From owner-ageing@net.bio.net Sun May 01 23:00:00 1994 Path: biosci!HAL.HAHNEMANN.EDU!springerj From: springerj@HAL.HAHNEMANN.EDU Newsgroups: bionet.molbio.ageing Subject: Does anyone out there know of a source of the FAS/Apo-1 cDNA? I am interested in Date: 2 May 1994 11:43:35 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 2 Sender: daemon@net.bio.net Distribution: bionet Message-ID: <0097DD52.3DF60860.2@hal.hahnemann.edu> NNTP-Posting-Host: net.bio.net studying mRNA expression levels in amyotrophic lateral sclerosis. I am also looking for a good human monoclonal as well. Thanks. Joe E. Springer. From owner-ageing@net.bio.net Sun May 01 23:00:00 1994 Path: biosci!NVEGW.CRL.AECL.CA!Clive.L.Greenstock From: Clive.L.Greenstock@NVEGW.CRL.AECL.CA Newsgroups: bionet.molbio.ageing Subject: IQ Date: 2 May 1994 14:55:51 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 2 Sender: daemon@net.bio.net Distribution: bionet Message-ID: <940502174120902-MTANVE*Clive.L.Greenstock@NVE.CRL.AECL.CA> NNTP-Posting-Host: net.bio.net I am trying to track down references ot articles on IQ and radiation exposure. Ant y leads? Clive Greenstock From owner-ageing@net.bio.net Mon May 02 23:00:00 1994 Path: biosci!bcm!mbcr.bcm.tmc.edu!th035681 From: th035681@mbcr.bcm.tmc.edu (Timothy R. Hughes) Newsgroups: bionet.molbio.ageing Subject: Re: Telomerase Date: 3 May 1994 04:07:48 GMT Organization: Baylor College of Medicine, Houston, Tx Lines: 20 Distribution: world Message-ID: <2q4imk$d17@gazette.bcm.tmc.edu> References: <2pg1c8$kbu@infa.central.susx.ac.uk> <2plpkd$p12@scunix2.harvard.edu> NNTP-Posting-Host: mbcr.bcm.tmc.edu Regarding a previous post: >Sydney Shall (bafa1@central.susx.ac.uk) wrote: >: The enzyme telomerase has been shown to be present in immortal >: cell lines. However, it has never been purified and therefore it has >: never been cloned. > >Yeast telomeres were first cloned in 1982 (Szostak & Blackburn; Cell >29:245). Tetrahymena telomerase was cloned in 1987 >(Greider & Blackburn; Cell 51: 887) and I suspect a mammalian homologue >has since been cloned. Telomerase turns out to be a protein which contains >a small RNA molecule, used to prime telomere synthesis. 1.) The RNA component of RNA telomerase has been cloned, but unless the data is unpublished or very recently published none of the protein components have been cloned, only purified. 2.) The cloning of a mammalian homologue has not yet been published. -- Tim Hughes From owner-ageing@net.bio.net Mon May 02 23:00:00 1994 Path: biosci!bcm!mbcr.bcm.tmc.edu!th035681 From: th035681@mbcr.bcm.tmc.edu (Timothy R. Hughes) Newsgroups: bionet.molbio.ageing Subject: FAQ Date: 3 May 1994 04:23:37 GMT Organization: Baylor College of Medicine, Houston, Tx Lines: 555 Distribution: world Message-ID: <2q4jk9$d17@gazette.bcm.tmc.edu> NNTP-Posting-Host: mbcr.bcm.tmc.edu The purpose of this FAQ is to address Frequently Asked Questions about the molbio.aging newsgroup. I will post around the first of the month every month. Hopefully this will increase participation, especially by people who read this newsgroup but don't write to it. If you have any thoughts or suggestions, or would like to see any additional topics or specific publications included, please email me at: th035681@mbcr.bcm.tmc.edu Contents include: 1.) brief descriptions of topics generally encompassed, in order to indicate what's going on in general; and 2.) a few references, reviews and/or recent publications regarding topics in aging research. All references should of course be taken to include "and references therein". Thanks, -- Tim Hughes Note: I am at the end of my final term of classes and have not had much time this month, so this FAQ is similar to last month's. I have dozens of additional articles and plan to include them over the (more relaxed) summer months. ======================================================================= I. Definition of Aging A. Senescence - Senescence refers to intrinsic adverse changes during aging in an organism. Strictly this is manifest as an increasing likelihood of death as a function of time, measured either from birth or from some developmental stage. [Also, strictly the term "senescence" should be used instead of "aging" in this FAQ but I haven't bothered.] Cell senescence refers to the limited proliferative capacity of cultured somatic cells (see below). 1. Gompertz Curve: A mathematical function called the "Gompertz curve" can be derived to describe expected mortality statistics for a population of organisms whose probability of death increases as a function of time. Many populations (including humans) demonstrate a survival curve which can be fit closely by a Gompertz curve. A critical parameter in the Gompertz expression is the MRDT (mortalitay rate doubling time) which is considered the index of how fast organisms in the population senesce, and it has been suggested that in scientific studies true slowing of the aging process occurs only when the MRDT increases, regardless of other aging parameters (i.e., mean, mode, maximum lifespan). General references on the study of aging: Finch, C. E. 1991. Longevity, Senescence, and the Genome. Univ. Chicago Press. 843 pages including references. Martin, George R. et al. 1993. Aging - Causes and Defenses. Annu. Rev. Med. 44:419-29. A quick overview, not entirely comprehensive but easy reading. Kirkwood, T.B.L. and Cremer, T. Cytogerontology Since 1881: A Reappraisal of August Weismann and a Review of Modern Progress. Human Genetics (1982) 60:101-121. A historical review of aging theories and arguments. II. Theories and evidence regarding the aging of multicellular organisms A. General Arguments. Population genetics [something I know little about] argues that no genetic trait which is detrimental late in life would be selected for, so no genes can survive throughout a population whose sole function is to cause senescence. The remaining possibilites are as follows: 1. Antagonistic Plieotropy: It is possible for genes which are benefical or necessary in youth or in the short term to be detrimental in the long term. An example is the cytochrome oxidase, a metabolic enzyme [detoxifant, I think] which is responsible for the initial step in transforming a number of dietary compounds into mutagenic agents. References: Aeschbacher, H-U. and Turesky, R.J. (1991) Mammalian cell mutagenicity and metabolism of heterocyclic aromatic amines. Mutation Research, 256:235-250. 2. Longevity Assurance Genes: It is also possible that genes which are designed to protect us from detriment be finite in capacity, as no selection may exist for alleles which protect for longer than the lifetime. [Example: genes involved in DNA damage control in somatic tissues.] B. Disposable Soma Theory: It has been suggested that the optimal allocation of energy for an organism which reproduces repeatedly is to invest no more energy in somatic maintenance than is necessary to ensure reproduction. [The original idea, I believe, referred primarily to DNA damage.] [Also, this argument seems unlikely to me to apply to humans. My understanding is that we consume 40% of our resting energy on brain activity, and about 30% of all ATP generated on maintaining transmembrane potentials (from which many cellular processes are driven, I'm not sure how much of that is converted into work and how much is lost by diffusion) and maintain a fairly warm body temperature. This suggests to me that energy conservation is not a significant selective advantage for mammals and humans in particular.] C. Somatic Mutation Hypothesis. DNA is inherently unstable and is susceptible to numerous modification and damaging agents. As genetic material it requires constant maintenance. One of the original ideas about the aging process is that the accumulation of somatic mutations throughout the lifespan is responsible for dysfunction of cells and consequently of organs and individuals. This has fallen out of favor as a mechanism for aging since DNA damage would be expected to be fairly random, and aging is largely consistent over a population. 2. free radicals: Reactive oxygen species are produced by mitochondria in oxidative phosphorylation, the biochemical pathway that allows us to utilize oxygen in energy production [conversion, rather]. Free radical species can also be produced by ionozing radiation. Free radicals can modify/damage a wide range of cellular molecules including DNA, lipids and proteins (see below). 2. carcinogens and mutagens: 3. cancer: 4. mitochondrial DNA damage: Mitochondria contain a small genome which due to its proximity to oxidative phosphorylation activity is more susceptible to oxidation than the nuclear DNA. Human mtDNA is 16.6 kb and encodes a small portion of the peptides involved in oxidative phosphorylation and also the rRNAs and tRNAs needed to translate these genes. It has been observed that the mutation rate of mtDNA is higher than that of the nuclear DNA, and also that there is a decline in oxidative phosphorylation activity in some tissues with age. Mitochondrial genetics is complex due to interaction with nuclear genes, predominant maternal inheritance, and the possibility that not all mitochondria in a cell need to be genetically identical. Nonetheless a number of genetic diseases are linked to mtDNA, and that mutations in nuclear genes can adversely affect mtDNA and/or oxidative phosphorylation. It has been proposed that accumulated mtDNA damage is a mechanism in aging, and that mitochondria with genomic deletions would be enriched due to a replicative advantage. [As with any theory involving genomic instability, one must reconcile the fact that babies are inevitably born young. In this case the question is: how do babies escape getting mom's 20-40 year old mitochondria?] References: Wallace, D.C. (1992) Mitochondrial Genetics: A Paradigm for Aging and Degenerative Diseases? Science 256:628-632 (May 1 1992). 5. apoptosis: D. Endocrine cascade E. Cell Senescence. A number of types of human cells will undergo less than about 100 divisions when cultured (grown in a dish or flask), at which point the cells adopt a distinctive appearance and will not divide any further. As stimulus to divide in mammalian tissues consists mainly of signaling factors it has been argued that senescence is a tissue culture artifact due to improper or inadequate signaling or an adaptive tolerance to signals. In large enough sample sizes, however, an inverse correlation between number of divisions obtained and age of donor is observed, and there also exists a rough correlation between species lifespan and number of divisions obtained. Furthermore cells from individuals with Werner's syndrome (premature aging) have a reduced proliferative capacity. It has been proposed that cell senescence occurs in vivo and could be responsible for loss of homeostasis in tissues of the elderly. Cells which senesce in culture include fibroblasts, lymphocytes, various epithelial cells, and adrenocortical cells. Tumor cells do not senesce in culture and it has also been proposed that senescence acts as a tumor-control mechanism by providing an additional hurdle for growth-errant cells. It is important to note that no direct evidence for cell senescence occuring in vivo has yet been obtained. References: Warner, H.R. et al. (1992) Control of Cell Proliferation in Senescent Cells. Journal of Gerontology 47(6):B185-B189. 1. DNA synthesis inhibition In an expression screen for cDNAs (expressed genes) in senescent cells which could inhibit DNA synthesis in "young" cells, the SDI-1 gene was cloned and found to be significantly up-regulated in senescent cells compered with their young counterparts. The gene was also cloned by two other groups simultaneously using completely different methods, and is thought to be the primary element responsible for p53-dependent cell-cycle arrest. References: Hunter, Tony (1993) Braking the cycle (minireview). Cell 75:839-841 (Dec 3 '93). 2. complementation studies: Cultured cells can be fused to one another and genetic properties analyzed in a manner analagous to yeast mating. Early cell fusion experiments clearly illustrated that senescence was a dominant trait in fused cultured cells (i.e. fusions of young to senescent are senescent; immortal to senescent are senescent.) This suggested that element(s) were missing from immortal cells which could be provided by senescent cells. To determine if immortal cells were all lacking the same thing or had different deletions, various immortal cells were fused, and it was found that some complemented (rescued) each other. In a specific case, a single inserted chromosome was sufficient to restore senescence. These complementation studies have recently been challenged, with apparently different results obtained using somewhat different methods. References: Pereira-Smith, O.M. & Smith, J.R. (1988) Genetic analysis of indefinite division in human cells: Identification of four complementation groups. PNAS 85:6042-6046. Ning, Y. et.al. (1991) Genetic analysis of indefinite division in human cells: Evidence for a cell-senescence-related gene(s) on human chromosome 4. PNAS 88:5635-5639. Ryan, P.A. et al (1994) Failure of Infinite Life span human cells from different immortality complementation groups to yield finite life span hybrids. J. Cell. Phys. (in press) 2. vs. DNA damage: [The fact that senescence is a dominant property suggests that DNA damage is not responsible for the senescence phenomenon. If senescent cells had lost a function that immortal cells retained, then immortality would be dominant. It seems unlikely that senescence would be due to a gain of function mutation in all senescent cells simultaneously. If immortality were due primarily to a gain of function mutation not present in senescent cells, again immortality would be expected to dominate. The remaining possibility then is that immortality is due to a loss of function, and that senescent cells have retained the normal genotype.] 3. telomere shortening: It was originally observed by Crick around 1960 (I think) that the DNA replication machinery, which can only synthesize in one direction, would always leave a little bit of unreplicated DNA on the lagging strand at the telomere (end of the chromosome). Proteins were identified which could extend telomeres, which have a special sequence. It is now well established that human telomeres get shorter on average as a function of age, that they are elongated in sperm cells, that as cells senesce in culture their telomeres shorten with a striking uniformity. It has been proposed that telomere shortening is responsible for cell senescence and hence is involved in the aging process, but no causal role has emerged. Evidence against the telomere hypothesis: Telomere shortening in yeast leads to cell death, not the phenotype seen in mammalian cell senescence; Mouse telomeres are up to ten times as long as human telomeres and do not shorten over the lifetime, and yet mouse cells senesce faster that human cells in culture. References: Kipling, D. & Cooke, H.J. (1990) Hypervariable ultra-long telomeres in mice. Nature 347:400-402. Lundblad, V. & Szostak, J. W. (1989) A Mutant with a Defect in Telomere Elongation Leads to Senescence in Yeast. Cell 57:633-643. Allsopp, R.C. et al. (1992) Telomere Length predicts replicative capacity of human fibroblasts. PNAS 89(21):10114-8. 3. senescence of the immune system: F. Cellular Aging G. Oxidative Stress Hypothesis With the random damage model falling out of favor, the free radical theory has evolved into what is termed the "oxidative stress hypothesis", which asserts that modification and damage to cellular molecules by free radicals is capable of altering "genetic programs" and disrupting cell function, thereby contributing to aging regardless of DNA damage. This model draws support from observations that (1) the free hydroxyl radical can clearly contribute to biochemical pathways producing not only damaged DNA but dysfunctional and/or deleterious proteins and lipids; (2) levels of such "oxidative stress" have been illustrated to increase throughout the lifespans of humans and drosophila [ and c. elegans? ], and is consistent with the results of rodent dietary restriction; (3) there is a clear correlation between lifespan and oxygen consumption/body weight weight in a number of species; (4) recent work in drosophila has extended lifespan by manipulating the biochemical pathway which metabolizes superoxide and hydrogen peroxide. There is extensive literature on oxidative stress. The genes/proteins involved in free radical metabolism are well-known (see SOD, catalase, glutathione peroxidase in any biochemistry textbook) but their regulation is not well understood. [Enzymes are regulated by their substrate and product levels, a "gimme"] Downstream events (i.e., exactly which important proteins and lipids are modified/damaged) is also not clear. References: Sohal, R.S. & Allen, R.G. (1990) Oxidative Stress as a causal factor in differentiation and aging: a unifying hypothesis. Exp. Gerontology 25:499-522. Stadtman, Earl R. (1992) Protein Oxidation and Aging. Science 257:1220-1224. H. DNA methylation Methylation of cytidine residues of DNA has been correlated with gene expression levels in a number of cases. It is unresolved whether methylation is a cause or result of altered chromatin structure. DNA methylation is thought to be responsible for imprinting, and has been implicated as a mechanism in both development and aging. Overall methylation levels in mice apparently decrease as a function of age from six to twenty-four months, and may subsequently increase. There is an extensive literature on DNA methylation and aging studies are only a small part of this active field. References: Singhal, R.P. (1987) DNA methylation in Aging of Mice. Mechanisms of Ageing and Development, 41:199-210. j. Other III. Aging in model organisms Traditional approaches to genetic and biochemical study include making mutants, and fractionating extracts and assaying for activity. Generating mutant humans and dissecting them is clearly not as ethical, so traditional laboratory organisms are used in many aging studies. This has an advantage that experiments can be performed ethically and efficiently, but a disadvantage that the results may not apply to humans. Aside from obvious morpohological differences, perhaps the strongest argument is that since humans live so long, our genome must have overcome whatever it is that causes other organisms to have such short lifespans. On the other hand, aging even in fruit flies and worms has a striking resemblance to that in humans. A. Humans 1. biomarkers of aging in humans: 2. causes of death: I am having a hard time finding a simple summary of U.S. mortality statistics and would appreciate anyone's contribution here. What I have found is that approximately 40% of all persons will have a neoplasm in their lifetime and that for about 20% of the population this is the cause of death. George Will discussed Sherwin B. Nuland's latest book "How We Die: Reflections on Life's Final Chapter" in the March 7 1994 Newsweek, and claimed that 85% of the aging population "succumbs[s] to one of seven ailments - atherosclerosis, hypertension, adult-onset diabetes, obesity, Alzheimer's and other dementias, cancer, and decreased resistance to infections". The book is apparently quite morbid in its attention to detail, and I suppose I will try to find it although I'm frankly not looking forward to reading the thing. 3. progeroid syndromes: A number of hereditary disorders result in short lifespans during which the senescence process is apparently accelerated. None of them exactly matches the wild-type aging phenotype, but the similarities are quite striking, and one would expect genes causing these syndromes to be significant in regulating the aging process. Traditional genetic linkage analyses are difficult because the diseases are very rare autosomal recessive. A linkage for Werner's syndrome was announced two years ago but I haven't heard of a gene yet. A number of progeroid syndromes have been linked to DNA repair deficiencies, and Werner's has a reported mutator phenotype. [The distinction between DNA repair and general transcription and replication is not entirely clear at this point. It is interesting that not all cellular mutator phenotypes result in premature aging syndromes in the organism.] References: Goto, M. et. al. (1992) Genetic Linkage of Werner's syndrome to five markers on chromosome 8. Nature, 355:735-737 (20 Feb '92) 4. linkages to longevity: A recent publication reports the distribution of alleles implicated in cardiovascular risk at two loci (genes) between French centenarians and a control population aged 20-70. The study was quite large and different distributions were found at both loci. The paper refers to an established linkage between longevity and HLA genotype as well. [Also I believe it is common knowledge that women live generally longer than men, making the Y chromosome a significant longevity determinant.] References: Schachter, F. et. al. (1994) Genetic associations with human longevity at the APOE and ACE loci. Nature Genetics 6:29-32 (january 1994). 5. hormone studies: B. Rodents - mice are the most common mammalian experimental model for genetic research. The mouse is considered to to fairly closely model humans. Murine cells are easily transformed in culture. Mice may have fewer defenses against dysplasia because they are smaller and don't live as long. 1. calorie restriction: It was first observed in the 1930's that rats which were fed less but supplied with proper nutrition lived longer. It has since been determined that the caloric intake is the sole determinant, suggesting that metabolic rate metabolic rate serves as a "genetic clock". However, metabolic rate is not necessarily lowered when the reduced mass of the animal is corrected for. The fact that a large number of physiological and pathological symptoms of aging are delayed in CR animals has made the phenomenon difficult to study. As glucose, insulin, and plasma-free glucocorticoid concentrations are affected, modulation of neuroendocrine regulatory systems has been implicated. The onset of tumors, which kill about 50% of all mice, is delayed in CR mice. No direct evidence exists for any hypothesis regarding the effects of CR. References: Masoro, E.J. (1993) Dietary Restriction and Aging. J. of the Am. Ger. Soc. 41:994-999. Weindruch, R. (1989) Dietary Restriction, Tumors, and Aging in Rodents. J. of Geron. 44(6):67-71. 2. SAM (senescence accelerated mouse): 3. SOD transgenics C. Drosophila 1. Genetic analysis 2. engineered mutants: Flies with extra copies of both Superoxide Dismutase, which converts superoxide anion radical to H2O2, and Catalase, which converts H2O2 to water and oxygen, were shown to have moderately increased lifespan and slightly delayed loss of physical activity. Cellular oxidative stress was clearly reduced as measured by protein carbonyl content. References: Orr, W.C. & Sohal, R.S. (1994) Extension of Life-Span by Overexpression of Superoxide Dismutase and Catalase in Drosophila melanogaster. Science 263:1128-1130 (25 Feb '94) D. C. Elegans 1. backcross analysis 2. age-1 mutant 2. "Methuselah": A recently reported mutant now holds the record for increase in lifespan. A mutation in daf-2, a developmental gene, more than doubles nematode lifespan (18 to 42 days mean). The mutants are "healthy and fertile". References: Kenyon, C. et al. (1993) A C. elegans mutant that lives twice as long as wild type. Nature 366:461-464. See also News & Views (Pertridge & Harvey) from the same issue. E. Other Species 1. yeast 2. sea urchin 3. calorie restriction in primates F. Relationship of biomarkers of aging in humans to those in model organisms IV. Other interesting phenomena, etc. =================================================================== +++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++ =================================================================== From owner-ageing@net.bio.net Mon May 02 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!EU.net!sunic!trane.uninett.no!daresbury!not-for-mail From: "Leonid Gavrilov" Newsgroups: bionet.molbio.ageing Subject: Mutation Theory of Ageing Date: 3 May 1994 13:09:05 +0100 Organization: A.N.Belozersky Institute, Moscow State University Lines: 112 Sender: daemon@mserv1.dl.ac.uk Distribution: bionet Message-ID: <2q5et1$r9j@mserv1.dl.ac.uk> X-Russian: Cyrillic Original-To: AGEING@dl.AC.UK May 3, 1994 Dear AGEING LIST subscribers, The purpose of this message is to invite you for scientific discussion of the recent paper in NATURE: Hughes, K.A. & Charlesworth, B. A GENETIC ANALYSIS OF SENESCENCE IN DROSOPHILA. Nature 367, 64-66 (1994). Our own comments on this paper are printed below. Your response would be greatly appreciated. Of special interest are responses of the authors: Kimberly A.Hughes (Chicago Zoological Society, Brookfield, Illinois) Brian Charlesworth (Department of Ecology and Evolution, Chicago) By the way, does anybody know their E-mail addresses ? Thanks, Dr.Leonid A.Gavrilov and Dr.Natalia S.Gavrilova ******************************************************************** TESTING THE MUTATION THEORY OF AGING: A SIMPLE EXPLANATION FOR MORTALITY DIVERGENCE SIR - Hughes and Charlesworth [1] provide a fascinating picture (Fig.1), demonstrating great increase in variability of mortality in male Drosophila melanogaster at very late ages, as predicted by the mutation accumulation hypothesis of senescence. In particular, they demonstrate that regression lines of log(mortality) on age, are starting virtually from the same point (similar intercepts) but are diverging greatly afterwards (different slopes). Since this observation is quite opposite to previous reports on relative convergence of mortality rates at late ages both in drosophila and humans (known as compensation effect of mortality) [2], we have tried to find out the reasons for such a fundamental contradiction. We suggest here a simple explanation for mortality divergence observed by Hughes and Charlesworth [1] and for the contradiction of this observation to previous reports [2]. Although Hughes and Charlesworth followed the Gompertz model (exponential increase of mortality rates with age) for data analysis, they used very unusual non-Gompertz transformation of data to receive straight regression lines: instead of calculating the logarithm of mortality rate as a function of age (as they indicated on the plots of their Fig.1), in fact they calculated log(mortality + 1) as it was written in legend for Fig.1. Since mortality rates are very small (less than 0.1) at young ages, even a great relative difference in mortality between populations will be completely masked after adding 1 to these very small numbers. For this reason only, all regression lines will inevitably have virtually the same starting point (similar intercepts). Since at very late ages the mortality rates are rather high (up to 0.8), the relative difference in mortality between populations will not be completely masked at high ages even after adding 1 to these numbers. Thus, observed divergence of mortality is an inevitable consequence of non conventional way of data transformation (adding 1 under the logarithm) used by the authors [1]. When conventional methods are used, quite opposite phenomenon of relative mortality convergence is observed both in drosophila and humans [2]. We can easily understand the reasons for non conventional transformation of data used by the authors: in small populations at young ages the observed mortality rates are often equal to zero (when nobody dies) and it is impossible to calculate the logarithm of mortality rate in such cases without adding some positive constant number under the logarithm. The problem is that this procedure produces artifacts through biased estimates of both intercept and slope parameters. For this reason the added constant should be extremely small to minimize biasing (say, 0.001 instead of 1.0). The best way to escape this problem completely is to estimate the Gompertz parameters directly by the methods of nonlinear regression [2]. Leonid A.Gavrilov Natalia S.Gavrilova A.N.Belozersky Institute Moscow State University Moscow 119899, Russia Fax: 7 (095) 939-0338/3181 1. Hughes, K.A. & Charlesworth, B. Nature 367, 64-66 (1994). 2. Gavrilov, L.A. & Gavrilova, N.S. The Biology of Life Span: A Quantitative Approach (Harwood Academic, Chur, London, 1991). Dr. Leonid A.Gavrilov, Ph.D. Dr. Natalia S.Gavrilova, Ph.D. ******************************THE END********************************* -- ________________________________________________________________ -- 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 gavrilov@aeiveos.uucp.free.msk.su Russia libro@genebee.msu.su aeiveos@glas.apc.org Please send your answer to my most reliable E-mail address: aeiveos@glas.apc.org if you wish to be sure to reach me. Thank you ! ___________________________________________________________________ From owner-ageing@net.bio.net Tue May 03 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!sunic!EU.net!howland.reston.ans.net!europa.eng.gtefsd.com!news.umbc.edu!davidson From: davidson@umbc.edu (Ms. Pamela Davidson; (GRAD) Newsgroups: bionet.molbio.ageing Subject: Glucose & Ageing Date: 4 May 1994 20:35:28 GMT Organization: University of Maryland, Baltimore County Lines: 13 Message-ID: <2q90ug$lm7@news.umbc.edu> NNTP-Posting-Host: umbc7.umbc.edu X-Newsreader: TIN [version 1.2 PL2] Hello, I am a graduate student at the University of Maryland and in the process of developing my thesis project. It is well documented that caloric restriction retards the aging process. Caloric restriction also lowers blood glucose levels. It has been recently demonstrated that high blood glucose levels results in the non-enzymatic glycosylation of extracellular proteins. During my search through the literature, I have come across several hypotheses that suggest non-enzymatic glycosylation also occurs to intracellular proteins. However I have not been able to find any published data on this. Does any one know of any information on on intracellular non-enzymatic glycosylation? Any information would be greatly appreciated. Please e-mail at davidson@umbc.edu Thank you for your help. From owner-ageing@net.bio.net Tue May 03 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!sunic!EU.net!howland.reston.ans.net!vixen.cso.uiuc.edu!newsrelay.iastate.edu!hobbes.physics.uiowa.edu!news.uiowa.edu!icaen!saluri From: saluri@icaen.uiowa.edu (Srinivas Aluri) Newsgroups: bionet.molbio.ageing Subject: Atherosclerosis Date: 4 May 1994 21:09:12 GMT Organization: Iowa Computer Aided Engineering Network, University of Iowa Lines: 12 Distribution: world Message-ID: <2q92to$dc4@news.icaen.uiowa.edu> NNTP-Posting-Host: l_ecn10.icaen.uiowa.edu Originator: saluri@l_ecn10 Keywords: aging Iam working on a report on Atherosclerosis and aging and would like to know if Ican get any help (ideas) regarding the progress of atherosclerosis (any causes for atherosclerotic plaque formation and its progress other than Hypertension , Diabetes , high LDLcontens) Iwould really appritiate if Ican get some help. Thanks you S Aluri (Iwould appritiate if Ican get reply to my mailing address ) saluri@icaen.uiowa.edu From owner-ageing@net.bio.net Wed May 11 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!sunic!EU.net!uunet!portal.com!portal!cup.portal.com!Marc_R_Rice From: Marc_R_Rice@cup.portal.com Newsgroups: bionet.molbio.ageing Subject: Ageing questions Message-ID: <111543@cup.portal.com> Date: Thu, 12 May 94 12:56:07 PDT Organization: The Portal System (TM) Lines: 10 To the Reader: The reason you are reading this article is because you are curious about ageing and if it can be reversed. I feel the same way. I mean I don't believe in magic but in science. I would welcome any replies. Even arguments are welcome. You can reply to me at this adress or send mail to riot@masc.com Thanks, Roy Hall III PS-any mail sent may not be read until after summer break. however I am cap- able to read any mail sent within the next two weeks (deadline May 25). After that don't expect any replies. Thanks again!!! From owner-ageing@net.bio.net Thu May 12 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: Ageing questions Date: 12 May 1994 21:03:17 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 20 Sender: daemon@net.bio.net Distribution: bionet Message-ID: <9405130405.AA12637@pclsp2> NNTP-Posting-Host: net.bio.net Roy Hall wrote: >To the Reader: >The reason you are reading this article is because you are curio us >about ageing and if it can be reversed. I feel the same way. I mean I don't >believe in magic but in science. I would welcome any replies. Even arguments >are welcome. You can reply to me at this adress or send mail to riot@masc.com > Thanks, > Roy Hall III I think the subject is of course very interesteing and I would appreciate if the answeres were made public, that means, directly to ageing@net.bio.net. Bye -- Vincenzo From owner-ageing@net.bio.net Thu May 12 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!sunic!EU.net!howland.reston.ans.net!cs.utexas.edu!swrinde!sdd.hp.com!decwrl!portal.com!portal!cup.portal.com!Marc_R_Rice From: Marc_R_Rice@cup.portal.com Newsgroups: bionet.molbio.ageing Subject: Ageing Group Message-ID: <111638@cup.portal.com> Date: Fri, 13 May 94 12:59:28 PDT Organization: The Portal System (TM) Lines: 8 Thanks For any responses to my original post. I would like to hear more about what the public thinks and I would like it if I can receive a professional opinion. Roy Hall PS-If you want to contact me you can do that by e-mailing me at the attached adress (Marc_R_Rice@cup.portal.com) or e-mail me at riot@masc.com. If you are going to post anything worthwhile please do that here making it available to other readers. Thank you!!!! From owner-ageing@net.bio.net Mon May 16 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!sunic!EU.net!howland.reston.ans.net!vixen.cso.uiuc.edu!sdd.hp.com!portal.com!portal!cup.portal.com!Marc_R_Rice From: Marc_R_Rice@cup.portal.com Newsgroups: bionet.molbio.ageing Subject: The Future... Message-ID: <111896@cup.portal.com> Date: Tue, 17 May 94 12:00:34 PDT Organization: The Portal System (TM) Lines: 7 To my Future... article I wold like some intersting replies. Unfortunately I was unable to finish it. Does anyone else share the same vision? or others about the evolution of mankind? Thaknki Thank you, Dreamer/Roy/Riot The Internet trinity!!! From owner-ageing@net.bio.net Mon May 16 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!sunic!EU.net!howland.reston.ans.net!gatech!swrinde!sdd.hp.com!portal.com!portal!cup.portal.com!Marc_R_Rice From: Marc_R_Rice@cup.portal.com Newsgroups: bionet.molbio.ageing Subject: The Human Future Message-ID: <111895@cup.portal.com> Date: Tue, 17 May 94 11:56:14 PDT Organization: The Portal System (TM) Lines: 11 The FUTURE of MANKIND I am somewhat of an idealist. What I see in OUR future is a world of scienti fic achievements and one that lives, if not in harmony with nature then at least with an environmental awareness that we lack today. I envisioned that with the advancements in medecine and genetics humans could have lifespans of hundreds of years to pursue what their heart desires. Paradise? No, man will still work and he will still have to solve his problems; however, humans will be free from threat of extinction after having populated worlds in this system and outside. What I want is a world of clear thinking, one with emotion, and one filled with humans and those small habits that make us. From owner-ageing@net.bio.net Mon May 16 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!bcm!cs.utexas.edu!howland.reston.ans.net!usenet.ins.cwru.edu!ns.mcs.kent.edu!kira.cc.uakron.edu!malgudi.oar.net!sun!oucsace!ouvaxa.cats.ohiou.edu!JANAPATI From: janapati@ouvaxa.cats.ohiou.edu Subject: reply to Marc R Rice Message-ID: Sender: news@oucsace.cs.ohiou.edu (news account) Reply-To: janapati@ouvaxa.cats.ohiou.edu Organization: Ohio University Computing & Technology Services Date: Tue, 17 May 1994 02:20:51 GMT Lines: 1 cing trophic factors etc. I understand ageing is evolutionarily determined by numerous factors. The only way one may try to prolong life span can be by suppressing or overexpressing certain genes involved in the above mentioned processes, at an early stage of life. From owner-ageing@net.bio.net Tue May 17 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!daresbury!trane.uninett.no!sunic!pipex!howland.reston.ans.net!usenet.ins.cwru.edu!lerc.nasa.gov!purdue!mozo.cc.purdue.edu!mace.cc.purdue.edu!barani From: barani@mace.cc.purdue.edu (NONAME.C) Subject: philosophy and ageing Sender: news@mozo.cc.purdue.edu (USENET News) Message-ID: Date: Wed, 18 May 1994 01:27:20 GMT Organization: Purdue University Lines: 46 Dreamer wants replies: The bionet.molbio.ageing is a forum for very serious yet mundane scientific ideas and discussions and it has not yet riped to the state of pedagogical matters. Therefore I would appreciate it, if a different newsgroup is used/created for that purpose. To dream about future is one thing; to unravel the ageing-mechanism is completely different. The ageing process leads various old age diseases and disorders which cause untold misery. The major aim of research in this topic is to solve these problems first. Nevertheless, in order not to discourage anyone from participating in this newsgroup (and due to the lack of a general newsgroup to discuss such issues), here are some questions to dreamer: Have you ever dreamt of being 200 years old and the possible world around you? What kind of relations and friends you would have? What kind of job you will be doing? If everyone wants to live to eternity and still want to reproduce their own kind, what would be the fate of earth? "I pay tax and therefore I have the right to know the results of ageing-research" will lead to everyone being immortal and the above situation will be inevitable. Does it mean the results of ageing-research can be classified? There are various mind boggling issues which would arise from political, philosophical backgrounds once there is significant progress in ageing research. However, it is still very far. Therefore I am going back to my work on phosphoglucomutase protein found in human heart and which is very essential for glucose activity and also why one of its domains strikingly resemble the heart itself! Good Luck to you dreamer. Have a nice day. barani@mace.cc.purdue.edu From owner-ageing@net.bio.net Tue May 17 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!daresbury!trane.uninett.no!eunet.no!nuug!EU.net!howland.reston.ans.net!cs.utexas.edu!swrinde!emory!news-feed-2.peachnet.edu!news-feed-1.peachnet.edu!news.duke.edu!godot.cc.duq.edu!nntp.club.cc.cmu.edu!news.mic.ucla.edu!library.ucla.edu!csulb.edu!csus.edu!netcom.com!jabowery From: jabowery@netcom.com (Jim Bowery) Subject: Telomere Research Message-ID: Organization: NETCOM On-line Communication Services (408 261-4700 guest) Date: Wed, 18 May 1994 19:43:02 GMT Lines: 26 I understand that telomeres are believed to be noncoding sections of the chromosomes, but what is the evidence for this other than the fact that they appear to serve no purpose? Also, since telomerase functions appropriately in cell division in some cell production (gametes for example) why is it that it cannot also function appropriately in the division of other cells? The incidence of cancer in cells that naturally utilize telomerase doesn't appear to be nearly as enormous as one would expect. Is eovoking telomerase in normal cells really that dangerous or would our other mechanisms for control of cancer control be adequate given a youthful immune system? In cases where those other cancer suppression mechanisms fail, is it unreasonable to expect that a telomerase antagonist might be developed to kill cancerous cells? Inquiring minds want to know (if ours will be the last generation to die of "old age"). -- 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 Tue May 17 23:00:00 1994 Path: biosci!bcm!cs.utexas.edu!sdd.hp.com!vixen.cso.uiuc.edu!news.eecs.uic.edu!uicvm.uic.edu!u56149 Organization: University of Illinois at Chicago, ADN Computer Center Date: Wed, 18 May 1994 12:58:06 CDT From: Message-ID: <94138.125806U56149@uicvm.uic.edu> Newsgroups: bionet.molbio.ageing Subject: Re: reply to Marc R Rice References: Lines: 22 In article , janapati@ouvaxa.cats.ohiou.edu says: > >cing trophic factors etc. I understand ageing is evolutionarily determined by >numerous factors. The only way one may try to prolong life span can be by >suppressing or overexpressing certain genes involved in the above mentioned >processes, at an early stage of life. It is more complicated than that. Numerous studies have demonstrated significant prolongation of maximal life span by lifelong restriction of caloric intake. Anyone interested in this may begin a search with the writings of Roy Walford - he has not been the major experimenter, but he is a prophet in this area. =============================================================================== + Gerald L. Bartlett, M.D., Ph.D. Phone: 309-671-8440 + + Professor and Chairman of Pathology FAX: 309-671-8439 + + University of Illinois College of Medicine @ Peoria + + Box 1649, Peoria, IL 61656-1649 e-mail: u56149@uicvm.cc.uic.edu + + 1 Illini Drive, Peoria, IL 61605-2576 u56149@uicvm.bitnet + =============================================================================== From owner-ageing@net.bio.net Tue May 17 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!bcm!cs.utexas.edu!howland.reston.ans.net!usenet.ins.cwru.edu!ns.mcs.kent.edu!kira.cc.uakron.edu!malgudi.oar.net!sun!oucsace!ouvaxa.cats.ohiou.edu!JANAPATI From: janapati@ouvaxa.cats.ohiou.edu Subject: rice/future Message-ID: Sender: news@oucsace.cs.ohiou.edu (news account) Reply-To: janapati@ouvaxa.cats.ohiou.edu Organization: Ohio University Computing & Technology Services Date: Wed, 18 May 1994 03:09:01 GMT Lines: 2 humans can not have a lengthy lifespan and faster evolution at the same time. In order to achieve more effecient system at short time an organism should have less lifespan but at the same time the body should be sufficiently exposed to the environment to get specific mutations. I think in future humans will have less lifespan but more healthy and with higher brain functions. From owner-ageing@net.bio.net Tue May 17 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!sunic!EU.net!uunet!nwnexus!zgi.com!venezia From: venezia@flames.zgi.com (Domenick Venezia) Newsgroups: bionet.molbio.ageing Subject: Telomeres Date: 18 May 94 22:46:47 GMT Organization: Northwest Nexus Inc. Lines: 4 Message-ID: NNTP-Posting-Host: flames.zgi.com Keywords: Telomere telomerase polymerase New to this new group and News in general so bear with me if I make some or have made some net-gaff. Has anybody been following the work on telomeres/telomerase coming out of Blackburn, Greider, Harley, etc? Is this the wrong forum for hard science? From owner-ageing@net.bio.net Wed May 18 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!uknet!EU.net!Austria.EU.net!newsfeed.ACO.net!info.univie.ac.at!lab8486.abc.univie.ac.at!ma From: ma@ABC.univie.ac.at (Manuel Simon) Newsgroups: bionet.molbio.ageing Subject: Re: telomeres Date: Thu, 19 May 1994 11:02:20 Organization: Inst. Biochemistry and Molecular Cell Biology Lines: 24 Distribution: world Message-ID: References: <9405190315.AA24155@pclsp2> NNTP-Posting-Host: lab8486.abc.univie.ac.at X-Newsreader: Trumpet for Windows [Version 1.0 Rev A] In article <9405190315.AA24155@pclsp2> vinz@PCLSP2.KUICR.KYOTO-U.AC.JP (Vincenzo Nardi-Dei) writes: >From: vinz@PCLSP2.KUICR.KYOTO-U.AC.JP (Vincenzo Nardi-Dei) >Subject: Re: telomeres >Date: 18 May 1994 20:12:47 -0700 >Also I am remembering, when I was child, my father used to cut a branch >from a tree, put it in the ground and it grew again to become a new tree. >From this second tree he could cut an other branch, put in the ground >and so on endlessly. So, do plants have telomeric regulation systems? >And if they have not, how do they in normal conditions do not develop >cancer, but cells grow in a differentiated way, generating organs, >stopping their growth at certain moments and, apoptosysly, leaves >fall? Vinc, I also remember some scenes, where we digged branches in our garden, but in fact, they never grew out! Highly specialized cells are necessary for *infinite* replication. You are right: most of the cells of a plant having undergone differentiation to specialized functions will not suffice the requirements for reproduction. Manuel From owner-ageing@net.bio.net Wed May 18 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: telomeres Date: 18 May 1994 20:12:47 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 24 Sender: daemon@net.bio.net Distribution: world Message-ID: <9405190315.AA24155@pclsp2> NNTP-Posting-Host: net.bio.net Telomeres shortening seems to be clearly implicated in regulation of cell ageing even though a stronger force should be the II principle of thermodinamic and its tendency to enthropy. Uncorrected DNA replication errors accumulate even affecting the same repairing system encoding genes provoking a cascade effect. But, is the limited number of cells replication that happens in the life span of an evoluted organism enough to provoke such number of errors? Also I am remembering, when I was child, my father used to cut a branch from a tree, put it in the ground and it grew again to become a new tree. From this second tree he could cut an other branch, put in the ground and so on endlessly. So, do plants have telomeric regulation systems? And if they have not, how do they in normal conditions do not develop cancer, but cells grow in a differentiated way, generating organs, stopping their growth at certain moments and, apoptosysly, leaves fall? -- Vincenzo Nardi-Dei Bio-functional Molecules Laboratory Institute for Chemical Research Kyoto University From owner-ageing@net.bio.net Wed May 18 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!daresbury!trane.uninett.no!sunic!EU.net!howland.reston.ans.net!usenet.ins.cwru.edu!ns.mcs.kent.edu!kira.cc.uakron.edu!malgudi.oar.net!sun!oucsace!ouvaxa.cats.ohiou.edu!JANAPATI From: janapati@ouvaxa.cats.ohiou.edu Subject: ageing/caloric restriction Message-ID: Sender: news@oucsace.cs.ohiou.edu (news account) Reply-To: janapati@ouvaxa.cats.ohiou.edu Organization: Ohio University Computing & Technology Services Date: Thu, 19 May 1994 22:23:04 GMT Lines: 4 So far the only way to prolong the lifespan was found to be caloric restriction at an early stage of life. But the mechanism by which the lifespan is extended is not known. Some believe it to be due to reduced metobolic rate and decrease in free radical production and damage. Where as others believe that a change in the levels of hormones in the blood. Free radicals damage is now found to beinvolved in several degenerative diseases. Free radical production was found to be only the terminal event in th e disease process. Moreover trophic factors are found to reverse degenerative changes in neurons. From these studies, it implies that changes in hormone or trophic factor levels or in signal transduction mechanism might be responsible for senescence. From owner-ageing@net.bio.net Wed May 18 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!sunic!trane.uninett.no!daresbury!not-for-mail From: Sydney Shall Newsgroups: bionet.molbio.ageing Subject: Telomeres and Hard Science Date: 19 May 1994 10:33:47 +0100 Lines: 50 Sender: daemon@mserv1.dl.ac.uk Distribution: bionet Message-ID: <2rfbpr$nf9@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk There has been a query whether this Bulletin Board - AGEING - is the approriate palce for contributions about telomeres and in general about "hard science"? The answers are quite categorical and are yes to both questions. There has been some discussion in recent weeks about telomeres in ageing, mostly derived from the work of Carol Greider at Cold Spring Harbor Labs., and of Cal harley now of Geron Corporation in California. It is clear that this hypothesis has a great deal of experimental support, although the precise mechanism and formal proof is still lacking. Interested people might consult the FAQ contribution that has been very generously prepared for this Bulletin Board. A separate thread of discusssion has arisen concerning plant tissues. It is clear that plant cells are behave very differently to animal cells in this regard. I am not aware of a detailed analysis od telomeres and of telomerase in plant cells. It would be an invaluable study. ************************************************************************** ************************************************************************** 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 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 Wed May 18 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!sunic!EU.net!howland.reston.ans.net!usc!nic-nac.CSU.net!charnel.ecst.csuchico.edu!psgrain!nntp.cs.ubc.ca!cyber2.cyberstore.ca!nwnexus!flames!venezia From: venezia@zgi.com (Domenick Venezia) Newsgroups: bionet.molbio.ageing Subject: telomeres Date: 18 May 1994 23:56:16 GMT Organization: Northwest Nexus Inc. Lines: 19 Message-ID: <2re9v0$mj7@nwfocus.wa.com> NNTP-Posting-Host: flames.zgi.com X-Newsreader: TIN [version 1.2 PL2] Jim Bowery mentions telomeres, but not telomeric shortening and its implications in human ageing. I'm trying to find out if this topic has been fully discussed in this forum so that I do not rehash old news. Here's the basic scheme: As we age more and more of our tissues' stem cells senesce and die. An example is that our skin thins with age. Eventually one tissue system or another no longer has enough functioning cells to mantain itself and we succumb to the cold, arbitrary, slimey hand of death. Why do stem cells senesce? Because with each replication a little bit ~100bp of the telomere is lost and eventually it reaches a point where it triggers some senescent process and the cell dies, just as it was programmed to do. My belief is that if every decade or so a way can be found to extend the telomeric sequence of each stem cell in the body we can increase the potential lifespan of the organism. Is this new ground? From owner-ageing@net.bio.net Thu May 19 23:00:00 1994 Path: biosci!ugene1.abbott.com!crosbys From: crosbys@ugene1.abbott.com (Seth Crosby 8-6999) Newsgroups: bionet.molbio.ageing Subject: ageing/caloric restr. Date: 19 May 1994 21:36:23 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 1 Sender: daemon@net.bio.net Distribution: world Message-ID: <9405200436.AA16990@ugene1.abbott.com> NNTP-Posting-Host: net.bio.net Keeping min in mind. This has only been shown in rodents. Not even monkeys yet, I believe. From owner-ageing@net.bio.net Thu May 19 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: telomeres Date: 20 May 1994 08:11:06 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 18 Sender: daemon@net.bio.net Distribution: world Message-ID: <9405201513.AA27260@pclsp2> NNTP-Posting-Host: net.bio.net Manuel answered: >..................... You are right: most of the cells of a plant having >undergone differentiation to specialized functions will not suffice the >requirements for reproduction. > >Manuel I wonder if such differentiated cells, unable to reproduct, have undergone a telomer-consumption-like effect and if, as "old" animal cells, they remain unable to replicate once separated from the plant and put in colture medium containing the appropriate growth factors and hormons, or will devlop a "callus" that will originate a new plant and not a "cancer-like" organism. -- Vincenzo From owner-ageing@net.bio.net Thu May 19 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!bcm!cs.utexas.edu!howland.reston.ans.net!vixen.cso.uiuc.edu!uchinews!ellis!bmdelane From: bmdelane@ellis.uchicago.edu (Brian Manning Delaney) Subject: Re: ageing/caloric restr. Message-ID: <1994May20.222900.11141@midway.uchicago.edu> Sender: news@uchinews.uchicago.edu (News System) Reply-To: bmdelane@midway.uchicago.edu Organization: University of Chicago References: <9405200436.AA16990@ugene1.abbott.com> Date: Fri, 20 May 1994 22:29:00 GMT Lines: 10 In article <9405200436.AA16990@ugene1.abbott.com> crosbys@ugene1.abbott.com (Seth Crosby 8-6999) writes: >Keeping min in mind. This has only been shown in rodents. Not even monkeys yet, I believe. No, it's been shown in oodles of species. True, though, it's not been demonstrated in primates yet, but two studies are underway, and results should start trickling in over the next few years. -- Brian M. Delaney or From owner-ageing@net.bio.net Fri May 20 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!uknet!EU.net!uunet!psinntp!sjuvm!ypjzbio Nntp-Posting-Host: 149.68.2.20 Date: Fri, 20 May 1994 17:17:00 -0400 From: "ZIMMERMAN, JAY A" Newsgroups: bionet.molbio.ageing Subject: Re: reply to Marc R Rice Message-ID: <20MAY94.18665145.0026@sjumusic.stjohns.edu> References: <94138.125806U56149@uicvm.uic.edu> Sender: usenet@sjumusic.stjohns.edu Organization: St. John's University Lines: 18 >In article , janapati@ouvaxa.cats.ohiou.edu >> >>numerous factors. The only way one may try to prolong life span can be by >>processes, at an early stage of life. > Bsignificant prolongation of maximal life span by lifelong restriction of >caloric intake. Anyone interested in this may begin a search with the >writings of Roy Walford - he has not been the major experimenter, but he >is a prophet in this area. >. Just a slight correction to the above - caloric restriction is only one of a variety of techniques which extends life span. One should include protein restriction (Bruce Ames), tryptophane restriction, and methionin restriction. This latter is probably unrelated to caloric restriction, since the energy intake of the met restricted animals (rats) was equal to or greater than in controls. >. From owner-ageing@net.bio.net Fri May 20 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!sunic!EU.net!uunet!nwnexus!flames!venezia From: venezia@zgi.com (Domenick Venezia) Newsgroups: bionet.molbio.ageing Subject: Re: telomeres Date: 21 May 1994 15:10:36 GMT Organization: Northwest Nexus Inc. Lines: 14 Distribution: world Message-ID: <2rl89c$rn7@nwfocus.wa.com> References: <9405190315.AA24155@pclsp2> NNTP-Posting-Host: flames.zgi.com X-Newsreader: TIN [version 1.2 PL2] Does anyone know if human telomerase has been cloned and sequenced? Either the protein or RNA moieties. I do not find it listed in PIR or SWISS-PROT and nothing shows up in local and/or global similarity searches of these databases or in the first 3 translation frames of Genbank and the unique sequences to EMBL. Have any of the "heavies" participated in this group? How many of the participants are actually working on biology related to ageing and on telomeres in particular? Domenick Venezia ZymoGenetics, Inc. Seattle, WA venezia@zgi.com From owner-ageing@net.bio.net Fri May 20 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!vixen.cso.uiuc.edu!sdd.hp.com!portal.com!portal!cup.portal.com!Marc_R_Rice From: Marc_R_Rice@cup.portal.com Newsgroups: bionet.molbio.ageing Subject: Re: rice/future Message-ID: <112189@cup.portal.com> Date: Sat, 21 May 94 00:29:13 PDT Organization: The Portal System (TM) References: Lines: 11 I am a mere hopeful. What I am hoping for is Genetic research to change the way we live and think. Our lifespans would be extended thanks to that research that is going on right now. By evolution we will have advanced past the care of chance and random radiation into carefully thought changes. However I agree that more evolution must occur before many humans are ready to accept such changes. The most important evolution would be in the social structure of the human race. It is apparent that not everyone can accept those chages immediately (i.e. Rwanda, Russia, and South Africa) Those countries in () signify the very countries that have proven themselves unable to accept a new order such as democracy (South Africa has at last taken a few steps toward change). Maybe my ideas are to early, but one can hope!!! From owner-ageing@net.bio.net Sat May 21 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!news.cac.psu.edu!news.pop.psu.edu!psuvax1!news.cc.swarthmore.edu!netnews.upenn.edu!ts5-58.upenn.edu!user From: ruthig@wista.wistar.upenn.edu (Lisa Ruthig) Newsgroups: bionet.molbio.ageing Subject: Re: telomeres Followup-To: bionet.molbio.ageing Date: 22 May 1994 22:02:34 GMT Organization: * Lines: 19 Distribution: world Message-ID: References: <9405190315.AA24155@pclsp2> <2rl89c$rn7@nwfocus.wa.com> NNTP-Posting-Host: ts5-58.upenn.edu In article <2rl89c$rn7@nwfocus.wa.com>, venezia@zgi.com (Domenick Venezia) wrote: > > Does anyone know if human telomerase has been cloned and sequenced? Either > the protein or RNA moieties. I do not find it listed in PIR or SWISS-PROT > and nothing shows up in local and/or global similarity searches of these > databases or in the first 3 translation frames of Genbank and the unique > sequences to EMBL. It has not been cloned, but people are working on it now. I will try to find out which group for you. > Have any of the "heavies" participated in this group? How many of the > participants are actually working on biology related to ageing and on > telomeres in particular? I work on mapping a human telomere "half-YAC" library in the lab of Harold Riethman. We have small projects studying the role of telomeres in aging and cancer. From owner-ageing@net.bio.net Sun May 22 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: Calories intake restriction Date: 22 May 1994 20:08:14 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 20 Sender: daemon@net.bio.net Distribution: world Message-ID: <9405230310.AA00858@pclsp2> NNTP-Posting-Host: net.bio.net I read often that reduction in intake of calories seems connected to increase in the life span: I would like to know if the tests have been done on the relative amount of calories or just roughly on the total-amount, with no consideration for other very important variabiles. I mean e.g., I burn, with my daily life activity and excercise, 5,000 Kcalories (is this the unit?) par day and I intake 5,000 Kcalories par day. My friend burns 2,000 Kcalories par day and intake 2,000 Kcalories. Is our life span expected to be different? or (as I believe) not? I would expect differences if both of us burn, with our daily life work and excercise, 2,000 Kcal par day and I intake 5,000 and my friend only 2,000 Kcal, due to overloading of catabolic pathways. I am not expert on ageing, but of course I have a lot of scientific curiosity on it, since its importance on our life. I would suppose, also, that in the first mentioned case, my life span would be longer then that one of my friend. -- Vincenzo From owner-ageing@net.bio.net Sun May 22 23:00:00 1994 Path: biosci!LAMAR.COLOSTATE.EDU!mouse From: mouse@LAMAR.COLOSTATE.EDU (Ann Baker) Newsgroups: bionet.molbio.ageing Subject: aging taste Date: 22 May 1994 20:54:52 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 6 Sender: daemon@net.bio.net Distribution: world Message-ID: <9405230355.AA107042@lamar.ColoState.EDU> NNTP-Posting-Host: net.bio.net 22 May 1994 An 80-y old woman asked me if I knew of any way to help her recover/retain her sense of taste. She is a semi-retired social worker, so references for informed layperson would be more appropriate, though any pertinent refs would be gratefully appreciated. AEM Baker From owner-ageing@net.bio.net Mon May 23 23:00:00 1994 Path: biosci!ugene1.abbott.com!crosbys From: crosbys@ugene1.abbott.com (Seth Crosby 8-6999) Newsgroups: bionet.molbio.ageing Subject: Re: Chromium Piccolinate, Supplements, etc. Date: 24 May 1994 10:29:14 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 4 Sender: daemon@net.bio.net Distribution: world Message-ID: <9405241729.AA09392@ugene1.abbott.com> NNTP-Posting-Host: net.bio.net Be on the look out for a small-molecular mimetic of GHRH coming out of Merck and Co. someday. I saw their prelim results at the small molecule meeting in Philidelphia (4/11-4/12) and this orally available drug looks promising. It's in clinical trials now. From owner-ageing@net.bio.net Wed May 25 23:00:00 1994 Path: biosci!agate!ihnp4.ucsd.edu!swrinde!pipex!doc.ic.ac.uk!susx.ac.uk!bafa1 From: bafa1@central.susx.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: L-Arginine Date: 24 May 1994 12:19:56 GMT Organization: University of Sussex Lines: 21 Message-ID: <2rsrdc$m0c@infa.central.susx.ac.uk> NNTP-Posting-Host: solx1.central.susx.ac.uk X-Newsreader: TIN [version 1.2 PL2] I am interested in the idea of eating supplements of L-arginine. Are there published reports on the effects of doing this? In addition, is there any information on the relationship between ingested ARGININE and the production of NO (nitric oxide) by NO synthase? Are there any known side-effects of over-dose of arginine or of arginine in the absnce of the any 19 amino-ecids? Any information received will be summarized and posted. Thanks. Sydney S.Shall@sussex.ac.uk -- ************************************************************************** ************************************************************************** From owner-ageing@net.bio.net Wed May 25 23:00:00 1994 Path: biosci!agate!ihnp4.ucsd.edu!usc!howland.reston.ans.net!pipex!lyra.csx.cam.ac.uk!warwick!not-for-mail From: cuhes@csv.warwick.ac.uk (Malcolm McMahon) Newsgroups: bionet.molbio.ageing Subject: Re: telomeres Date: 26 May 1994 15:37:05 +0100 Organization: University of Warwick, Coventry, UK Lines: 25 Message-ID: <2s2c6h$hj1@crocus.csv.warwick.ac.uk> References: <9405190315.AA24155@pclsp2> NNTP-Posting-Host: crocus-fddi.csv.warwick.ac.uk Mime-Version: 1.0 Content-Type: text/plain; charset=US-ASCII Content-Transfer-Encoding: 7bit In article <9405190315.AA24155@pclsp2>, vinz@PCLSP2.KUICR.KYOTO-U.AC.JP (Vincenzo Nardi-Dei) writes: > >Telomeres shortening seems to be clearly implicated in regulation of cell >ageing even though a stronger force should be the II principle of >thermodinamic and its tendency to enthropy. Uncorrected DNA replication >errors accumulate even affecting the same repairing system encoding >genes provoking a cascade effect. I don't think the entropy idea really holds water because errors would accumulate from one generation to the next as quickly as from one mitosis to the next. Just as lethal mutations are selected out in a species so they would be selected out in a group of cells. The death clock argument is the first suggested mechanism of aging that has ever made sense to me because it explains why there are no imortal mutants - they die of cancer before we notice they are immortal. Looking at the way that anomolous longevity seems to have quickly evolved in humans as soon as we found a use for grandparents suggests that it's actually rather easy for evolution to produce longevity (experiments with drosophelia show the same thing). To me this clearly points to aging being a "deliberate" mechanism rather than some wear and tear thing. Malcolm From owner-ageing@net.bio.net Wed May 25 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!gatech!swrinde!pipex!uknet!EU.net!uunet!newstf01.cr1.aol.com!search01.news.aol.com!not-for-mail From: abubu@aol.com (ABUBU) Newsgroups: bionet.molbio.ageing Subject: Telomerase animal studies? Date: 26 May 1994 12:36:07 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 11 Sender: news@search01.news.aol.com Message-ID: <2s2j5n$bfs@search01.news.aol.com> NNTP-Posting-Host: search01.news.aol.com I gather from reading other posts that while telomerase (and it's corresponding gene) have not been cloned, telomerase has been purified. Has anyone been conducting animal studies to see what the effect of introducing telomerase does? It seems that this would be the definitive way to answer the questions that have been posed. Perhaps purification of enough telomerase remains prohibitively expensive? If not, studies could be done to test its effect on cancer rates, and life-span. One problem that I can think of is delivery to the appropriate places in the animals. Will it cross cell membranes if injected? Probably not. What about using DMSO or another carrier? From owner-ageing@net.bio.net Wed May 25 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!uknet!EU.net!uunet!newstf01.cr1.aol.com!search01.news.aol.com!not-for-mail From: abubu@aol.com (ABUBU) Newsgroups: bionet.molbio.ageing Subject: Re: Glucose & Ageing Date: 26 May 1994 12:42:02 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 13 Sender: news@search01.news.aol.com Message-ID: <2s2jgq$bil@search01.news.aol.com> References: <2q90ug$lm7@news.umbc.edu> NNTP-Posting-Host: search01.news.aol.com In article <2q90ug$lm7@news.umbc.edu>, davidson@umbc.edu (Ms. Pamela Davidson; (GRAD) writes: >...intracellular non-enzymatic glycosylation... I don't really know alot about this subject, but one place that you might look (if you haven't already) is in literature dealing with diabeties. This disease causes increased blood glucose levels, and all it's related problem : cataracts, premature aging... I believe that most of these problems are a result of excessive cross-linking. There is a drug, aminoguanidine, available in Europe that is supposed to prevent this from happening by preventing the final bonding step. Don't know if that is helpful to you or not, hope so. From owner-ageing@net.bio.net Wed May 25 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!bcm!cs.utexas.edu!swrinde!pipex!uknet!EU.net!uunet!nih-csl!NewsWatcher!user From: jaizzo@helix.nih.gov (John A. Izzo) Subject: Re: Calories intake restriction Message-ID: Followup-To: bionet.molbio.ageing Sender: postman@alw.nih.gov (AMDS Postmaster) Organization: Natl. Inst. on Aging References: <9405230310.AA00858@pclsp2> Date: Thu, 26 May 1994 18:19:25 GMT Lines: 29 In article <9405230310.AA00858@pclsp2>, vinz@PCLSP2.KUICR.KYOTO-U.AC.JP (Vincenzo Nardi-Dei) wrote: > > I read often that reduction in intake of calories seems connected > to increase in the life span: I would like to know if the tests > have been done on the relative amount of calories or just roughly > on the total-amount, with no consideration for other very important > variabiles. > I mean e.g., I burn, with my daily life activity and excercise, > 5,000 Kcalories (is this the unit?) par day and I intake 5,000 Kcalories > par day. My friend burns 2,000 Kcalories par day and intake 2,000 > Kcalories. Is our life span expected to be different? or > (as I believe) not? I would expect differences if both of > us burn, with our daily life work and excercise, 2,000 Kcal par day > and I intake 5,000 and my friend only 2,000 Kcal, due to overloading > of catabolic pathways. Vincenzo, I work at the Natl. Inst. on Aging as a postdoc. While my area of expertise is not diet restriction, however from what I understand the studies have only focused on a reduction of the caloric intake relative to what the rat (or other species) would ingest ad librum (ie unrestricted access to food).Your second example is an good approximation of what we know based on current research. I will inquire about the effect of metabolism and external factors and post any noteworthy information. From owner-ageing@net.bio.net Thu May 26 23:00:00 1994 Path: biosci!GEOG.LEEDS.AC.UK!malcolm From: malcolm@GEOG.LEEDS.AC.UK (Malcolm McMahon) Newsgroups: bionet.molbio.ageing Subject: desirability of aging. Date: 27 May 1994 04:39:31 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 17 Sender: daemon@net.bio.net Distribution: world Message-ID: <15498.9405270859@mailer.leeds.ac.uk> References: <9405270056.AA05681@possum.murdoch.edu.au> NNTP-Posting-Host: net.bio.net I'm familiar with the Sruldbruggs but the argument doesn't hold much water. A cure for ageing is far from being the same as immortality. You can be as ageing proof as you like - it doesn't stop you from being hit by a bus. I'd estimate if you removed ageing and disease the human live expectancy would go up to maybe 300 - 400 years (depending mostly on social stability). In wild animals, of course, it doesn't make any significant difference at all. Immortality for them would, I believe, convey a slight evolutionary advantage since more experienced animals presumably make better parents. At the moment much of the structure of our lives revolves arround the inevitability of ageing. What new structures would evolve if it where removed noone can say. I, for one, am looking foreward to the next century and hope to see the whole of it. Malcolm From owner-ageing@net.bio.net Thu May 26 23:00:00 1994 Path: biosci!agate!cat.cis.Brown.EDU!noc.near.net!news.delphi.com!usenet From: proctorp@delphi.com Newsgroups: bionet.molbio.ageing Subject: Re: L-Arginine Date: Thu, 26 May 94 21:02:10 -0500 Organization: Delphi (info@delphi.com email, 800-695-4005 voice) Lines: 5 Message-ID: References: <2rsrdc$m0c@infa.central.susx.ac.uk> NNTP-Posting-Host: bos1c.delphi.com X-To: Sydney Shall Re: Oral arginine I tell my hair loss patients to take oral arginine under the radionale that NO is the "natural" minoxidil. Peter H. Proctor, PhD, Md From owner-ageing@net.bio.net Thu May 26 23:00:00 1994 Path: biosci!POSSUM.MURDOCH.EDU.AU!cummins From: cummins@POSSUM.MURDOCH.EDU.AU (Dr Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Re: desirability of aging. Date: 26 May 1994 17:52:27 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 23 Sender: daemon@net.bio.net Distribution: world Message-ID: <9405270056.AA05681@possum.murdoch.edu.au> NNTP-Posting-Host: net.bio.net Swift wrote about the awful possibilities of eternal life in"Gulliver's Travels". The "Struldbruggs" were a group of (mutated?) individuals who lived for ever. They were awful bores and miserable with their pointless existence. Somebody should resurrect the term as a metaphor in aging studies. Check the story out :-) Yours, virtually Jim 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 "Nothing in biology makes sense except in the light of evolution" Dobzhansky, 1973 From owner-ageing@net.bio.net Thu May 26 23:00:00 1994 Path: biosci!daresbury!not-for-mail From: Sydney Shall Newsgroups: bionet.molbio.ageing Subject: Telomerase enzyme Date: 27 May 1994 10:58:13 +0100 Lines: 46 Sender: daemon@mserv1.dl.ac.uk Distribution: bionet Message-ID: <2s4g7l$4tt@mserv1.dl.ac.uk> Original-To: ageing@dl.ac.uk There have been several messages about the enzyne telomerase. This enzyme consists of an RNA fragment as well as a very large protein. The RNA fragment has been identified and the relevant DNA cloned. However the protein portion of this enzyme has not been purified at all. Moreover, while a good enzyme assay is available, it seems to be the case that it is not an easy assay because often the enzyme is present in very small amounts. Because the enzyme has not been purified there is no possibility at the moment of achieving the molecular cloning of the cDNA or of the gene. It is clear however that this enzyme is of tremendous interest. Sydney ************************************************************************** ************************************************************************** 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 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 May 26 23:00:00 1994 Path: biosci!biosci!not-for-mail From: leach@mbcrr.harvard.edu (Martin Leach) Newsgroups: bionet.announce,bionet.general,bionet.molbio.ageing,bionet.molbio.bio-matrix,bionet.molbio.methds-reagnts,bionet.neuroscience Subject: **VIRTUAL SEMINAR** BIOMOO Neuroscience Journal Club meeting notice. Date: 26 May 1994 18:26:52 -0700 Organization: Boston University Dept. of Pharmacology Lines: 134 Sender: kristoff@net.bio.net Approved: bionews-moderator@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Xref: biosci bionet.announce:1161 bionet.general:9351 bionet.molbio.ageing:782 bionet.molbio.bio-matrix:484 bionet.molbio.methds-reagnts:14659 bionet.neuroscience:3443 * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * _ ..._---_---_..._ * * * * B i o M O O .-~ ~. `. .' .' .~-. * * * * (__) (_. o o o o o o . \ * * * * (@*) Neuroscience ( o o _ o o o | * * * * /-------\u' Journal Club (_ .o o /' o o ______| * * * * / | || `\______( o /======/' * * * * ||----|| will be presenting \_____/'=====/' * * * * ^^ ^^ the paper | | * * * * `\ | * * * * 66 Neurotoxicity of a 99 * * * * Prion Protein Fragment * * * * * * * * ( Nature 1993 Apr 8; 362 (6420): 543-6 ) * * * * * * * * on Monday 6th June, ( 9 am EST, 2 pm GMT ) * * * * * * * * * * * * * * * * BioMOO is at bioinfo.weizmann.ac.il 8888 * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * Dear Bionetters, Neville Percy (Nev in Biomoo) and I (Martin) are going to present the following paper at the next BioMOO journal club. A short article gives some background to prions (if you want some background info) - Neville recommends....A 'unified theory' of prion propagation. Nature 1991 Nov 7;354(6348):25-6 We are proposing for the next journal club to be on Monday 6th June (9AM EST - 2PM GMT) This may be subject to change - ie the computer system goes down - mega-lag etc.. Good luck reading the article Nev and Martin TI: Neurotoxicity of a prion protein fragment. AU: Forloni-G; Angeretti-N; Chiesa-R; Monzani-E; Salmona-M; Bugiani-O; Tagliavin i-F SO: Nature. 1993 Apr 8; 362(6420): 543-6 PY: 1993 LA: ENGLISH AB: The cellular prion protein (PrPC) is a sialoglycoprotein of M(r) 33-35K that is expressed predominantly in neurons. In transmissible and genetic neurodegene rative disorders such as scrapie of sheep, spongiform encephalopathy of cattle a nd Creutzfeldt-Jakob or Gerstmann-Straussler-Scheinker diseases of humans, PrPC is converted into an altered form (termed PrPSc) which is distinguishable from i ts normal homologue by its relative resistance to protease digestion. PrPSc accu mulates in the central nervous system of affected individuals, and its protease- resistant core aggregates extracellularly into amyloid fibrils. The process is a ccompanied by nerve cell loss, whose pathogenesis and molecular basis are not un derstood. We report here that neuronal death results from chronic exposure of pr imary rat hippocampal cultures to micromolar concentrations of a peptide corresp onding to residues 106-126 of the amino-acid sequence deduced from human PrP com plementary DNA. DNA fragmentation of degenerating neurons indicates that cell de ath occurred by apoptosis. The PrP peptide 106-126 has a high intrinsic ability to polymerize into amyloid-like fibrils in vitro. These findings indicate that c erebral accumulation of PrPSc and its degradation products may play a role in the nerve cell degeneration that occurs in related encephalopathi es AN: 93218742 If you do not know how to connect to BioMOO or are just interested in this virtual scientific community please refer to the latest issue of Science which talks about BioMOO and gives instructions how to get there. The Science article is: Science - 13th May 1994, Vol. 263, pages 900-901 Martin Leach and Neville Percy (co-organisers of this journal club) emails: leach@mbcrr.harvard.edu or spbcnsp@ucl.ac.uk (respectively) If you have any problems please feel free to contact either of us. -- ..... Martin Leach Email:leach@mbcrr.harvard.edu _|____ Dept. of Pharmacology Phone: (617) 638-5323 / o / Boston Univ. School of Med. Fax: (617) 638-4329 _/ |-/__==/ 80 E. Concord St. (L603) (BULLDOZER) \_ Boston MA 02118 "Not the old underpants on your USA head.....WIBBLE" -BLACKADDER From owner-ageing@net.bio.net Thu May 26 23:00:00 1994 Path: biosci!rutgers!gatech!howland.reston.ans.net!spool.mu.edu!sgiblab!news.cs.indiana.edu!noose.ecn.purdue.edu!mozo.cc.purdue.edu!mace.cc.purdue.edu!barani From: barani@mace.cc.purdue.edu (Make-Me-Happy;Gift-Cash!) Newsgroups: bionet.molbio.ageing Subject: Cell-Death Message-ID: Date: 27 May 94 20:44:18 GMT Sender: news@mozo.cc.purdue.edu (USENET News) Organization: Purdue University Lines: 12 Science, Vol.264 (1994) 677-683 contains an article "Genetic Control of programmed cell death in Drosophila" authors: K.White,M.E.Grether,J.M.Abrahms,L.Young,K.Farrell, and H.Steller. also see a review related to the above in the same issue pp668-669 titled "Cell Death genes: Drosophila Enters the field" by M.C.Raff From owner-ageing@net.bio.net Thu May 26 23:00:00 1994 Path: biosci!rutgers!gatech!swrinde!ihnp4.ucsd.edu!sdcc12!jeeves!wsun From: wsun@jeeves.ucsd.edu (Fiberman) Newsgroups: bionet.molbio.ageing Subject: Re: telomeres Message-ID: <68388@sdcc12.ucsd.edu> Date: 27 May 94 20:28:30 GMT References: <9405190315.AA24155@pclsp2> <2s2c6h$hj1@crocus.csv.warwick.ac.uk> Sender: news@sdcc12.ucsd.edu Organization: University of California, San Diego Lines: 36 Nntp-Posting-Host: jeeves.ucsd.edu In article <2s2c6h$hj1@crocus.csv.warwick.ac.uk> cuhes@csv.warwick.ac.uk (Malcolm McMahon) writes: > >I don't think the entropy idea really holds water because errors would >accumulate from one generation to the next as quickly as from one >mitosis to the next. Just as lethal mutations are selected out in a >species so they would be selected out in a group of cells. This is a very good argument. One would think that deleterious but silent mutations could accumulate from one generation to another until an entire species is wiped out. But that does not happen. >The death clock argument is the first suggested mechanism of aging that >has ever made sense to me because it explains why there are no imortal >mutants - they die of cancer before we notice they are immortal. But using the same argument as above. There must be a way to prevent cancer in old age. A single cell can develop into an organism without any problems, why would an adult organism eventually develop cancer? >Looking at the way that anomolous longevity seems to have quickly evolved >in humans as soon as we found a use for grandparents suggests that it's >actually rather easy for evolution to produce longevity (experiments >with drosophelia show the same thing). To me this clearly points to >aging being a "deliberate" mechanism rather than some wear and tear thing. >Malcolm I don't know about aging being deliberate, but perhaps there are some deleterious genes or aging genes that is present in our DNA. There's no selection for longevity genes since as long as an organsim reaches the reproductive age, it has survived well in the evolutionary sense. -fm From owner-ageing@net.bio.net Thu May 26 23:00:00 1994 Path: biosci!daresbury!trane.uninett.no!eunet.no!nuug!EU.net!howland.reston.ans.net!cs.utexas.edu!usc!nic-nac.CSU.net!charnel.ecst.csuchico.edu!olivea!news.bu.edu!ppp-7-15.bu.edu!user From: leach@mbcrr.harvard.edu (Martin Leach) Newsgroups: bionet.molbio.ageing Subject: REPOST: **VIRTUAL SEMINAR** BioMOO Neuroscience Journal Club Followup-To: bionet.molbio.ageing Date: 27 May 1994 22:05:03 GMT Organization: Boston University Dept. of Pharmacology Lines: 99 Message-ID: NNTP-Posting-Host: ppp-7-15.bu.edu * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * _ ..._---_---_..._ * * * * B i o M O O .-~ ~. `. .' .' .~-. * * * * (__) (_. o o o o o o . \ * * * * (@*) Neuroscience ( o o _ o o o | * * * * /-------\u' Journal Club (_ .o o /' o o ______| * * * * / | || `\______( o /======/' * * * * ||----|| will be presenting \_____/'=====/' * * * * ^^ ^^ the paper | | * * * * `\ | * * * * 66 Neurotoxicity of a 99 * * * * Prion Protein Fragment * * * * * * * * ( Nature 1993 Apr 8; 362 (6420): 543-6 ) * * * * * * * * on Monday 6th June, ( 9 am EST, 2 pm GMT ) * * * * * * * * * * * * * * * * BioMOO is at bioinfo.weizmann.ac.il 8888 * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * Dear Bionetters, Neville Percy (Nev in Biomoo) and I (Martin) are going to present the following paper at the next BioMOO journal club. A short article gives some background to prions (if you want some background info) - Neville recommends....A 'unified theory' of prion propagation. Nature 1991 Nov 7;354(6348):25-6 We are proposing for the next journal club to be on Monday 6th June (9AM EST - 2PM GMT) This may be subject to change - ie the computer system goes down - mega-lag etc..Good luck reading the article Nev and Martin TI: Neurotoxicity of a prion protein fragment. AU: Forloni-G; Angeretti-N; Chiesa-R; Monzani-E; Salmona-M; Bugiani-O; Tagliavin i-F SO: Nature. 1993 Apr 8; 362(6420): 543-6 PY: 1993 LA: ENGLISH AB: The cellular prion protein (PrPC) is a sialoglycoprotein of M(r) 33-35K that is expressed predominantly in neurons. In transmissible and genetic neurodegene rative disorders such as scrapie of sheep, spongiform encephalopathy of cattle and Creutzfeldt-Jakob or Gerstmann-Straussler-Scheinker diseases of humans, PrPC is converted into an altered form (termed PrPSc) which is distinguishable from its normal homologue by its relative resistance to protease digestion. PrPSc accumulates in the central nervous system of affected individuals, and its protease-resistant core aggregates extracellularly into amyloid fibrils. The process is accompanied by nerve cell loss, whose pathogenesis and molecular basis are not understood. We report here that neuronal death results from chronic exposure of primary rat hippocampal cultures to micromolar concentrations of a peptide corresponding to residues 106-126 of the amino-acid sequence deduced from human PrP complementary DNA. DNA fragmentation of degenerating neurons indicates that cell death occurred by apoptosis. The PrP peptide 106-126 has a high intrinsic ability to polymerize into amyloid-like fibrils in vitro. These findings indicate that c erebral accumulation of PrPSc and its degradation products may play a role in the nerve cell degeneration that occurs in related encephalopathies AN: 93218742 If you do not know how to connect to BioMOO or are just interested in this virtual scientific community please refer to the latest issue of Science which talks about BioMOO and gives instructions how to get there. The Science article is: Science - 13th May 1994, Vol. 263, pages 900-901 Martin Leach and Neville Percy (co-organisers of this journal club) emails: leach@mbcrr.harvard.edu or spbcnsp@ucl.ac.uk (respectively) If you have any problems please feel free to contact either of us. -- ..... Martin Leach Email:leach@mbcrr.harvard.edu _|____ Dept. of Pharmacology Phone: (617) 638-5323 / o / Boston Univ. School of Med. Fax: (617) 638-4329 _/ |-/__==/ 80 E. Concord St. (L603) (BULLDOZER) \_ Boston MA 02118 "Not the old underpants on your USA head.....WIBBLE" -BLACKADDER p.s. try BioMOO (virtual biology on the internet - telnet bioinfo.weizmann.ac.il 8888) From owner-ageing@net.bio.net Fri May 27 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!agate!ihnp4.ucsd.edu!sdd.hp.com!col.hp.com!csn!gbuell From: gbuell@teal.csn.org (Greg Buell) Subject: Re: desirability of aging. Message-ID: Sender: news@csn.org (The Daily Planet) Nntp-Posting-Host: teal.csn.org Organization: Colorado SuperNet, Inc. References: <9405270056.AA05681@possum.murdoch.edu.au> <15498.9405270859@mailer.leeds.ac.uk> Date: Sat, 28 May 1994 17:43:12 GMT Lines: 49 In article , Fergus Doherty wrote: >In article <15498.9405270859@mailer.leeds.ac.uk>, malcolm@GEOG.LEEDS.AC.UK >(Malcolm McMahon) wrote: >> > >> At the moment much of the structure of our lives revolves arround the >> inevitability of ageing. What new structures would evolve if it where >> removed noone can say. I, for one, am looking foreward to the next >> century and hope to see the whole of it. >> >Would it really be desirable to live for 3-400 years? This would lead to >an increased population, perhaps even more so if it led to more children >spread over a longer period (child bearing period for women would be >greater if ageing slowed?). What effect of such older people would there >be on innovation and social change, might not such a society be dangerously >static? > >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 INVENTION PROJECT... THAT AGES YOU DIFFERENTLY --- so you still die at 80 but you have the body of a 29 year old. THIS INVENTION WOULD BE A GODSEND FOR WOMEN.... CONSIDERING ALL THE 60 YEAR OLD MD'S WHO MARRY 19 YEAR OLD WOMEN.... GRIN GREG BUELL 303 443 6270 PO BOX 1113 BOULDER CO 80306 LIGHT YEAR CONQUEST CORP. -- C:\dir PATH to the 10 nearest SOLAR SYSTEMS >> marries OS/2 to INTERNET "The Light Year Conquest Corp."->>> Lovestars on their honeymoon A-BOMB "1,001 Things You Can Invent" ->>>> You must invent gravity control !!! FIVE POINTS IF YOU CAN NAME THE 10 NEAREST STARS TO EARTH --> GENIUS ?? From owner-ageing@net.bio.net Fri May 27 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!europa.eng.gtefsd.com!news.ans.net!newstf01.cr1.aol.com!search01.news.aol.com!not-for-mail From: abubu@aol.com (ABUBU) Newsgroups: bionet.molbio.ageing Subject: Re: telomeres Date: 28 May 1994 18:34:02 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 13 Sender: news@search01.news.aol.com Message-ID: <2s8gsq$jql@search01.news.aol.com> References: <68388@sdcc12.ucsd.edu> NNTP-Posting-Host: search01.news.aol.com In article <68388@sdcc12.ucsd.edu>, wsun@jeeves.ucsd.edu (Fiberman) writes: >There's no selection for longevity genes since as long as >an organsim reaches the reproductive age, it has survived well >in the evolutionary sense. I have heard this several times, but I do not see why. Wouldn't an organism that stayed as a reproductive adult permanently have a great advantage? It could have ten times (just to pick a number) as many offspring as another organism that aged normally. It would also have a better chance of staying alive, and rearing it's young by virtue of experience. From owner-ageing@net.bio.net Fri May 27 23:00:00 1994 Path: biosci!agate!doc.ic.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: Re: desirability of aging. Followup-To: bionet.molbio.ageing Date: 27 May 1994 15:22:30 GMT Organization: Nottingham University, UK. Lines: 22 Distribution: world Message-ID: References: <9405270056.AA05681@possum.murdoch.edu.au> <15498.9405270859@mailer.leeds.ac.uk> NNTP-Posting-Host: macfd.biochem.nottingham.ac.uk In article <15498.9405270859@mailer.leeds.ac.uk>, malcolm@GEOG.LEEDS.AC.UK (Malcolm McMahon) wrote: > > At the moment much of the structure of our lives revolves arround the > inevitability of ageing. What new structures would evolve if it where > removed noone can say. I, for one, am looking foreward to the next > century and hope to see the whole of it. > Would it really be desirable to live for 3-400 years? This would lead to an increased population, perhaps even more so if it led to more children spread over a longer period (child bearing period for women would be greater if ageing slowed?). What effect of such older people would there be on innovation and social change, might not such a society be dangerously static? 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 Fri May 27 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!pipex!sunic!EU.net!uunet!nwnexus!flames!venezia From: venezia@zgi.com (Domenick Venezia) Newsgroups: bionet.molbio.ageing Subject: telomerase Date: 28 May 1994 00:11:30 GMT Organization: Northwest Nexus Inc. Lines: 15 Message-ID: <2s627i$d9s@nwfocus.wa.com> NNTP-Posting-Host: flames.zgi.com X-Newsreader: TIN [version 1.2 PL2] Sidney Shall says that the RNA moiety has been cloned but the protein moiety has not been. I'm not sure which organisms Sidney is talking about, but at least the yeast protein moiety has been cloned. Lundblad, V. and Szostak, J.W. "A Mutant with a Defect in Telomere Elongation Leads to Senescence in Yeast", Cell 57:633-643. Search for locus EST1 in PIR and/or EST1_YEAST in SWISS-PROT. The RNA moiety has been cloned from about 8 ciliates (Cell 67:343-353). Sidney, if you are speaking of the human moieties, please email or post the reference(s). Thanks. Domenick Venezia ZymoGenetics Seattle, WA venezia@zgi.com From owner-ageing@net.bio.net Fri May 27 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!cs.utexas.edu!swrinde!gatech!news-feed-1.peachnet.edu!news.duke.edu!solaris.cc.vt.edu!news.ans.net!newstf01.cr1.aol.com!search01.news.aol.com!not-for-mail From: abubu@aol.com (ABUBU) Newsgroups: bionet.molbio.ageing Subject: Re: desirability of aging. Date: 27 May 1994 20:23:01 -0400 Organization: America Online, Inc. (1-800-827-6364) Lines: 15 Sender: news@search01.news.aol.com Message-ID: <2s62t5$65c@search01.news.aol.com> References: <15498.9405270859@mailer.leeds.ac.uk> NNTP-Posting-Host: search01.news.aol.com In article <15498.9405270859@mailer.leeds.ac.uk>, malcolm@GEOG.LEEDS.AC.UK (Malcolm McMahon) writes: >You can be as ageing proof as you like - it doesn't stop you from >being hit by a bus. I'd estimate if you removed ageing and disease the >human live expectancy would go up to maybe 300 - 400 years (depending >mostly on social stability). The statistics that I have seen (doubt they include wars and such) say that if you were a careful driver (auto accidents being the main cause of accidental death), and if safety continues to inprove with better technology as it has been, you could expect to live over 100,000 years. From owner-ageing@net.bio.net Fri May 27 23:00:00 1994 Path: biosci!agate!spool.mu.edu!howland.reston.ans.net!gatech!prism!prism!not-for-mail From: gt8623b@prism.gatech.edu (William Shelly Hayes) Newsgroups: bionet.molbio.ageing Subject: Re: desirability of aging. Date: 28 May 1994 13:24:41 -0400 Organization: Georgia Institute of Technology Lines: 52 Sender: gt8623b@prism.gatech.edu Message-ID: <2s7uop$p5n@acmex.gatech.edu> References: <15498.9405270859@mailer.leeds.ac.uk> <2s62t5$65c@search01.news.aol.com> NNTP-Posting-Host: acmex.gatech.edu X-Newsreader: TIN [version 1.2 PL2] If aging is conquered, there are several aspects that few people seem to consider. Old age and infirmity is a disease. I think that our natural (without aging) physical maturity would stop in the early twenties. This physical age would also have an effect on our minds. As we get older, 'crystallized' knowledge is more prevalent - 'fluid' knowledge is less prevalent. This is one of the reasons that older people are more conservative (generally speaking). There was some research I remember hearing about at one time that was experimenting with rats. The object of the research was a drug that allowed the 'fluid' learning ability of younger rats in the older rats. The adage that one cannot teach an old dog new tricks has an enormous impact on our society - some of which is good. Rational conservatism can keep devastating trends from taking over (hot-headed youngsters). A population composed of just old (in body and mind) but immortal people (which I believe is impossible as one is trying to keep a deteriorated condition stable) would become a static and boring society. I do not believe that immortality (barring accidental death) would become static except for possibly a stronger safety conciousness. People would live until they got tired of it, and then they would make themselves stop living (and all of us would go to hell for committing suicide :) ). The initial aspects of a means to stop aging if it were cheap enough to be generally available would be devastating to our society. One third of our society would be back at work (as they would be essentially very knowledgeable twenty year olds) and the birth rate would not slow down significantly. This cannot help but to generate a lot of war and other craziness as the population increases. The way I hope aging research progresses is for it to reduce old age infirmity (as it is doing now), but still keep the limit at ~85 years. As our society progresses, the age limit will hopefully move upwards with the onset of the disease getting closer and closer to the maximum age limit. Basically, people staying young until they die. I think this would be the smoothest transition for aging remedies to make it into our society. No matter what, as immortality approaches, some means of enforced birth control is going to have to be instituted. Unfortunately, I believe that research will only unveil a total fix for aging and not an incremental one. Medicine now only treats symptoms of aging and that will not get us far enough for the total fix not to be somewhat catastrophic. Of course the preceding is only my opinion, it can always stand improvement and refining. -- May I recommend the book 'Ain't Nobody's Business If You Do' by Peter McWilliams aka 'The Absurdity of Consensual Crimes in a Free Society' From owner-ageing@net.bio.net Sun May 29 23:00:00 1994 Path: biosci!agate!howland.reston.ans.net!news.intercon.com!udel!news2.sprintlink.net!news.sprintlink.net!news.world.net!news.teleport.com!ip-cc.teleport.com!user From: jbechtol@reed.edu (J. Bechtold) Newsgroups: bionet.molbio.ageing Subject: Re: telomeres Followup-To: bionet.molbio.ageing Date: Sun, 29 May 1994 18:56:17 -0700 Organization: Reed College Lines: 8 Message-ID: References: <9405190315.AA24155@pclsp2> <2s2c6h$hj1@crocus.csv.warwick.ac.uk> <68388@sdcc12.ucsd.edu> NNTP-Posting-Host: ip-c12.teleport.com In article <68388@sdcc12.ucsd.edu>, wsun@jeeves.ucsd.edu (Fiberman) wrote: > In article <2s2c6h$hj1@crocus.csv.warwick.ac.uk> cuhes@csv.warwick.ac.uk (Malcolm McMahon) writes: If you are interested in this subject, I suggest you read two articles in PNAS, early April of this year by Harley (research), and especially the interesting commentary by Titia deLange. In addition, the cited refs are brief and to the point of this thread. From owner-ageing@net.bio.net Sun May 29 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!agate!howland.reston.ans.net!wupost!csus.edu!netcom.com!jabowery From: jabowery@netcom.com (Jim Bowery) Subject: Re: telomeres Message-ID: Organization: NETCOM On-line Communication Services (408 261-4700 guest) References: <68388@sdcc12.ucsd.edu> <2s8gsq$jql@search01.news.aol.com> Date: Mon, 30 May 1994 09:20:45 GMT Lines: 22 abubu@aol.com (ABUBU) writes: > In article <68388@sdcc12.ucsd.edu>, wsun@jeeves.ucsd.edu (Fiberman) > writes: > > >There's no selection for longevity genes since as long as > >an organsim reaches the reproductive age, it has survived well > >in the evolutionary sense. > > I have heard this several times, but I do not see why. Wouldn't an > organism that stayed as a reproductive adult permanently have a great > advantage? It could have ten times (just to pick a number) as many > offspring as another organism that aged normally. It would also have > a better chance of staying alive, and rearing it's young by virtue of > experience. The basic answer is that the "unit of selection" is not the individual, but the "gene". Genes are already "immortal" so there is no inherent selective advantage for increasing the longevity of the bodies carrying them. -- 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 Sun May 29 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: telomeres Date: 30 May 1994 03:41:16 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 48 Sender: daemon@net.bio.net Distribution: world Message-ID: <9405301043.AA17560@pclsp2> NNTP-Posting-Host: net.bio.net >>I don't think the entropy idea really holds water because errors would >>accumulate from one generation to the next as quickly as from one >>mitosis to the next. Just as lethal mutations are selected out in a >>species so they would be selected out in a group of cells. > >This is a very good argument. One would think that deleterious >but silent mutations could accumulate from one generation to >another until an entire species is wiped out. But that does not >happen. I don't see how easily deleterious but silent mutations could accumulate until an entire species is wiped out. Mutations, as matter of fact, happen in continuation in every living species, beeing this the basis of evolution, but I can not see entire species wiped out. Moreover, at species level, the mutations select them selves, the deleterious ones making the organism less competitive and less able to reproduce and the opposite happens for the favorable mutations. This is the basis for the evolution where mutations play a very important role and I see no need to discuss further. At individual organism the situation is a little different beeing not always easy for all the kind of cells to be replaced when some damage reduce their efficiency, especially in determinate kind of cells and in the adulthood. Replacement can be effective only in open growth system, as is the case of species, but not in controlled growth system, as the individual organisms. Moreover, the mutation could be favourable for the single cell and deleterious for the organism (e.g. cancer mutations), making completely lose the sense of a selection from one mitosis to the next, even if the cells of the individual were free to replicate at will. >The death clock argument is the first suggested mechanism of aging that >has ever made sense to me because it explains why there are no imortal >mutants - they die of cancer before we notice they are immortal. Normal cells, should not develop in cancer-like form even when their clock is not terminated; cells are inhibited in the growth by the contact with the surrounding cells. This contact makes the cell to "understand" its position and role in the organism. When for some mutation the information on the contact inhibition is lost in the cell, it could become cancer-like. Bye, -- Vincenzo From owner-ageing@net.bio.net Mon May 30 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!agate!overload.lbl.gov!dog.ee.lbl.gov!ihnp4.ucsd.edu!usc!nic-nac.CSU.net!charnel.ecst.csuchico.edu!olivea!uunet!zib-berlin.de!math.fu-berlin.de!chemie.fu-berlin.de!a_kowald From: a_kowald@chemie.fu-berlin.de (Axel Kowald) Subject: Lifespan without ageing Message-ID: Sender: news@math.fu-berlin.de (Math Department) Nntp-Posting-Host: glycin.chemie.fu-berlin.de Organization: Kristallographic Institute FU Berlin References: <15498.9405270859@mailer.leeds.ac.uk> <2s62t5$65c@search01.news.aol.com> Date: Tue, 31 May 1994 14:36:07 GMT Lines: 22 Hello everybody ! Just to get the numbers right. Assuming the current knowledge of medicine and an environment as you find it in Europe or the States it is fairly straightforward to calculate the life expectancy using life tables. The life expectancy is around 1200 years, not 300 and not 100000. That means you have a 50% chance to life for 1200 years. The important thing is that if you are lucky and you managed to survive for those 1200 years you have another 50% chance to live for the next 1200 years !!! That means that you have a chance of 25% to live for 2400 years. This is totally different from today. If you survive for 75 years you have NOT another 50% chance to survive the next 75 years. The reason is that the ageing process increases your mortality in an exponential way (doubling it every 8 years) while you have a constant mortality if you could switch off ageing. I just wanted to mention that, because one normally doesn't think about it. Axel Kowald (a_kowald@chemie.fu-berlin.de) From owner-ageing@net.bio.net Mon May 30 23:00:00 1994 Path: biosci!agate!overload.lbl.gov!dog.ee.lbl.gov!ihnp4.ucsd.edu!library.ucla.edu!europa.eng.gtefsd.com!howland.reston.ans.net!news.cac.psu.edu!news.pop.psu.edu!psuvax1!news.cc.swarthmore.edu!netnews.upenn.edu!parvati1-7.wistar.upenn.edu!user From: ruthig@wista.wistar.upenn.edu (Lisa Ruthig) Newsgroups: bionet.molbio.ageing Subject: Re: telomerase Followup-To: bionet.molbio.ageing Date: 31 May 1994 22:37:53 GMT Organization: Wistar Institute Lines: 25 Distribution: world Message-ID: References: <2s627i$d9s@nwfocus.wa.com> NNTP-Posting-Host: parvati1-7.wistar.upenn.edu In article <2s627i$d9s@nwfocus.wa.com>, venezia@zgi.com (Domenick Venezia) wrote: > > Sidney Shall says that the RNA moiety has been cloned but the protein > moiety has not been. I'm not sure which organisms Sidney is talking about, > but at least the yeast protein moiety has been cloned. Lundblad, V. and > Szostak, J.W. "A Mutant with a Defect in Telomere Elongation Leads to > Senescence in Yeast", Cell 57:633-643. Search for locus EST1 in > PIR and/or EST1_YEAST in SWISS-PROT. The RNA moiety has been cloned from > about 8 ciliates (Cell 67:343-353). > From " An Alternative Pathway for Yeast Telomerase Maintenance Rescues ext1- Senescence," Cell 73:347-360 Lundblad and Blackburn: EST1 mutants show a continuous decline in telomere length and increases in frequency of cell death and chromosome loss. "These phenotypes are consistent with the hypothesis that the EST1 gene encodes an essential component of the yeast telomere replication machinery, such as telomerase, although other mechanisms for the failure to replicate telomeres are not excluded." Note that they do not claim to have definitely cloned telomerase. Lisa Ruthig ruthig@wista.wistar.upenn.edu From owner-ageing@net.bio.net Tue May 31 23:00:00 1994 Newsgroups: bionet.molbio.ageing Path: biosci!agate!howland.reston.ans.net!torn!nott!emr1!news From: woodgold@seismo.emr.ca (Cathy Woodgold) Subject: Re: aging taste Message-ID: <1994Jun1.163326.861@emr1.emr.ca> Sender: news@emr1.emr.ca Nntp-Posting-Host: saw19.seismo.emr.ca Reply-To: woodgold@seismo.emr.ca Organization: Geological Survey of Canada References: <9405230355.AA107042@lamar.ColoState.EDU> Date: Wed, 1 Jun 1994 16:33:26 GMT Lines: 16 In article AA107042@lamar.ColoState.EDU, mouse@LAMAR.COLOSTATE.EDU (Ann Baker) writes: > 22 May 1994 > An 80-y old woman asked me if I knew of any way to help her recover/retain > her sense of taste. She is a semi-retired social worker, so references for > informed layperson would be more appropriate, though any pertinent refs would > be gratefully appreciated. > AEM Baker Not sure if this will help your friend, but a deficiency in zinc causes many people to lose their sense of taste (and appetite). Zinc supplements might help. Cathy