.edu> References: <36vqoc$dme@agate.berkeley.edu> <37dofb$3ln@infa.central.susx.ac.uk> Sender: usenet@sjumusic.stjohns.edu Organization: St. John's University Lines: 27 In article norm@chico.uucp (Norman E. Andrews [ MT 2C-402 9089575786 NC6241000 ]) writes: >Hello, Sidney Shall, > >Thank you for your reply about the Hayflick limit. > >I don't think you mentioned in vivo tests, but I'll bring that subject up. There are at least two in vivo tests of which I am aware, both dating back several years. David Harrison transplanted hematopoeitic stem on cells in mice over a few generations. He found that the stem cell line from survived well past the normal lifespan of the mouse, but only through vitro. two or three generations beyond that. Try J. Gerontol. or Mech. Ageing ed and Development. Along the same line, someone in England performed skin grafts in mice differing only in the gene for coat color. This graft lains survived two or three generations of transplantation but eventually was have lost from the host mice, presumptively because of failure to continue divisions. Although some consider that immunologic senescence, common at advanced age, might be a reflection of limited lifespan of cells, for the most part noone believes that we die because we run out of cells. The biological phenomenon is extremely interesting, however, and exit from mitotic phase presumably reflects changes in the cells that are very relevant to the decreased adaptiveness that characterizes aging. Richard A. Lockshin/Dept. Biol. Sci. St. John's U.8000 Utopia Pkwy Jamaica NY 11439 USA/Phone 718: 990-1854/ Fax 718: 380-8543 yprlbio@sjumusic.stjohns.edu or rick@sjubiol.stjohns.edu From owner-ageing@net.bio.net Fri Oct 14 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!sunic!pipex!uunet!newstf01.cr1.aol.com!newsbf01.news.aol.com!not-for-mail From: lifeextser@aol.com (LifeExtSer) Newsgroups: bionet.molbio.ageing Subject: Hayflick number and Telemorase Date: 15 Oct 1994 15:59:04 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 5 Sender: news@newsbf01.news.aol.com Message-ID: <37pca8$sd5@newsbf01.news.aol.com> NNTP-Posting-Host: newsbf01.news.aol.com Anybody have any info on this enzyme? It is supposed to add telomeres back onto the end of DNA, and thereby reset the Hayflick counter. It was on this group, or perhaps sci.life-extension awhile back, but I haven't seen any study results from testing on live animals. Seems like this would be a great way to see just how important the Hayflick number is. From owner-ageing@net.bio.net Sat Oct 15 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!agate!howland.reston.ans.net!europa.eng.gtefsd.com!newsxfer.itd.umich.edu!zip.eecs.umich.edu!caen!msuinfo!harbinger.cc.monash.edu.au!news.cs.su.oz.au!metro!OzEmail!joi From: joi@ozemail.com.au (Jonathon Alexander) Subject: Have u seen sci.life-extension? Message-ID: Sender: news@ozemail.com.au (System Administrator) Organization: OzEmail Pty Ltd Sydney Australia Date: Sun, 16 Oct 1994 10:39:39 GMT X-Newsreader: TIN [version 1.2 PL2] Lines: 4 Some of you may not know there is also a sci.life-extension newsgroup. - more pragmatic, less scientific, but perhaps still useful and interesting. Regards, John Alexander From owner-ageing@net.bio.net Sat Oct 15 23:00:00 1994 Path: biosci!agate!auxin.hip.berkeley.edu!user From: tjyeh@soda.CSUA.berkeley.edu (Raymond Yeh) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick number and Telemorase Date: Sun, 16 Oct 1994 06:45:46 -0800 Organization: UC Berkeley Lines: 15 Message-ID: References: <37pca8$sd5@newsbf01.news.aol.com> NNTP-Posting-Host: auxin.hip.berkeley.edu In article <37pca8$sd5@newsbf01.news.aol.com>, lifeextser@aol.com (LifeExtSer) wrote: > Anybody have any info on this enzyme? It is supposed to add telomeres > back onto the end of DNA, and thereby reset the Hayflick counter. It was > on this group, or perhaps sci.life-extension awhile back, but I haven't > seen any study results from testing on live animals. Seems like this > would be a great way to see just how important the Hayflick number is. As far as I know, in cancer cells, there is no telomeric shortening due to the increased activity of telomerase. I remember it was mentioned in this newsgroup a while back that telomerases are hard to purify because they are in such low quantities in the cell. Raymond Yeh From owner-ageing@net.bio.net Sat Oct 15 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!agate!spool.mu.edu!howland.reston.ans.net!vixen.cso.uiuc.edu!uwm.edu!caen!msuinfo!harbinger.cc.monash.edu.au!news.cs.su.oz.au!metro!OzEmail!joi From: joi@ozemail.com.au (Jonathon Alexander) Subject: Any info smart drug sideeffects Message-ID: Sender: news@ozemail.com.au (System Administrator) Organization: OzEmail Pty Ltd Sydney Australia Date: Sun, 16 Oct 1994 10:49:05 GMT X-Newsreader: TIN [version 1.2 PL2] Lines: 6 Hi, I'm seriously considering trying some smart drugs. I wondered if any of you have any information on (a) side-effects (b) most cost-effective where cost is measured in risk of self-damage. Thanks and regards John Alexander From owner-ageing@net.bio.net Sat Oct 15 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!agate!howland.reston.ans.net!europa.eng.gtefsd.com!newsxfer.itd.umich.edu!zip.eecs.umich.edu!caen!msuinfo!harbinger.cc.monash.edu.au!news.cs.su.oz.au!metro!OzEmail!joi From: joi@ozemail.com.au (Jonathon Alexander) Subject: Re: Hayflick number and Telemorase Message-ID: Sender: news@ozemail.com.au (System Administrator) Organization: OzEmail Pty Ltd Sydney Australia Date: Sun, 16 Oct 1994 10:43:23 GMT References: <37pca8$sd5@newsbf01.news.aol.com> X-Newsreader: TIN [version 1.2 PL2] Lines: 12 LifeExtSer (lifeextser@aol.com) wrote: : Anybody have any info on this enzyme? It is supposed to add telomeres : back onto the end of DNA, and thereby reset the Hayflick counter. It was : on this group, or perhaps sci.life-extension awhile back, but I haven't : seen any study results from testing on live animals. Seems like this : would be a great way to see just how important the Hayflick number is. There was a brief but significant article near the front of a recent Scientific American, might be June, July, August, on Telomeres. I posted a reference to it to sci.life-extension. I believe it is called telomerase. Regards John Alexander From owner-ageing@net.bio.net Sat Oct 15 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!usc!howland.reston.ans.net!pipex!uunet!olivea!charnel.ecst.csuchico.edu!csusac!csus.edu!netcom.com!netcomsv!lafn.org!lafn.org!ad368 From: ad368@lafn.org (Jim Day) Subject: Re: Have u seen sci.life-extension? Message-ID: <1994Oct16.161430.5393@lafn.org> Sender: news@lafn.org Nntp-Posting-Host: lafn.org Organization: Los Angeles Free-Net Date: Sun, 16 Oct 1994 16:14:30 GMT Lines: 7 Besides the Scientific American article, another article that mentions the role of telomerase was published in the April 25, 1994 issue of U.S. News and World Report, p79-82. Regards, Jim Day -- From owner-ageing@net.bio.net Sun Oct 16 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!usenet.ins.cwru.edu!lerc.nasa.gov!purdue!mozo.cc.purdue.edu!not-for-mail From: barani@dart.cc.purdue.edu (barani) Newsgroups: bionet.molbio.ageing Subject: Don't worry; Be Happy! Date: 17 Oct 1994 01:59:47 -0500 Organization: Purdue University Computing Center Lines: 15 Distribution: world Message-ID: <37t7d3$kgg@dart.cc.purdue.edu> NNTP-Posting-Host: dart.cc.purdue.edu Why worry about death? As long as you are going to live, you aint going to die; And if you die, you wont be around to worry about it anyway. And if you die, you will go to Heaven; So, no need to worry; And in case you go to Hell, then you will be shaking hands with all your friends you won't have anytime to worry! :) S.Baranidharan B-146 Lilly Hall of Life Sciences Purdue University W.Lafayette IN 47907 USA From owner-ageing@net.bio.net Sun Oct 16 23:00:00 1994 Path: biosci!PCLSP2.KUICR.KYOTO-U.AC.JP!vinz From: vinz@PCLSP2.KUICR.KYOTO-U.AC.JP (Vincenzo Nardi-Dei) Newsgroups: bionet.molbio.ageing Subject: Re: Don't worry; Be Happy! Date: 17 Oct 1994 02:15:55 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 17 Sender: daemon@net.bio.net Distribution: world Message-ID: <9410170913.AA03235@pclsp2> NNTP-Posting-Host: net.bio.net >Why worry about death? >As long as you are going to live, you aint going to die; >And if you die, you wont be around to worry about it anyway. That's very true, when you will be death no more desire of living... >And if you die, you will go to Heaven; So, no need to worry; >And in case you go to Hell, then you will be shaking hands with >all your friends you won't have anytime to worry! This second part looks more funny... :-) From owner-ageing@net.bio.net Sun Oct 16 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!swrinde!ihnp4.ucsd.edu!munnari.oz.au!news.uwa.edu.au!newsman.csu.murdoch.edu.au!Jim.Cummins From: cummins@possum.murdoch.edu.au (Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick number and Telemorase Date: 17 Oct 1994 08:21:28 GMT Organization: Murdoch University, Western Australia Lines: 25 Sender: -Not-Authenticated-[6523] Message-ID: <37tc68INNj2j@newsman.csu.murdoch.edu.au> References: <37pca8$sd5@newsbf01.news.aol.com> NNTP-Posting-Host: vetmac3.csu.murdoch.edu.au X-Posted-From: InterNews 1.0@newsman.csu.murdoch.edu.au. Xdisclaimer: No attempt was made to authenticate the sender's name. See the following: Shay JW, Wright WE, Werbin H (1993): Loss of telomeric DNA during aging may predispose cells to cancer (review). International Journal Of Oncology 3:559-563. Shay JW, Wright WE, Werbin H (1993): Toward a molecular understanding of human breast cancer - a hypothesis. Breast Cancer Research And Treatment 25:83-94. Martin GR, Danner DB, Holbrook NJ (1993): Aging - causes and defenses. Annual Review Of Medicine 44:419-429. Recent studies have shown that chromosomes shorten as cells divide and become senescent. Also, deletions in mitochondrial DNA increase markedly with advancing age, presumably secondary to damage from oxygen radicals. Since host defenses against environmental factors also become attenuated, the molecular damage associated with aging may increasingly perturb normal homeostasis and increase the susceptibility to disease and disability. Such age-associated dysfunctions can be targeted and interrupted. Jim "I refuse to have a signature" Cummins School of Veterinary Studies Murdoch University Western Australia 6150 Tel +61-9-360 2668 Fax +61-9-310 4144 E-mail cummins@possum.murdoch.edu.au From owner-ageing@net.bio.net Sun Oct 16 23:00:00 1994 Path: biosci!ilr.uucp.free.net!gavrilov From: gavrilov@ilr.uucp.free.net ("Leonid Gavrilov") Newsgroups: bionet.molbio.ageing Subject: Hayflick Limit - Debates in BioEssays Date: 17 Oct 1994 10:30:31 -0700 Organization: A.N.Belozersky Institute, Moscow State University Lines: 239 Sender: daemon@net.bio.net Distribution: world Message-ID: <2ea2c4e2.ilr@ilr.uucp.free.net> NNTP-Posting-Host: net.bio.net TO: FROM: Dr. Leonid A.Gavrilov, Ph.D. A.N.Belozersky Institute Moscow State University 119899 Moscow, RUSSIA FAX: 7 (095) 939-0338 7 (095) 939-3181 October 17, 1994 Dear Sirs, Recently we have received a lot of E-mail messages asking me to reproduce on the AGEING list the scientific debates between Dr.Leonard Hayflick and ourselves (Dr.L.A.Gavrilov and Dr.N.S.Gavrilova) that were published recently by BioEssays (16/8 AUG 1994, p.591-593). Because of copyright restrictions, we cannot do that for Hayflick's paper: please see BioEssays. But we can reproduce here our response to Hayflick's paper in its original form, since BioEssays has eliminated many important parts of it because of the limited journal space. Sincerely yours, Dr.Leonid A.Gavrilov, Ph.D. and Dr.Natalia S.Gavrilova, Ph.D. P.S.: Our original paper submitted to BioEssays (and published in abridged form) is printed below: -------------------------------------------------------------------------- The Weismann-Swim-Hayflick concept of proliferative limit: historical and critical comments by Leonid A.Gavrilov and Natalia S.Gavrilova Although the Weismann-Swim-Hayflick concept of proliferative limit was already discussed in great detail in our book (1) which has received a lot of attention from many scientific journals including BioEssays (2-20), we are very pleased by invitation of BioEssays to return to this discussion again and to reply to Dr.Hayflick's comments. Since his comments have a lot of quite different declarations mixed together, and since not all the readers of BioEssays have read our book, we shall start our reply from the very beginning in a chronological manner (in an abridged form since all the details could be found in our book): 1. The idea that the limited lifespan of organisms is determined by the limited capacity of somatic cells for division was originally created not by Dr.Hayflick in 1961, but by the famous German biologist August Weismann a century ago (21). Moreover, it was Weismann who postulated that the differences in the longevity of animal species are caused by the different number of generations that the somatic cells of each species can produce (the cells of long-lived species are capable for completing more divisions). Weismann's idea has received a lot of attention in our century too. For example, the Nobel Prize winner and the founder of gerontology (and the father of the term 'gerontology') Ilya Mechnikov devoted a special chapter for discussing and criticizing the Weismann's theory of cell division limit in his famous book "Essais optimistes" (22). Since this book was published for many times (at least in 1907, 1908, 1913, 1964, 1987) any scientist interested in aging research had an opportunity to read about Weismann's theory of cell division limit. Certainly, it is very nice that Dr.Hayflick after some delay of about 20 years has finally received some knowledge about the Weismann's theory too and there is a complete mutual understanding now at least in this issue. 2. The author of the first convincing experimental evidence and clear conclusion that animal cells in culture cannot be propagated indefinitely was not Dr.Hayflick but another American scientist, Dr. H. Earle Swim from Western Reserve University School of Medicine in Cleveland, Ohio, together with his co-authors, Dr. Robert F. Parker and Dr. R.F.Haff (23-25). In 1959 after analyzing results from 336 publications, including the results of his own experiments on the serial cultivation of 23 strains of fibroblasts derived from normal tissues of the rabbit and chick embryo (23), as well as 51 strains of human fibroblasts derived from foreskin, placenta, testicle, uterus and embryonic tissues (24), Dr. Swim came to the following fundamentally important conclusions: "... in most instances where growth occurs the cells eventually undergo nonspecific degeneration" (25, see p.145). "The common experience of many investigators indicates that the early cultivation of cells usually follows a characteristic course which can be conveniently divided into three phases. In phase I the cells proliferate rapidly after an initial lag and usually can be transferred serially without difficulty. Phase II is characterized by a decrease in multiplication to a point where it usually ceases and the cells are eventually lost as a result of nonspecific degeneration" (25, p.159). "This was accompanied at first by an increase in the number of granules in the cytoplasm of the cells; later, degenerating cells were observed and their numbers increased progressively until the bottoms of the flasks were covered with a dense layer of cellular debris..." (23, p.201). The important conclusion was also drawn that when cells stop multiplying, this is not a methodological artifact caused by such factors as inoculum size, toxic media, or their inability to proliferate on glass (24). Finally, Dr. Swim (25) notes that "infrequently a third stage is recognized by the appearance of actively proliferating cells in phase II cultures." (p.159). "It should be emphasized that phases I and II represent the usual pattern, while phase III is a relatively rare event." (25, p.160). Dr.Swim (25) also noted that in these rare cases of re-appearance of active proliferation the new proliferating cells often differ from the original cells both in morphology and growth pattern (cell transformation). 3. In view of the above mentioned quotations from Dr. Swim it is clear that such Dr.Hayflick's statements as "Swim ... describe no phases" and "Moorhead and I were the first to ... describe the three phases" are absolutely wrong. Moreover, the notations used by Dr.Hayflick are unbelievably similar to notations of three phases introduced earlier by Dr. Swim (including even the same Roman numbers I, II and III !). Perhaps Dr.Hayflick might wish to give a rational explanation for such a fantastic similarity between his papers and the earlier paper by Dr. Swim (25). 4. It is true that Dr.Hayflick was the first to declare that limited proliferative capacity is the property of all diploid cells and diploid cells only. Unfortunately, this declaration is wrong in both directions: First, there are a lot of aneuploid and polyploid cells in 'old' cultures, thus the lack of diploid karyotype per se is not sufficient for unlimited proliferation. Second, virtually unlimited proliferation could be observed for normal diploid cells too (if these cells do not embark on terminal differentiation). For example, it turns out that normal diploid mouse embryo cells, which under standard conditions manifest a growth crisis after 7-10 population doublings, may be successfully cultivated without any sign of an approaching growth crisis for at least 200 population doublings. All that is necessary is to change the composition of the culture medium (excluding blood serum and adding a number of ingredients, including the epidermal growth factor). In this case the cells, which are apparently capable of unlimited multiplication, remain diploid and nontumorigenic (26). Certain normal diploid cells show a practically inexhaustible capability for proliferation not only in vitro, but also in vivo. For example, it is well known that normal cells of drosophila imaginal discs can proliferate indefinitely if their differentiation inductors are absent (27). It is also well established that there is no any intrinsic limit to the proliferation of normal hemopoietic stem cells (27). Thus, the declaration of Dr.Hayflick that proliferation limit "is an intrinsic property of all normal cells" is definitely not true. 5. We would agree with Dr.Hayflick that cells "do eventually die". The only problem is that this declaration means nothing. For example, the atoms of radioactive elements also "do eventually die", but they do not age (their 'rate of dying' is constant and does not increase with age). The same is true for cell cultures: there is no evidence for real aging, i.e., age- dependent increase in cellular mortality rates. Instead, the cellular cultures are surprisingly claimed to be senescent and dead simply because they stopped active proliferation. This is definitely unacceptable definition of death since according to it all of us have dead brains ! It is clear that decrease in proliferation rates is not necessarily a manifestation of cell deterioration and aging; instead, it might be a consequence of 'healthy' cell differentiation (see our book for details). For this reason the so-called 'aging' in cell cultures may have no any relation to the problems of real cellular aging. 6. Since Dr.Hayflick decided to "raise serious questions about the judgement and competence" of Dr.Downes, we would like to mention that Dr. Downes was very careful in the review of our book and in discussion of Dr.Hayflick's scientific contribution. Some other book reviewers, for example, Dr.Brian Merry, made much more definite conclusions: "the authors justifiably devote a large proportion of this important chapter to a careful study of the phenomenon of limited in vitro cell division, often referred to as the Hayflick limit. They present a most thorough and timely re-appraisal of this data and they question the relevance of this popular model to the ageing process" (5). Similar comments could be found in other book reviews published by Free Radical Biology & Medicine (6), Human Biology (7), British Medical Journal (8), Population and Development Review (9). Thus, the waiting list for receiving Dr.Hayflick's penalties is too long to "raise serious questions about the judgement and competence" of Dr.Downes and any other person who has his own opinion on Dr.Hayflick's work. 7. Finally, we would like to emphasize that Dr.Hayflick has made a significant contribution into promotion of the Weismann's ideas, reproducing Dr. Swim's experimental results as well as their further development. For this reason in our book we called this scientific approach the Weismann-Swim-Hayflick concept. The fact that the name of Dr.Hayflick is mentioned not on the first place was due to historical reason only and should not be considered as an attack on him personally (perhaps he might wish to consult his psychologist for this purpose). Instead Dr.Hayflick might wish to organize a scientific meeting in 1997 to celebrate the 40th anniversary of the Dr. Swim's discovery at the School of Medicine at Cleveland where Dr. Swim worked. This meeting might be sponsored by American Federation for Aging Research where Dr.Hayflick is a key person, and we would be happy to take part in such a meeting together with Dr. Hayflick and Dr.Downes to discuss the issues of mutual interest. Such meeting might be interesting to many readers of BioEssays too. References 1. Gavrilov, L.A. and Gavrilova, N.S. (1991). The Biology of Life Span: a Quantitative Approach. Harwood Academic Publishers GMBH, Chur, etc. ISBN: 3-7186-4983-7. 2. Downes, C.S. (1993). Senescence and the genome or, change and decay in all except lobsters I see. BioEssays, 15, 359-362. 3. Kirkwood, T.B.L. (1991). Tales of old. The Biology of Life Span. Nature, 352, 767-768. 4. Masoro, E.J. (1993). The Biology of Life Span: A Quantitative Approach. Quarterly Review of Biology, 68, 92. 5. Merry, B. (1991). The Biology of Life Span: A Quantitative Approach. Ageing and Society, 11, 509-510. 6. Pryor, W.A. (1992). The Biology of Life Span: A Quantitative Approach. Free Radical Biology & Medicine, 12, 331-332. 7. Akiyama, M.M. (1992). The Biology of Life Span: A Quantitative Approach. Human Biology, 64, 630-632. 8. Grundy, E. (1992). When your time's up. The Biology of Life Span: A Quantitative Approach. British Medical Journal, 305, 431. 9. Olshansky, S.J. (1992). The Biology of Life Span: A Quantitative Approach. Population and Development Review, 18, 555-558. 10. Fairweather, D.S. (1992). The Biology of Life Span: A Quantitative Approach. Age and Ageing, 21, 386-387. 11. Izsak, J. (1992). The Biology of Life Span: A Quantitative Approach. Archives of Gerontology and Geriatrics, 15, 192-194. 12. Gracy, R.W. (1993). The Biology of Life Span: A Quantitative Approach. Educational Gerontology, 19, 92-93. 13. Dean, W. (1992). The Biology of Life Span: A Quantitative Approach. Experimental Gerontology, 27, 251-253. 14. Walford, R.L. (1991). Booknote from Biosphere II. The Biology of Life Span: A Quantitative Approach. Gerontologist, 31, 707. 15. Hipkiss, A. (1992). The Biology of Life Span: A Quantitative Approach. International Journal of Geriatric Psychiatry, 7, 614. 16. Crews, D.E. (1993). Biological aging. The Biology of Life Span: A Quantitative Approach. Journal of Cross-Cultural Gerontology, 8, 281-290. 17. Vetter, N. (1992). The Biology of Life Span: A Quantitative Approach. Journal of Epidemiology & Community Health, 46, 630. 18. Barnett, H.A.R. (1992). The Biology of Life Span: A Quantitative Approach. Journal of the Institute of Actuaries, 119, 379-381. 19. Hoffer, A. (1993). The Biology of Life Span: A Quantitative Approach. Journal of Orthomolecular Medicine, 8, 59-60. 20. Kannisto, V. (1992). The Biology of Life Span: A Quantitative Approach. Population Studies, 46, 366-367. 21. Weismann, A. (1892). Uber Leben und Tod. Verlag von Gustav Fisher, Jena. 22. Mechnikov, I.I. (1907). Essais optimistes. Paris, 438p. 23. Haff, R.F. and Swim, H.E. (1956). Serial propagation of 3 strains of rabbit fibroblasts; their susceptibility to infection with Vaccinia virus. Proc.Soc.Exp.Biol.Med., 93, 200-204. 24. Swim, H.E. and Parker, R.F. (1957). Culture characteristics of human fibroblasts propagated serially. Am.J.Hygiene, 66, 235-243. 25. Swim, H.E. (1959). Microbiological aspects of tissue culture. Ann.Rev.Microbiol. 13, 141-176. 26. Loo, D.T., Fuquay, J.I., Rawson, C.L. and Barnes, D.W. (1987). Extended culture of mouse embryo cells without senescence: inhibition by serum. Science 236, 200-202. 27. Finch, C.E. (1991). Longevity, Senescence and the Genome. University of Chicago Press. ******************************THE END************************************* From owner-ageing@net.bio.net Mon Oct 17 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!rutgers!gatech!howland.reston.ans.net!agate!news.ucdavis.edu!csus.edu!netcom.com!ix.netcom.com!netcomsv!lafn.org!lafn.org!ad368 From: ad368@lafn.org (Jim Day) Subject: Re: Hayflick number and Telemorase Message-ID: <1994Oct17.230047.13423@lafn.org> Sender: news@lafn.org Nntp-Posting-Host: lafn.org Organization: Los Angeles Free-Net Date: Mon, 17 Oct 1994 23:00:47 GMT Lines: 44 I'm a writer, not a scientist, but those looking for information on telomerase activity may find something of interest in the papers listed below. Jim Day ========================================================= Counter, C.M., et al., "Telomere shortening associated with chromosome instability is arrested in immortal cells which express telomerase activity," EMBO Journal, May 1992, p1921. Counter, C.M., et al., "Stabilization of short telomeres and telomerase activity accompany immortalization of Epstein-Barr virus-transformed human B lymphocytes," Journal of Virology, May 1994, p3410. Greider, Carol W., "Telomerase is processive," Molecular and Cellular Biology, September 1991, p4572. Lamond, Angus I., "Tetrahymena telomerase contains an internal RNA template," Trends in Biochemical Sciences, June 1989, p202. Romero, D.P., and E.H. Blackburn, "A conserved secondary structure for telomerase RNA," Cell, October 18, 1991, p343. ten Dam, Edwin, et al., "A conserved pseudoknot in telomerase RNA," Nucleic Acids Research, December 25, 1991, p6951. Yu, Guo-Liang, et al., "In vivo alteration of telomere sequences and senescence caused by mutated Tetrahymena telomerase RNAs," Nature, March 8, 1990, p126. Yu, Guo-Liang, et al., "Developmentally programmed healing of chromosomes by telomerase in Tetrahymena," Cell, November 15, 1991, p823. -- From owner-ageing@net.bio.net Wed Oct 19 23:00:00 1994 Path: biosci!daresbury!not-for-mail From: Graham Pawelec Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Date: 20 Oct 1994 14:22:33 +0100 Lines: 53 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <385qup$ldg@mserv1.dl.ac.uk> Reply-To: Graham Pawelec Original-To: "bionet discussion group imm. & ageing" In the discussion on different limits to the proliferative lifespan for different tissues, it was mentioned that lymphocytes may manage only ca. 23 PD in vitro. While some authors from the ageing field have concluded this, most immunologists working with T cell lines and clones know that this cannot be the case. Leaving aside mouse T cells for the moment, and concentrating on less-prone-to-transformation human T cells, simple arithmetic demonstrates that to obtain a T cell clone in sufficient numbers to experiment with, more than 23 PD are required. Starting from one cell, 23 PD represents 4 million cells; commonly (but not always) T cell clones are obtained which have experienced at least twice this number of PD. Indeed, many immunologists simply assume that T cell clones are immortal. In our hands, however, in well over a decade of T cell cloning, we have not seen a single immortal human line. Average life span of established clones is estimated at perhaps 40 - 50 PD, with the most long-lived clones achieving ca. 80 PD (and thus conforming to the "Weismann-Swim-Hayflick" limit, as Gavrilov & Gavrilova have suggested it should be designated). There is a great deal of clonal heterogeneity and many clones survive even less than 23 PD. How to resolve the discrepancy between a maximum in vitro lifespan of ca. 23 PD established by "T cell gerontologists" and the 80 PD or more established by "T cell immunologists"? I think that this may have something to do with the fact that the former have exclusively used uncloned T cell lines, rather than monoclonal populations. We have observed that uncloned lines manifest shorter lifespans than monoclonal lines obtained from the same starting population. Therefore, we believe that this is more to do with interactions between different T cell clones in the bulk population, where inhibitory effects predominate after a relatively short time, and that this has nothing to do with the actual potential lifespan of the cells. Separating suppressive cells by cloning results in the isolation of populations with extended lifespan; however, recloning monoclonal populations does not result in further extension of lifespan beyond the ca. 80 PD maximum, showing that the cloning procedure per se is not responsible for extending lifespan. Although T cells may be a special case, it might be conceivable that studies on other cell types would show similar discrepancies between the behaviour of cloned - versus - uncloned populations. Maybe some of the controversies in the literature on different potential lifespans could be resolved in this way. Perhaps someone in this discussion group could comment on that? Graham Pawelec, Section for Transplantation Immunology & Immunohematology, University Hospital, Tuebingen, Germany Coordinator, European Union Concerted Action on the Molecular Biology of Immunosenescence, EUCAMBIS From owner-ageing@net.bio.net Wed Oct 19 23:00:00 1994 Path: biosci!news.Stanford.EDU!rutgers!gatech!swiss.ans.net!potogold.rmii.com!ksc.com!garys From: garys@ksc.com (Gary F. Stevens) Newsgroups: bionet.molbio.ageing Subject: Glycation Date: Thu, 20 Oct 1994 15:38:33 Organization: Kaman Sciences Corp Lines: 3 Message-ID: NNTP-Posting-Host: starship.ksc.com X-Newsreader: Trumpet for Windows [Version 1.0 Rev A] Anyone up on this subject? I would like to learn more about it... Gary From owner-ageing@net.bio.net Wed Oct 19 23:00:00 1994 Path: biosci!news.Stanford.EDU!hsdndev!dartvax.dartmouth.edu!usenet From: Matthew.R.Cooperberg@dartmouth.edu (Matthew R. Cooperberg) Newsgroups: bionet.molbio.ageing,bionet.molbio.proteins,bionet.general Subject: Collagen Query Date: 20 Oct 1994 21:51:16 GMT Organization: Dartmouth College, Hanover, NH Lines: 16 Message-ID: <386ook$2mp@dartvax.dartmouth.edu> NNTP-Posting-Host: at-3-sn-149.dartmouth.edu X-Posted-From: InterNews 1.0.3@dartmouth.edu Xref: biosci bionet.molbio.ageing:963 bionet.molbio.proteins:2903 bionet.general:11660 Correct me if any of these assumptions are incorrect: As mammals age, flabby skin results from a cumulative increase in covalent cross-links among collagen subunits. Lathyrism is caused by overconsumption of sweet peas, whose beta-aminopropionitrile >reduces< intramolecular cross-linking to a debilitating extent. Would consumption of sweat peas (or treatment w/ beta-aminoproprionitrile) in any way slow or reverse the deterioration of skin elasticity? Thanks! From owner-ageing@net.bio.net Thu Oct 20 23:00:00 1994 Newsgroups: bionet.molbio.ageing,bionet.molbio.proteins,bionet.general Path: biosci!daresbury!bioftp.unibas.ch!doelz From: doelz@comp.bioz.unibas.ch (Reinhard Doelz) Subject: Re: Collagen Query Message-ID: <1994Oct21.060009.6164@comp.bioz.unibas.ch> Followup-To: bionet.molbio.ageing,bionet.molbio.proteins,bionet.general Organization: EMBnet Switzerland [Basel] X-Newsreader: TIN [version 1.2 PL2] References: <386ook$2mp@dartvax.dartmouth.edu> Date: Fri, 21 Oct 1994 06:00:09 GMT Lines: 36 Xref: biosci bionet.molbio.ageing:964 bionet.molbio.proteins:2907 bionet.general:11666 Matthew R. Cooperberg (Matthew.R.Cooperberg@dartmouth.edu) wrote: : Correct me if any of these assumptions are incorrect: : Lathyrism is caused by overconsumption of sweet peas, whose : beta-aminopropionitrile >reduces< intramolecular cross-linking to a : debilitating extent. : Would consumption of sweat peas (or treatment w/ : beta-aminoproprionitrile) in any way slow or reverse the deterioration : of skin elasticity? Basically, this is true. However, beta-aminoproprionitrile affects the generation of allysine in general, which is the primary precursor of collagen crosslinks in both juvenile (azomethine, two-membered) and adult (three and possibly four side changes involving) crosslink compounds. Therefore, the reason for decreasing skin elasticity, i.e. the 'maturation' from juvenile to adult crosslinks, is targeted with such a chemical.However, a certain amount of crosslinking is required for the mechanical stability of tissue. Experiments ('60s or '70s) in vivo with chemically induced Lathyrism showed that the life of the animals was drastically reduced because of breaking aortas and similar important devices. Regards Reinhard maybe worth reading: Bailey,A.J., Robins, S.P., Balian, G. Nature 251, 105 (1974). Waite, J.H., Tanzer, M.L. CRC Handbook of Chemistry in aging, 1981, 195f. Doelz,R. and Heidemann, E. Int. J. Peptide Protein Res. 32, 307 (1988). Doelz, R. and Heidemann, E. Conn. Tissue Research 18, 255 (1989). -- R.Doelz Klingelbergstr.70| Tel. x41 61 267 2247 Fax x41 61 267 2078| Biocomputing CH 4056 Basel| electronic Mail doelz@ubaclu.unibas.ch| Biozentrum der Universitaet Basel|-------------- Switzerland ---------------| EMBnet Switzerland:info@ch.embnet.org From owner-ageing@net.bio.net Thu Oct 20 23:00:00 1994 Path: biosci!ESSEX.HSC.COLORADO.EDU!kruged From: kruged@ESSEX.HSC.COLORADO.EDU (Edward Krug) Newsgroups: bionet.molbio.ageing Subject: Diurnal hormones and Hayflick limit Date: 20 Oct 1994 23:46:19 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 16 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Dirunal hormone cycles are acknowledged to be important in ageing of intact animals, but when "in vitro" cell doubling limits are discussed the standard model is steady state medium composition. Does anyone out there know of any studies where the tissue culture media has been regulated to mimic the normal "in vivo" hormonal pattern? Edward C. Krug Ph.D. Instructor Campus Box B-168 Dept. of Infectious Diseases Univ. of Colorado Health Sciences Center 4200 E. Nineth Ave. Denver, Colorado, 80262 e-mail = kruged@essex.hsc.colorado.edu From owner-ageing@net.bio.net Fri Oct 21 23:00:00 1994 Path: biosci!daresbury!bioftp.unibas.ch!citi2.fr!jussieu.fr!jabba.fdn.org!uunet!psinntp!sjuvm!yprlbio Nntp-Posting-Host: 149.68.2.20 Date: Fri, 21 Oct 1994 14:30:06 -0400 From: "LOCKSHIN, RICHARD A" Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Message-ID: <21OCT94.15657444.0020@sjumusic.stjohns.edu> References: <36vqoc$dme@agate.berkeley.edu> <37dofb$3ln@infa.central.susx.ac.uk> <37lkp2$63m@infa.central.susx.ac.uk> Sender: usenet@sjumusic.stjohns.edu Organization: St. John's University Lines: 100 Following up the question of in vivo demonstration of a Hayflick Limit in vivo: Sydney Shall asked for these references. The Krohn referenc is courtesy of Jay Zimmerman, also at StJohns, ypjzbio@sjumusic.stjohns. Krohn also has a book from approximately the same period. See also the Finch et al Handbook of the Biology of Aging. Krohn PL Heterochronic transplantation in the study of ageing. Proc. Roy Soc. B. 157: 128 (1962) (transplantation of skin; apparently this was not different pigments but reversed anterior-posterior orientation.) Stem cell transplantation (from PaperChase/MedLine) 1. Loss of stem cell repopulating ability upon transplantation. Effects of donor age, cell number, and transplantation procedure. [ABSTRACT ONLINE] Harrison: J Exp Med (1982 Dec 1) 156(6):1767-7 2. Loss of proliferative capacity in immunohemopoietic stem cells caused by serial transplantation rather than aging. [ABSTRACT ONLINE] Harrison: J Exp Med (1978 May 1) 147(5):1526-31 1. Effects of transplantation and age on immunohemopoietic cell growth in the splenic microenvironment. [ABSTRACT ONLINE] Harrison: Exp Hematol (1988 Mar) 16(3):213- 2. The decrease in long-term marrow repopulating capacity seen after transplantation is not the result of irradiation-induced stromal... [ABSTRACT ONLINE] Gardner: Exp Hematol (1988 Jan) 16(1):49-54 Richard A. Lockshin Dept. Biol. Sci. St. John's U. 8000 Utopia Pkwy Jamaica NY 11439 USA/Phone 718: 990-1854/ Fax 718: 380-8543 In article <37lkp2$63m@infa.central.susx.ac.uk> bafa1@central.susx.ac.uk (Sydney Shall) writes: >Sydney Shall (bafa1@central.susx.ac.uk) wrote: >: Tsung-Jui Yeh (tjyeh@soda.CSUA.Berkeley.EDU) wrote: > >: : I was wondering about the Hayflick limit for rapid dividing cells like >: : ones that line the stomach and also cells of the cornea. Do these cells >: : have the same Hayflick limit as fibroblasts? If so, why can these cells >: : afford to divide so fast? > >: : Thanks >: Cells from different tissues display different Hayflick limits. This >: means that some cells like fibroblasts may go through about 50 to 70 >: population doublings, in about 150 cell generations. On the other hand, >: adult dermal fibroblasts, chondrocytes experience many fewer >: generations. Lymphocytes seem in most growth media, to experience only >: about 23 population doublings. So, at the moment we do not really know >: whether there is one fixed Hayflick limit; the evidence available so far >: would suggest that there are specific Hayflick limits for different >: tissues. This clearly has important implications for the homeostasis of >: each individual tissue. >: Moreover, it is very well established that the same cell type from >: different animal species show a species-specific Hayflick limit; this is >: part of the evidence for the notion that the Hayflick limit is >: genetically controlled. > >: -- >: Sydney SHALL, >: Laboratory of Cell and Molecular Biology, >: Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. >: Telephone: +44.273.67.83.03 FAX: +44.273.67.84.33 > > >RESPONSE: > >I think the major question to arise from this discussion is whether a >Hayflick limit exists in vivo, that is in intact bodies. Regrettably, >there is very little published evidence on this question. The only >evidence that I can adduce is (1) Werner's syndrome, where a very >evident premature ageing is correlated with a changed Hayflick limit in >vitro, and (2) secondly a paper by Rohme in which he convincingly shows >a correlation between both average and maximum lifespans of different >animals and the life-span of there cells in vitro (their Haflick limit >number). >Both of these items of evidence are correlations; so although they are >persuasive to me, I would say the question as to whether there is an in >vivo Hayflick limit is completely open and unresolved. > >The second question raised abou whether the Hayflick limit has an >COMPONENT of culture conditions in it is different. I think that the >question being asked is whether the hayflick limit is an artifact; this >means, is it TOTALLY due to the way we grow the cells. There is no >doubt that the way we grow cells influences the value of the Hayflick >limit. But the direct question is: can we grow cells in such a way that >there is NO Hayflick limit. This question has been directly addressed >by one author, who has given the answer that for mice one can grow cells >in the absence of serum and then they are immortal. But I understand >that the same author says that this does NOT work for human cells. >Furthermore, I observe that so far there is no published confirmation of >this one report. So, I think that this must be viewed with some >caution. Again, I would say that culture conditions modulate the value >of the Hayflick limit, but the existence of such a limit is abiological >property of the cells. The real issue in my view is whether this limit >is a biological property, at least in part, or SOLELY,a consequence of >the culture conditions. If the latter, then one should not look for >genes which are important in this process. If the former is true, then >one is probably justified in searching for genes which are relevant to >the phenomenon. > >-- >Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, >University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. >Tel:+44.273.67.83.03 FAX:+44.273.67.84.33; E-Mail:Janet:S.Shall@uk.ac.sussex >Elsewhere:S.Shall@sussex.ac.uk EARN/BITNET:S.Shall%sussex@ukacrl >. >. From owner-ageing@net.bio.net Sun Oct 23 22:00:00 1994 Path: biosci!agate!howland.reston.ans.net!news.sprintlink.net!nwnexus!news.halcyon.com!flames!venezia From: venezia@zgi.com (Domenick Venezia) Newsgroups: bionet.molbio.ageing Subject: Telomerase and Reality Testing Date: 24 Oct 1994 01:34:34 GMT Organization: Northwest Nexus Inc. Lines: 8 Message-ID: <38f2va$33i@news.halcyon.com> NNTP-Posting-Host: flames.zgi.com X-Newsreader: TIN [version 1.2 PL2] As far as I am aware no mammalian telomerase gene has yet been cloned. If I'm wrong please send the reference(s) via private email. Domenick Venezia ZymoGenetics, Inc. Seattle, WA venezia@zgi.com From owner-ageing@net.bio.net Mon Oct 24 22:00:00 1994 Path: biosci!agate!doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Re: Hayflick limit for rapid dividing cells Date: 25 Oct 1994 11:56:36 GMT Organization: University of Sussex Lines: 71 Distribution: bionet Message-ID: <38irpk$2nh@infa.central.susx.ac.uk> References: <385qup$ldg@mserv1.dl.ac.uk> NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] Graham Pawelec (olxpa01@mailserv.zdv.uni-tuebingen.de) wrote: : In the discussion on different limits to the proliferative lifespan for : different tissues, it was mentioned that lymphocytes may manage only ca. : 23 PD in vitro. While some authors from the ageing field have concluded : this, most immunologists working with T cell lines and clones know that : this cannot be the case. Leaving aside mouse T cells for the moment, and : concentrating on less-prone-to-transformation human T cells, simple : arithmetic demonstrates that to obtain a T cell clone in sufficient : numbers to experiment with, more than 23 PD are required. Starting from : one cell, 23 PD represents 4 million cells; commonly (but not always) T : cell clones are obtained which have experienced at least twice this : number of PD. Indeed, many immunologists simply assume that T cell clones : are immortal. In our hands, however, in well over a decade of T cell : cloning, we have not seen a single immortal human line. Average life span : of established clones is estimated at perhaps 40 - 50 PD, with the most : long-lived clones achieving ca. 80 PD (and thus conforming to the : "Weismann-Swim-Hayflick" limit, as Gavrilov & Gavrilova have suggested it : should be designated). There is a great deal of clonal heterogeneity and : many clones survive even less than 23 PD. : How to resolve the discrepancy between a maximum in vitro lifespan of ca. : 23 PD established by "T cell gerontologists" and the 80 PD or more : established by "T cell immunologists"? I think that this may have something : to do with the fact that the former have exclusively used uncloned T cell : lines, rather than monoclonal populations. We have observed that uncloned : lines manifest shorter lifespans than monoclonal lines obtained from the : same starting population. Therefore, we believe that this is more to do with : interactions between different T cell clones in the bulk population, where : inhibitory effects predominate after a relatively short time, and that : this has nothing to do with the actual potential lifespan of the cells. : Separating suppressive cells by cloning results in the isolation of : populations with extended lifespan; however, recloning monoclonal : populations does not result in further extension of lifespan beyond the : ca. 80 PD maximum, showing that the cloning procedure per se is not : responsible for extending lifespan. : Although T cells may be a special case, it might be conceivable that : studies on other cell types would show similar discrepancies between the : behaviour of cloned - versus - uncloned populations. Maybe some of the : controversies in the literature on different potential lifespans could be : resolved in this way. Perhaps someone in this discussion group could : comment on that? : Graham Pawelec, : Section for Transplantation Immunology & Immunohematology, : University Hospital, : Tuebingen, Germany : Coordinator, European Union Concerted Action on the Molecular Biology : of Immunosenescence, EUCAMBIS Graham Pawelec is correct, I think, in drawing attention to the specific features of T-lymphocyte biology. However, there is also an aspect of the growth of T-lymphocytes which is consistent with a life-span of 20-30 population doublings. When we grow T-lymphocytes we grow a mass culture of millions of clones; therefore, we do not need to first establish a clone from an individual cell, which would certainly add a minimum of 20 population doublings to the total. This fact also possibly leads to waves of clonal successions, as different clonal populations take over the culture. It is a feature of T-cell growth that the growth rate is erratic, which would be consistent with this explanation, but I would emphasise that this has not been experimentally demonstrated. -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Tel:+44.273.67.83.03 FAX:+44.273.67.84.33; E-Mail:Janet:S.Shall@uk.ac.sussex Elsewhere:S.Shall@sussex.ac.uk EARN/BITNET:S.Shall%sussex@ukacrl From owner-ageing@net.bio.net Tue Oct 25 22:00:00 1994 Path: biosci!rutgers!gatech!newsfeed.pitt.edu!uunet!news.delphi.com!usenet From: jarice@delphi.com Newsgroups: bionet.molbio.ageing Subject: Re: Telomerase and Reality Testing Date: Tue, 25 Oct 94 21:37:09 -0500 Organization: Delphi (info@delphi.com email, 800-695-4005 voice) Lines: 33 Message-ID: References: <38f2va$33i@news.halcyon.com> NNTP-Posting-Host: bos1d.delphi.com X-To: Domenick Venezia Domenick Venezia writes: >As far as I am aware no mammalian telomerase gene has yet been cloned. >If I'm wrong please send the reference(s) via private email. I believe the original question was whether telomerase has ever been exogenously applied to an organism to invesitgate it's effects. I would imagine that two things are possible: the cancer rate would increase, and the organism may live longer. Remember, many cell types in the human body do not ordinarily divide. So even if telomerase was successful with dividing cells, non-dividing cells would continue to age and deteriorate. There is a problem with the telomere theory of aging, however. If the length of the telomere serves roughly as a limit to the number of divisions a cell is capable of, how does one explain various experiments that extend the life of an organism, for example: > Particularly striking was a paper entitled "Pineal Cross-Transplantation in > Mice (Old to Young and Vice-Versa) as evidence for an Endogenous "Aging > Clock", quote: "A remarkable acceleration of aging and death was seen in the > young mice grafted with an "old" pineal, while a very significant delay of agi ng > and death was observed in the old mice grafted with a "young" pineal gland." > The old mice lived an average of 1021 days, while the young mice lived an > average of 510 days. Control mice lived an average of 719 days. In the case of the rats that lived longer, did the cells that divided get a few extra divisions, and if so, was this extra life mediated by telomerase? If the dividing cells did not get extra divisions, was the young pineal gland somehow increasing the interval between divisions? Jim Rice From owner-ageing@net.bio.net Tue Oct 25 22:00:00 1994 Path: biosci!POSSUM.MURDOCH.EDU.AU!cummins From: cummins@POSSUM.MURDOCH.EDU.AU (Dr Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Extended ageing in Microchiroptera Date: 25 Oct 1994 19:16:19 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 23 Sender: daemon@net.bio.net Distribution: world Message-ID: <9410260221.AA08400@possum.murdoch.edu.au> NNTP-Posting-Host: net.bio.net A recent report in a local journal (Tideman, CR "Meat Markets and Chastity Belts" Australian Natural History 1994 p 66-67) suggests that Microchiropteran bats, with body masses equivalent to mice, can nevertheless live more than 30 years. (1) Does anyone in this group know of active research on ageing in bats; (2) Any ideas as to the possible mechanism(s)? Yours, virtually:- Jim "Spermatology rules o~ o~ o~ o~" Cummins Associate Professor in Veterinary Anatomy Murdoch University, Murdoch Western Australia 6150 Tel +61-9-360 2668 Fax +61-9-310 4144 E mail cummins@possum.murdoch.edu.au From owner-ageing@net.bio.net Tue Oct 25 22:00:00 1994 Path: biosci!agate!howland.reston.ans.net!EU.net!uunet!solaris.cc.vt.edu!news.duke.edu!godot.cc.duq.edu!newsfeed.pitt.edu!dsinc!netnews.upenn.edu!netnews.CC.Lehigh.EDU!ns1.CC.Lehigh.EDU!not-for-mail From: x011@ns1.CC.Lehigh.EDU Newsgroups: bionet.molbio.ageing Subject: Aloe vera? Date: 26 Oct 1994 08:11:22 -0400 Organization: Lehigh University Lines: 4 Message-ID: <38lh1a$6cvk@ns1.CC.Lehigh.EDU> NNTP-Posting-Host: ns1.cc.lehigh.edu Has anyone done any research on aloe vera as an anti-aging chemical. I believe it is an anti-oxidant and reduces cell division. It may also cause nerve cells to duplicate. The status of the nervous system I suspect is linked to longevity. Ron Blue From owner-ageing@net.bio.net Tue Oct 25 22:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!bcm!cs.utexas.edu!swrinde!elroy.jpl.nasa.gov!lll-winken.llnl.gov!enews.sgi.com!decwrl!netcomsv!netcom.com!jabowery From: jabowery@netcom.com (Jim Bowery) Subject: Re: Telomerase and Reality Testing Message-ID: Organization: NETCOM On-line Communication Services (408 261-4700 guest) X-Newsreader: TIN [version 1.2 PL1] References: <38f2va$33i@news.halcyon.com> Date: Wed, 26 Oct 1994 16:10:51 GMT Lines: 38 First, I want to emphasize that I am simply asking a question about reality testing as oppose to theoretic speculation. Treating rats with telomerase would be an interesting experiment regardless of the outcome and it may even help us engage in more fruitful lines of theoretic speculation. Has it been done? If not, why not? Does the telomerase gene have to be cloned before such reality testing can commence? jarice@delphi.com wrote: : of divisions a cell is capable of, how does one explain various : experiments that extend the life of an organism, for example: : : > Particularly striking was a paper entitled "Pineal Cross-Transplantation in : > Mice (Old to Young and Vice-Versa) as evidence for an Endogenous "Aging : > Clock", quote: "A remarkable acceleration of aging and death was seen in the : > young mice grafted with an "old" pineal, while a very significant delay of agi : ng : > and death was observed in the old mice grafted with a "young" pineal gland." : > The old mice lived an average of 1021 days, while the young mice lived an : > average of 510 days. Control mice lived an average of 719 days. : : In the case of the rats that lived longer, did the cells that divided : get a few extra divisions, and if so, was this extra life mediated by : telomerase? If the dividing cells did not get extra divisions, was the : young pineal gland somehow increasing the interval between divisions? This is a very interesting experiment, of course. But there is no necessary relationship between the observed effect and telomerase even if both telomerase and the pineal gland are keys to the riddle of aging. It would be nice if we discovered a central "control system" which mediated telomerase and other age-related phenomena, of course. But all redundant speculation aside: I'm really confused as to why the experiment with telomerase hasn't been done (if indeed it hasn't). -- The promotion of politics exterminates apolitical genes in the population. The promotion of frontiers gives apolitical genes a route to survival. From owner-ageing@net.bio.net Wed Oct 26 22:00:00 1994 Path: biosci!daresbury!not-for-mail From: Newsgroups: bionet.molbio.ageing Subject: Telomere information Date: 27 Oct 1994 11:32:37 -0000 Lines: 7 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <38o34l$bbg@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk Once again there h ve been enquiries about some basic information about telomeres. For those of you who want to have a very general introduction to telomere research and progress, a well-written simple article by a science-journalist Jean Marx is available in the journal SCIENCE, vol. 265, pp 1656, issue dated 16 September 1994, titled CHROMOSOME ENDS CATCH FIRE. Wish you a good reading. From owner-ageing@net.bio.net Wed Oct 26 22:00:00 1994 Path: biosci!daresbury!not-for-mail From: Newsgroups: bionet.molbio.ageing Subject: More information on telomeres Date: 27 Oct 1994 11:35:05 -0000 Lines: 10 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <38o399$bg4@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk In the previous posting, I forgot to mention two more interesting write-ups on telomeres: 1, by T.R. Cech in SCIENCE, vol. 266, pp 387, 21st October 1994 issue: giving enough background and discussing the publication of a paper in the same issue of SCIENCE, pp 404 reporting the discovery of the gene for telomerase RNA in the yeast. These two papers should bring any one up-to-date in telomere research. Wishing you good reading, Suresh Rattan/Aarhus/Denmark From owner-ageing@net.bio.net Wed Oct 26 22:00:00 1994 Path: biosci!agate!howland.reston.ans.net!vixen.cso.uiuc.edu!uwm.edu!psuvax1!rutgers!netnews.upenn.edu!netnews.CC.Lehigh.EDU!ns1.CC.Lehigh.EDU!not-for-mail From: x011@ns1.CC.Lehigh.EDU Newsgroups: bionet.molbio.ageing Subject: Chromosome #1 Date: 27 Oct 1994 08:23:30 -0400 Organization: Lehigh University Lines: 3 Message-ID: <38o642$4fjq@ns1.CC.Lehigh.EDU> NNTP-Posting-Host: ns1.cc.lehigh.edu Several years ago in Science and interesting article said that if you remove chromosome #1 the human cell will be immortal. Is there any connection to telemerase? Ron Blue From owner-ageing@net.bio.net Thu Oct 27 22:00:00 1994 Path: biosci!ESSEX.HSC.COLORADO.EDU!kruged From: kruged@ESSEX.HSC.COLORADO.EDU (Edward Krug) Newsgroups: bionet.molbio.ageing Subject: NON-Hayflick fibroblast ageing assay Date: 28 Oct 1994 01:49:31 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 16 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Hans Selye and others, paraphrased, suggested that ageing is the decreased range of response to stress. I have an approach for producing a physiologically valid Non-Hayflick form of ageing in fibroblasts in tissue culture. I have standard tissue culture facilities and both high and low passage human fibroblasts in culture. I am looking for stimulus-response pairs with which to challenge my fibroblasts and see if they do display a decreased response in absence of increased passage number. Any suggestions?? Please send suggestions to me at kruged@essex.hsc.colorado.edu From owner-ageing@net.bio.net Thu Oct 27 22:00:00 1994 Path: biosci!rutgers!gatech!howland.reston.ans.net!pipex!lyra.csx.cam.ac.uk!sunsite.doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Re: Diurnal hormones and Hayflick limit Date: 28 Oct 1994 17:08:53 GMT Organization: University of Sussex Lines: 26 Distribution: world Message-ID: <38rb75$ih9@infa.central.susx.ac.uk> References: NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] Edward Krug (kruged@ESSEX.HSC.COLORADO.EDU) wrote: : Dirunal hormone cycles are acknowledged to be important in ageing : of intact animals, but when "in vitro" cell doubling limits are discussed : the standard model is steady state medium composition. Does anyone out : there know of any studies where the tissue culture media has been regulated : to mimic the normal "in vivo" hormonal pattern? : Edward C. Krug Ph.D. : Instructor : Campus Box B-168 : Dept. of Infectious Diseases : Univ. of Colorado Health Sciences Center : 4200 E. Nineth Ave. : Denver, Colorado, 80262 : e-mail = kruged@essex.hsc.colorado.edu I am not aware of any reports which mimic the diurnal rythm. But there are numerous reports on the effects of a variety of hormones. I would recommend that you seek out some papers by Vincent Cristafalo, who has also written a very review of this topic. -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Tel:+44.273.67.83.03 FAX:+44.273.67.84.33; E-Mail:Janet:S.Shall@uk.ac.sussex Elsewhere:S.Shall@sussex.ac.uk EARN/BITNET:S.Shall%sussex@ukacrl From owner-ageing@net.bio.net Fri Oct 28 22:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!lyra.csx.cam.ac.uk!macx20.mrc-lmb.cam.ac.uk!user From: jong@mrc-cpe.cam.ac.uk (Jong Park) Newsgroups: bionet.molbio.ageing Subject: Information.... Jong Followup-To: bionet.molbio.ageing Date: Sat, 29 Oct 1994 15:35:43 +0000 Organization: Centre For Protein Engineering, Room308, Hills Road, CB2 2QH, Cambridge, UK Lines: 14 Message-ID: NNTP-Posting-Host: macx20.mrc-lmb.cam.ac.uk I am a student in Protein Science and I am very much interested in Ageing. I already have read a lot of papers and want to keep following the development of Ageing research. If anybody want to release any data, articles, and wish to make a list of subscribers please add my name and address. Also if you all send me your mail address I will summarize info. I got and direct them to you. Jong Park -- Jong PARK, MRC Centre For Protein Engineering, Cambridge, Korean Tim Hubbard's student. jong@mrc-cpe.cam.ac.uk, (44) 01223 402134 From owner-ageing@net.bio.net Sat Oct 29 22:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!agate!spool.mu.edu!howland.reston.ans.net!ix.netcom.com!netcom.com!jimwork From: jimwork@netcom.com (James A. Work) Subject: Re: Aloe vera? Message-ID: Organization: NETCOM On-line Communication Services (408 261-4700 guest) X-Newsreader: TIN [version 1.2 PL1] Date: Sun, 30 Oct 1994 21:41:10 GMT Lines: 4 I doubt that you can have it both ways. How does it inhibit cell division but encourage nerve cell division? -- James A. Work a major skew. jimwork@netcom.com From owner-ageing@net.bio.net Sun Oct 30 22:00:00 1994 Path: biosci!bcm!cs.utexas.edu!howland.reston.ans.net!news.sprintlink.net!EU.net!uunet!olivea!charnel.ecst.csuchico.edu!waldorf.csc.calpoly.edu!decwrl!tribune.usask.ca!quartz.ucs.ualberta.ca!gpu!ooskin From: ooskin@gpu.srv.ualberta.ca (Alec Oskin) Newsgroups: bionet.molbio.ageing Subject: Request: Information on Current Research Date: 31 Oct 1994 20:19:44 GMT Organization: University of Alberta Lines: 13 Message-ID: <393jh0$ed4@quartz.ucs.ualberta.ca> NNTP-Posting-Host: gpu3.srv.ualberta.ca X-Newsreader: TIN [version 1.2 PL2] Does anyone have a list of labs currently working in this field (i.e. telomerase characterization / function) and what, specifically these labs are doing? I would appreciate it if you could either post such a list here or e-mail me directly. Also, can anyone recommend any reviews/current papers that would bring me "up to par" on the research being done in this field. ----------- """""" " """"" """"" Alec Oskin " " " " " """""" " """ " University of Alberta, Edmonton, Canada " " " " " " " """""" """""" """""" From owner-ageing@net.bio.net Sun Oct 30 22:00:00 1994 Path: biosci!agate!howland.reston.ans.net!news.cac.psu.edu!news.pop.psu.edu!hudson.lm.com!godot.cc.duq.edu!newsfeed.pitt.edu!dsinc!netnews.upenn.edu!netnews.CC.Lehigh.EDU!ns1.CC.Lehigh.EDU!not-for-mail From: x011@ns1.CC.Lehigh.EDU Newsgroups: bionet.molbio.ageing Subject: Re: Aloe vera? Date: 31 Oct 1994 09:03:47 -0500 Organization: Lehigh University Lines: 12 Message-ID: <392tg3$45cs@ns1.CC.Lehigh.EDU> NNTP-Posting-Host: ns1.cc.lehigh.edu In article , jimwork@netcom.com (James A. Work) wr ites: >I doubt that you can have it both ways. How does it inhibit cell >division but encourage nerve cell division? >-- >James A. Work a major skew. jimwork@netcom.com > Why don't nerve cell divide but normal cells do. The reverse could be the way. Nerve cell divide if exposed to the hormone that causes epidermal tissue to divide. Aloe taken internally slows recovery from surgery. Aloe externally helps the skin repair damage. Therefore .... Ron Blue From owner-ageing@net.bio.net Sun Oct 30 22:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!sunsite.doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Re: Extended ageing in Microchiroptera Date: 31 Oct 1994 11:03:24 GMT Organization: University of Sussex Lines: 31 Distribution: world Message-ID: <392its$qsi@infa.central.susx.ac.uk> References: <9410260221.AA08400@possum.murdoch.edu.au> NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] : A recent report in a local journal (Tideman, CR "Meat Markets and Chastity : Belts" Australian Natural History 1994 p 66-67) suggests that : Microchiropteran bats, with body masses equivalent to mice, can : nevertheless live more than 30 years. : : (1) Does anyone in this group know of active research on ageing in bats; : (2) Any ideas as to the possible mechanism(s)? : Yours, virtually:- : Jim "Spermatology rules o~ o~ o~ o~" Cummins : Associate Professor in Veterinary Anatomy : Murdoch University, : Murdoch Western Australia 6150 : Tel +61-9-360 2668 : Fax +61-9-310 4144 : E mail cummins@possum.murdoch.edu.au RESPONSE Is there any reason to suppose that there is a correlation between body size and longevity? -- Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Tel:+44.273.67.83.03 FAX:+44.273.67.84.33; E-Mail:Janet:S.Shall@uk.ac.sussex Elsewhere:S.Shall@sussex.ac.uk EARN/BITNET:S.Shall%sussex@ukacrl From owner-ageing@net.bio.net Mon Oct 31 22:00:00 1994 Path: biosci!rutgers!gatech!howland.reston.ans.net!news2.near.net!news.delphi.com!usenet From: proctorp@delphi.com Newsgroups: bionet.molbio.ageing Subject: Re: Extended ageing in Microchiroptera Date: Mon, 31 Oct 94 20:46:11 -0500 Organization: Delphi (info@delphi.com email, 800-695-4005 voice) Lines: 14 Message-ID: References: <9410260221.AA08400@possum.murdoch.edu.au> <392its$qsi@infa.central.susx.ac.uk> NNTP-Posting-Host: bos1d.delphi.com X-To: Sydney Shall Sydney Shall writes: >Is there any reason to suppose that there is a correlation between body >size and longevity? Yes, sort of. Among mammals, longevity is roughly correlated with body surface area. Same is true of birds-- Except, a typical bird lives twice as long as the same-size mammal. Reason unknown. However, birds do not break down uric acid an antioxidant which has been correlated with increased lifespan in primates. Dr. Dr. Peter Proctor From owner-ageing@net.bio.net Mon Oct 31 22:00:00 1994 Path: biosci!internet!biosci!not-for-mail From: biohelp (BIOSCI Administrator) Newsgroups: bionet.molbio.ageing Subject: UNSUBSCRIBING, BIOSCI ARCHIVES, ADDRESS DATABASE & BIOSCI FAQ Date: 1 Nov 1994 02:00:16 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 322 Sender: daemon@net.bio.net Distribution: world Message-ID: <199411011000.CAA19661@net.bio.net> NNTP-Posting-Host: net.bio.net Four important items follow: How to cancel e-mail subscriptions to BIOSCI newsgroups, BIOSCI archive searching, the BIOSCI FAQ, and the BIOSCI User Address Directory form. If you have not yet listed yourself in our BIOSCI user directory, please take a few minutes to complete and return the form below. If your personal information has changed since you listed yourself, please send us a complete new updated form. We can not make manual revisions to existing entries. Sincerely, Dave Kristofferson BIOSCI/bionet Manager biosci-help@net.bio.net **** How to cancel a BIOSCI e-mail subscription **** If you want to cancel your e-mail subscription to this group, PLEASE DO NOT POST YOUR UNSUBSCRIBE REQUEST TO THE NEWSGROUP ADDRESS (NOR REPLY TO A MESSAGE POSTED TO THE NEWSGROUP)!!! This would send your request to all of the readers of the newsgroup, but it might still not be seen by the BIOSCI staff - thus you would annoy many people and possibly not accomplish your goal anyway. IF YOU ARE LOCATED IN THE AMERICAS OR PACIFIC RIM COUNTRIES, please send a message to biosci@net.bio.net Instructions will be returned automatically, so the contents of your message do not matter. IF YOU ARE LOCATED IN EUROPE, AFRICA OR CENTRAL ASIA, please send a message to MXT@dl.ac.uk containing the word help in the body of the message to retrieve e-mail server instructions. Any text placed on the Subject: line of your message will be ignored, so be sure to put the "help" command in the body of the message. If you need personal assistance, a BIOSCI staff member can be contacted at either of the following addresses. Please contact the address designated for your location. Support Address Location --------------- -------- biosci@daresbury.ac.uk Europe, Africa, and Central Asia biosci-help@net.bio.net Americas and the Pacific Rim **** SEARCHING BIOSCI ARCHIVES **** The easiest way to search the BIOSCI archives is to use gopher software and connect over the Internet to net.bio.net, the U.S. BIOSCI computer. We maintain three indexes which are searchable from the main gopher menu on net.bio.net: (1) an index of all BIOSCI postings; (2) an index of individual journal article references from the Table of Contents postings on the BIO-JOURNALS newsgroup; and (3) an index of BIOSCI users including regular mail and e-mail addresses, phone/FAX numbers, research interests, and newsgroup participation. E-mail users can search the BIOSCI archives by using our waismail e-mail server. For instructions send the message help to waismail@net.bio.net. Leave the Subject: line blank (anything entered on the Subject: line is ignored). WAIS software can also be used to search the archives as described in the BIOSCI FAQ (see below). Finally, the BIOSCI archive files are accessible by anonymous FTP to net.bio.net [134.172.2.69] in the directory pub/BIOSCI. **** BIOSCI FREQUENTLY ASKED QUESTIONS (FAQ) SHEET **** New users of BIOSCI/bionet may want to read the "Frequently Asked Questions" or "FAQ" sheet for BIOSCI. The FAQ provides details on how to participate in these forums and is available for anonymous FTP from net.bio.net [134.172.2.69] in pub/BIOSCI/doc/biosci.FAQ or for retrieval by gopher to net.bio.net, port 70. It may also be requested by sending the command info faq in the body of an e-mail message to the Internet address biosci-server@net.bio.net. Please do not enter the info faq command on the Subject: line of your message since the e-mail server ignores text on the Subject: line. The FAQ is also posted on the first of each month to the newsgroup BIONEWS/bionet.announce immediately following the posting of the BIOSCI information sheet. **** BIOSCI USER ADDRESS DIRECTORY **** Please take this opportunity to add your name and address information to the BIOSCI User Address Database if you have not already done so. Below is the address form that we would like each reader of the BIOSCI/bionet newsgroups to complete and return if you would like to be listed in our database. The database serves as a directory that enables biologists, who are currently using (or even just reading) the BIOSCI newsgroups, to look up e-mail addresses and other information about our users. The address database is reindexed nightly for WAIS, waismail, and gopher access. If you have access to gopher, connect to net.bio.net to search the database. If you have access to WAIS, please use our WAIS source biologists-addresses.src. If you are not on the Internet, please use our waismail server (send the word "help" to waismail@net.bio.net to get instructions; any text on the Subject: line of your message will be ignored, so put the help command in the body of the mail message.). Please carefully follow the instructions for completing the form below and return it to either of the following two addresses (whichever is more convenient for you). Thanks in advance for taking the time to complete and return the form. Addresses for returning forms Location Network ----------------------------- -------- ------- biovote@net.bio.net U.S.A. Internet/BITNET biovote@daresbury.ac.uk U.K. JANET MAKING SURE THAT YOUR INFORMATION IS CURRENT This notice will be mailed bimonthly to each newsgroup. You should check your database entry from time-to-time to see if your address information is still up-to-date. Using Gopher to complete the form --------------------------------- If you don't want to use a text editor, you can also use Dan Jacobson's gopher site to fill out the address database form as follows. Otherwise skip this section on gopher and proceed to the instructions for filling out the form below. > To add yourself to the database just point your > gopher client at merlot.gdb.org and select the following: > > --> 15. Searching For Biologists/ > > --> 9. E-mail Addresses of Biosci-Bionet Users/ > > --> 1. Add (or Correct) Your Address to the BIOSCI User Address > Data.. > > > And fill out the form. or Rob Harper's gopher site in Europe as follows: > Europeans can point their gopher client at gopher.csc.fi and add their > information to the database. All entries will be mailed directly to > Dave for incorporation in a wais source. > > The path to the questionare is as follows. > > ---> 10. Finnish EMBnet BioBox/ > > ---> 8. FAQ Files/ > > FAQ Files > > 1. EMBnet: Information. > 2. EMBnet: Internet resources guide. > 3. A Biologist's Guide to Internet Resources/ > 4. All FAQs (Frequently Asked Questions) Searches and Archives/ > --->5. Bionauts Address Database (questionaire) IMPORTANT INSTRUCTIONS - PLEASE READ CAREFULLY Please enter all responses after the : on each line, leaving one (1) blank space after the : (i.e., before the start of your text). Please do NOT extend your responses past the end of each line (80 characters). PLEASE DO NOT alter any of the field identifiers such as "first name: ". If you have nothing to enter after a field identifier, PLEASE LEAVE IT - do not delete it even if there is no data on the line in question. Several lines are provided at the end of the form for comments, but, please adhere to the line length restriction. On the date: line, please enter the date in the DD-MM-YY format, e.g., 15-05-93 for 15 May 1993. This line will tell others when the information was last updated. Please be sure to include the 0's for single digit days or months, e.g., 15-05-93, not 15-5-93. Note that the "e-mail network: " line below is for specifying, e.g., "Internet," "BITNET," "EARN," "JANET," or whatever other network that your computer may be on. If you are uncertain about any field, please feel free to leave it blank, but please DO NOT DELETE the field identifier from the form! In the first field below, "New information or Update ...", please enter "N" if this is the first time that you have registered in the directory or "U" if you are correcting a listing that you sent to us previously. The comment: lines may be used for anything that you like but PLEASE DO NOT DELETE THEM FROM THE FORM OR ALTER THEM. One suggested use is to list the names of the newsgroups in which you participate. Please use the MAILING LIST name (see below - the latest version of the list can be requested from biosci@net.bio.net) instead of the USENET name even if you don't participate by e-mail. WAIS might get confused by the periods in the USENET names. This allows one to retrieve via WAIS or waismail the list of participants in a particular group. For example: comment: ARABIDOPSIS PLANT-BIOLOGY BIONEWS On the comment: lines use these names below ---- NOT the USENET names below MAILING LIST NAME USENET Newsgroup Name ----------------- --------------------- ACEDB-SOFT bionet.software.acedb AGEING bionet.molbio.ageing AGROFORESTRY bionet.agroforestry ARABIDOPSIS bionet.genome.arabidopsis BIOFORUM bionet.general BIO-INFORMATION-THEORY bionet.info-theory BIONAUTS bionet.users.addresses BIONEWS bionet.announce BIO-JOURNALS bionet.journals.contents BIO-MATRIX bionet.molbio.bio-matrix BIOPHYSICAL-SOCIETY bionet.prof-society.biophysics BIOPHYSICS bionet.biophysics BIO-SOFTWARE bionet.software BIOTHERMOKINETICS bionet.metabolic-reg CELL-BIOLOGY bionet.cellbiol CHLAMYDOMONAS bionet.chlamydomonas CHROMOSOMES bionet.genome.chromosomes COMPUTATIONAL-BIOLOGY bionet.biology.computational CYTONET bionet.cellbiol.cytonet DROSOPHILA bionet.drosophila EMBL-DATABANK bionet.molbio.embldatabank EMPLOYMENT bionet.jobs GDB bionet.molbio.gdb GENBANK-BB bionet.molbio.genbank GENETIC-LINKAGE bionet.molbio.gene-linkage GRASSES-SCIENCE bionet.biology.grasses HIV-MOLECULAR-BIOLOGY bionet.molbio.hiv HUMAN-GENOME-PROGRAM bionet.molbio.genome-program IMMUNOLOGY bionet.immunology INFO-GCG bionet.software.gcg JOURNAL-NOTES bionet.journals.note METHODS-AND-REAGENTS bionet.molbio.methds-reagnts MOLECULAR-EVOLUTION bionet.molbio.evolution MYCOLOGY bionet.mycology NEUROSCIENCE bionet.neuroscience N2-FIXATION bionet.biology.n2-fixation PARASITOLOGY bionet.parasitology PHOTOSYNTHESIS bionet.photosynthesis PLANT-BIOLOGY bionet.plants POPULATION-BIOLOGY bionet.population-bio PROTEIN-ANALYSIS bionet.molbio.proteins PROTEIN-CRYSTALLOGRAPHY bionet.xtallography PROTISTA bionet.protista RAPD bionet.molbio.rapd SCIENCE-RESOURCES bionet.sci-resources STRUCTURAL-NMR bionet.structural-nmr TROPICAL-BIOLOGY bionet.biology.tropical VIROLOGY bionet.virology WOMEN-IN-BIOLOGY bionet.women-in-bio YEAST bionet.molbio.yeast Listing newsgroups on the comment: line is optional, of course. Thanks again for your cooperation! --------------- please cut here and return portion below --------------- New information or Update to old record (enter N or U): date (DD-MM-YY): first name: middle initial: family name: job title: e-mail address: e-mail network: phone number: FAX number: institution: address1: address2: address3: city: state/province: country: postal code: research interest: research interest: comment: comment: comment: comment: comment: