From owner-ageing@net.bio.net Thu Jun 03 23:00:00 1993 Path: biosci!uwm.edu!wupost!kuhub.cc.ukans.edu!hubble.asymetrix.com!netnews.nwnet.net!news.u.washington.edu!hardy.u.washington.edu!rbradbur From: rbradbur@hardy.u.washington.edu (Robert Bradbury) Newsgroups: bionet.molbio.ageing Subject: Mitochondrial aging (was Re: Ageing in yeast) Summary: Mitochondrial aging is minimal Message-ID: <1uoatuINNi3t@news.u.washington.edu> Date: 4 Jun 93 20:22:22 GMT References: <9305272035.AA28754@net.bio.net> Distribution: bionet Organization: University of Washington, Seattle Lines: 22 NNTP-Posting-Host: hardy.u.washington.edu In article cummins@CSUVAX1.MURDOCH.EDU.AU (Dr Jim Cummins) writes: >There's currently a lot of interest in the role of mitochondrial DNA >deletions in ageing phenomena. mtDNA deletions occur much faster than in >somatic DNA (in eukaryotic organisms) and accumulate preferentially in >postmitotic cells such as muscle and brain. The end result is disorded >oxidative phosphorylation and spin-off of free radicals. It's possible >that individual yeast cells might age but the colony as a whole survives >through mitosis and the selective elimination of cells with defective >mitochondria? Just one idea. > The articles I've seen on mitochondrial deletion accumulation/genetic defects indicate that the effect is very small (1-2% of mitochondrial genomes are defective). Given cells contain 200-700 mitochondria I have a very difficult time accepting the idea that a few defective genomes causing the problem. Additionally the aging "phenotype" does not appear to be the same as that of people with genetic diseases of the mitochondria which usually show up as heart/muscle disorders. To think of it as part of the the aging process makes sense because the deletions do accumulate/accelerate with age. However to consider it a major player seems a bit of a stretch. From owner-ageing@net.bio.net Thu Jun 03 23:00:00 1993 Path: biosci!uwm.edu!math.ohio-state.edu!sdd.hp.com!decwrl!decwrl!netcomsv!netcom.com!dman From: dman@netcom.com (Dallman Ross) Newsgroups: bionet.molbio.ageing Subject: Re: Is this real science or dupication of sci.life-extension? Message-ID: Date: 4 Jun 93 13:43:15 GMT References: <1umobnINN65g@news.u.washington.edu> Organization: NETCOM On-line Communication Services (408 241-9760 guest) Lines: 23 X-Newsreader: TIN [version 1.1 PL9] John Saario (sjohn@u.washington.edu) wrote: > Cell division can be correlated with youth, of course, since developing > organisms must increase cell number and are "young" by definition. Does > this necessarily mean that if cells never stopped dividing we would never > age or die and that this is the answer to stop the process of ageing? It > seems a likely point to start research but I don't think that the > restriction on the number of times a cell may divide is limiting life span > in our society. Pardon the answer of a non-scientist-but-interested-amateur; but I think cell division-rate is only part of the equation. The DNA of older organisms is much more at the effect of free-radical attack that leads to mutation. The more exposure over time, the more mutation and the more problems there will be dividing successfully. Well, I think that's close. -- __ ___ dman@netcom.com (/ \ _ /) /) _ _ _ _ _ (/__) _ _ _ dross@well.sf.ca.us /` )(_(_( _(__/|/|/(_(_(_/| ( / ( (_)_/_)_/_)_ 350 Perkins St., #108 (___/ ` ( \ Oakland, CA 94610-3422 From owner-ageing@net.bio.net Thu Jun 03 23:00:00 1993 Path: biosci!daresbury!daresbury!news From: bafa1@central.sussex.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: cell division and ageing Message-ID: <1993Jun4.175804.29917@gserv1.dl.ac.uk> Date: 4 Jun 93 16:56:44 GMT Sender: list-admin@daresbury.ac.uk Distribution: bionet Lines: 45 Original-To: ageing@uk.ac.daresbury X-Mailer: ELM [version 2.3 PL11] Recent discusion has touched upon the question as to whether cell division is related to human ageing. The answer is clearly that cell division is related to human ageing. There is some indirect evidence for this statement; but there is direct evidence in the human genetic condition known as Werner's Syndrome. In this condition, there is severe premature ageing and the life-span is approximately halved. Cells from these patients show a much reduced (between 3 and 5 fold) ability to proliferate, thus it is now clear that there is some, currently unclear connection between cell proliferation and human ageing. Sydney Shall ************************************************************************** ************************************************************************** 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: +44.273.67.83.33 E-Mail: Janet: BAFA1@uk.ac.sussex.central Elsewhere: BAFA1@central.sussex.ac.uk EARN/BITNET: BAFA1%sussex.central@ukacrl ******************************************************************************* ******************************************************************************* From owner-ageing@net.bio.net Thu Jun 03 23:00:00 1993 Path: biosci!agate!usenet.ins.cwru.edu!howland.reston.ans.net!usc!sdd.hp.com!saimiri.primate.wisc.edu!usenet.coe.montana.edu!netnews.nwnet.net!news.u.washington.edu!hardy.u.washington.edu!rbradbur From: rbradbur@hardy.u.washington.edu (Robert Bradbury) Newsgroups: bionet.molbio.ageing Subject: Protein inactivation and aging Message-ID: <1uobt2INNib4@news.u.washington.edu> Date: 4 Jun 93 20:38:58 GMT References: <1umobnINN65g@news.u.washington.edu> Organization: University of Washington, Seattle Lines: 49 NNTP-Posting-Host: hardy.u.washington.edu In article <1umobnINN65g@news.u.washington.edu> sjohn@u.washington.edu (John Saario) writes: > >Cell division can be correlated with youth, of course, since developing >organisms must increase cell number and are "young" by definition. Does >this necessarily mean that if cells never stopped dividing we would never >age or die and that this is the answer to stop the process of ageing? It >seems a likely point to start research but I don't think that the >restriction on the number of times a cell may divide is limiting life span >in our society. There are several problems with cell-division forever. 1) Eventually you would weight more than the planet. 2) You would require a huge energy input (as well as C+H+O+N...) 3) Cell replication is not perfect and errors would accumulate. It seems clear that telomere shortening plays a key role in the aging process primates. It probably shows up as decreased cell replication and/or cancer from misrepair of shortened chromosomes. The real question is it simply a side-effect of turning off telomerase at some point in development or is it a "fail-safe" mechanism which normally acts to "disable" cells which have divided a certain number of times and have accumulated a number of DNA mutations due to DNA polymerase errors. If a computer scientist were to design a biological system for extended lifespan he might do some of the things nature has done but he would probably add some more reliability & redundancy, e.g. 1) Make DNA polymerase more accurate (although slower replicating) and compensate by having more origins of replication. 2) Keep telomerase on at sufficient levels to maintain telomere length. 3) Move more of the mitochondrial genome into the nucleus where it would be more protected from oxidative damage. 4) Have a protein recycling system which kept significantly ahead of damage accumulation (requires increased energy input). etc. > >I recently heard a seminar which compared the amount of certain inactivated >metabolic enzymes with age of donor of tissue sample. As much as 60% of the >protein appeared to be inactive by comparision of Western and activities in >older individuals. Inactivation was postulated to be by some sort of peroxide >modification and accumulation of inactive protein due to a decrease in amount >of a scavenger protein. What is the current state of this research? > Clearly oxidative damage to proteins (as well as other modifications) plays an important role in protein inactivation and decreased functioning of organisms. This may be one of the aging factors which is offset by calorie/protein/amino-acid restriction. The tradeoff is that by increasing protein recycling you increase your energy consumption over "minimal" levels which will lead to increased O2 consumption leading eventually to higher levels of DNA damage... catch-22. From owner-ageing@net.bio.net Thu Jun 03 23:00:00 1993 Path: biosci!daresbury!doc.ic.ac.uk!agate!usenet.ins.cwru.edu!magnus.acs.ohio-state.edu!math.ohio-state.edu!sdd.hp.com!saimiri.primate.wisc.edu!usenet.coe.montana.edu!netnews.nwnet.net!news.u.washington.edu!sjohn From: sjohn@u.washington.edu (John Saario) Newsgroups: bionet.molbio.ageing Subject: Is this real science or dupication of sci.life-extension? Message-ID: <1umobnINN65g@news.u.washington.edu> Date: 4 Jun 93 05:59:19 GMT Organization: University of Washington Lines: 21 NNTP-Posting-Host: goren1.u.washington.edu I think I have been posting to the wrong group since it didn't seem I was responding to scientific postings. Question then: Cell division can be correlated with youth, of course, since developing organisms must increase cell number and are "young" by definition. Does this necessarily mean that if cells never stopped dividing we would never age or die and that this is the answer to stop the process of ageing? It seems a likely point to start research but I don't think that the restriction on the number of times a cell may divide is limiting life span in our society. I recently heard a seminar which compared the amount of certain inactivated metabolic enzymes with age of donor of tissue sample. As much as 60% of the protein appeared to be inactive by comparision of Western and activities in older individuals. Inactivation was postulated to be by some sort of peroxide modification and accumulation of inactive protein due to a decrease in amount of a scavenger protein. What is the current state of this research? sjohn@u.washington.edu From owner-ageing@net.bio.net Fri Jun 04 23:00:00 1993 Path: biosci!CSUVAX1.MURDOCH.EDU.AU!cummins From: cummins@CSUVAX1.MURDOCH.EDU.AU (Dr Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Re: cell division and ageing Message-ID: Date: 5 Jun 93 08:44:54 GMT References: <9306041807.AA28128@net.bio.net> Sender: daemon@net.bio.net Distribution: bionet Lines: 66 On 4 Jun 1993, Sydney Shall wrote: > Recent discusion has touched upon the question as to whether cell division > is related > to human ageing. The answer is clearly that cell division is related > to human ageing. There is some indirect evidence for this statement; > but there is direct evidence > in the human genetic condition known as Werner's Syndrome. > In this condition, there is severe premature ageing and the life-span > is approximately halved. Cells from these patients show a much > reduced (between 3 and 5 fold) ability to proliferate, thus it > is now clear that there is some, currently unclear connection between > cell proliferation and human ageing. > > Sydney Shall > > > ************************************************************************** > > ************************************************************************** > > > > 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: +44.273.67.83.33 > > E-Mail: > > Janet: BAFA1@uk.ac.sussex.central > > Elsewhere: BAFA1@central.sussex.ac.uk > > EARN/BITNET: BAFA1%sussex.central@ukacrl > > > ******************************************************************************* > > ******************************************************************************* One powerful model is that ageing is related also to deletions to mitochondrial DNA. A common deletion that is seen in mitochondrial myopathies and also in aging post mitotic tissues such as muscle, cuts out about 2/3 of the oxidative phosphorylation pathway and results in depleted energy production and disordered release of free radicals. Rapidly dividing cells may eliminate defective mitochondria by active selection. We've recently identified this deletion in testis biopsies from men with spermatogenic failure: this is consistent with the hypothesis that some forms of male infertility are due to premature testis ageing. The link between free radicals and sperm dysfunction is well established. If netters are interested in this area email me directly and I can give more info. Jim Cummins Murdoch University Western Australia> From owner-ageing@net.bio.net Fri Jun 04 23:00:00 1993 Path: biosci!CSUVAX1.MURDOCH.EDU.AU!cummins From: cummins@CSUVAX1.MURDOCH.EDU.AU (Dr Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Re: Mitochondrial aging (was Re: Ageing in yeast) Message-ID: Date: 5 Jun 93 08:59:28 GMT References: <9306042055.AA14736@net.bio.net> Sender: daemon@net.bio.net Distribution: bionet Lines: 36 On 4 Jun 1993, Robert Bradbury wrote: > In article cummins@CSUVAX1.MURDOCH.EDU.AU (Dr Jim Cummins) writes: > >There's currently a lot of interest in the role of mitochondrial DNA > >deletions in ageing phenomena. mtDNA deletions occur much faster than in > >somatic DNA (in eukaryotic organisms) and accumulate preferentially in > >postmitotic cells such as muscle and brain. The end result is disorded > >oxidative phosphorylation and spin-off of free radicals. It's possible > >that individual yeast cells might age but the colony as a whole survives > >through mitosis and the selective elimination of cells with defective > >mitochondria? Just one idea. > > > > The articles I've seen on mitochondrial deletion accumulation/genetic > defects indicate that the effect is very small (1-2% of mitochondrial > genomes are defective). Given cells contain 200-700 mitochondria > I have a very difficult time accepting the idea that a few defective > genomes causing the problem. Additionally the aging "phenotype" > does not appear to be the same as that of people with genetic diseases > of the mitochondria which usually show up as heart/muscle disorders. > > To think of it as part of the the aging process makes sense because > the deletions do accumulate/accelerate with age. However to consider > it a major player seems a bit of a stretch. Check out an article by Doug Wallace in Science last year, May I think. The mtDNA-somatic mutation theory is rapidly gaining acceptance. Threshold effects are important, as cells don't express the defective phenotype until they have passed through a specific threshold level of defective mitochodria. Thismay be quite low. Jim Cummins> From owner-ageing@net.bio.net Wed Jun 09 23:00:00 1993 Path: biosci!daresbury!daresbury!news From: bafa1@central.sussex.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Mitochondrial ageing Message-ID: <1993Jun10.115651.29929@gserv1.dl.ac.uk> Date: 10 Jun 93 11:28:09 GMT Sender: list-admin@daresbury.ac.uk Distribution: bionet Lines: 40 Original-To: ageing@uk.ac.daresbury X-Mailer: ELM [version 2.3 PL11] There have been several messages pointing to the notion that deletions and mutations in mitochondrial DNA significantly contribute to either cell or animal ageing. The idea is very attractive, and there is some interesting, but very indirect evidence for this notion. But, can anyone direct us to specific data (references) in which AGEING rather tthan disease is correlated with mitochondrial DNA deletions. I have studied thearticle in Science last year, to which Jim Cummings referred, but there is I think, no direct evidence for this connection with ageing. The relationship of mit. DNA changes with human diseases, especially muscle, is sound. is there any evidence for such a connection with ageing, say of the heart; again, I emphasise, not just with cardiomyopathy which is rather rare. Any bits of direct evidence would be most worthwhile to examine. ************************************************************************** ************************************************************************** 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: +44.273.67.83.33 E-Mail: Janet: BAFA1@uk.ac.sussex.central Elsewhere: BAFA1@central.sussex.ac.uk EARN/BITNET: BAFA1%sussex.central@ukacrl ******************************************************************************* ******************************************************************************* From owner-ageing@net.bio.net Thu Jun 10 23:00:00 1993 Path: biosci!CSUVAX1.MURDOCH.EDU.AU!cummins From: cummins@CSUVAX1.MURDOCH.EDU.AU (Dr Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Re: Mitochondrial ageing Message-ID: Date: 11 Jun 93 02:46:47 GMT References: <9306101207.AA18800@net.bio.net> Sender: daemon@net.bio.net Distribution: bionet Lines: 28 The evidence linking mtDNA deletions and aging is accumulating rapidly. Netters should check out the following references. Zhang et al (1992) FEBS 297: 34-38 Torii et al (1992) Am J Respir Cell Mol Biol 6:543-549 Cortopassi $ Arnheim (1990) NAR 18(23): 6927-6933 Miquel (1991) Arch Gerontol Geriatr 12: 99-117 Linnane et al (1992) Mutation Res 275: 195-208 Linnane et al (1992) In Adenine Nucleotides in Cellular Energy Transfer and Signal Transduction, S Papa, A Azzi and JM Tager (eds) Birkhauser Verlag, Basel/Switzerland, pp 137-149. This last also contains information on mtDNA deletions in rats with aging and uses an interesting cell model lacking mtDNA. Leprat et al (1990) in Mechanisms of Ageing and Development 52: 149-167 have described a technique for monitoring cell ageing and mitochondrial function using fluorescent probes. I hope we can keep this discussion going, as the mtDNA theory of aging has great explanatory potential. In addition, it opens the way to rational approaches to treating age-related disorders using redox therapy (eg Coenzyme Q10). One could even speculate on doing mitochondrial transfers or perfusions to combat ege! Jim Cummins Murdoch University Western Australia From owner-ageing@net.bio.net Thu Jun 10 23:00:00 1993 Path: biosci!BROWNVM.BROWN.EDU!DRAND From: DRAND@BROWNVM.BROWN.EDU (David Rand) Newsgroups: bionet.molbio.ageing Subject: Re: Mitochondrial ageing Message-ID: <9306111341.AA02905@net.bio.net> Date: 11 Jun 93 13:26:40 GMT Sender: daemon@net.bio.net Distribution: bionet Lines: 14 We have some preliminary data suggesting a connection between ageing and mtDNA (but not necessarily between mtDNA and ageing). When Drosophila females heteroplasmic for two different-sized length variants of mtDNA (due to an insertion in the A+T-rich control region [non-coding]) are allowed to lay eggs in cohorts, the age of the mother is related to the transmission of the two mtDNAs. When the mother is young, her offspring show an increase in the frequency of the smaller mtDNA; when the same mother lays eggs after 15-20 days, the larger mtDNA has an advantage in transmission. To now clarify my first sentence, all I am prepared to say now is that as the female ages, she transmits mtDNAs differently; it may be going to far to say that the reason she ages is that the proportions of mtDNAs in her cells (germline) changes. More later: there are many blots to hybridize and a freezer full of young and old flies to grind up. --David Rand, Brown University, Bio Med Box G-W, Providence, RI 02912 USA From owner-ageing@net.bio.net Sun Jun 13 23:00:00 1993 Path: biosci!vigyan.ernet.in!mbu!barani From: mbu!barani@vigyan.ernet.in Newsgroups: bionet.molbio.ageing Subject: Eternity! Message-ID: <9306141807.AA01564@iisc.ernet.in> Date: 14 Jun 93 18:07:17 GMT Sender: daemon@net.bio.net Distribution: bionet Lines: 37 The lineage between deletions/insertions in mtDNA and ageing can be befuddling. How does one prove that the mutations in mtDNA precede ageing? Even then how does one find the cause for mtDNA mutations? It is also necessary to find similar mechanisms in lower organisms in which an equivalent process takes place to support this theory. Also it is quite a wishful thinking that mutations in mtDNA alone are responsible for an almost programmed cell ageing. I am not being pessimistic, but just trying to control the euphoria over the mtDNA-ageing theory. We need to to be more exhaustive in analysis. For whatever be its worth, I record here a finding related to the mitochondria genomes. I have analysed the sequences of three mammalian mitochondria (human, rodent and finwhale) and found a single 52 nucleotide long conserved sequence. This conserved sequence lies approximately at the same location in all the three genomes. This region codes for the 16s rRNA. This is the longest conserved sequence between these three. I can send further details for those interested. S.Baranidharan Molecular Biophysics Unit Indian Institute of Science Bangalore 560 012 India. barani@mbu.iisc.ernet.in fax: 912-080-341683 From owner-ageing@net.bio.net Mon Jun 14 23:00:00 1993 Path: biosci!daresbury!daresbury!news From: bafa1@central.sussex.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: What is ageing?????? Message-ID: <1993Jun15.143745.20282@gserv1.dl.ac.uk> Date: 15 Jun 93 11:46:30 GMT Sender: list-admin@daresbury.ac.uk Distribution: bionet Lines: 82 Original-To: ageing@uk.ac.daresbury X-Mailer: ELM [version 2.3 PL11] In response to a previous contribution, someone has asked me (privately) how one measure ageing except as disease. This is in my view a very profound question, so I have taken the liberty of publishing my (private) response, becuase I should like to hear the views of other people. I am aware that this can be a very controversial discussion. The point is very well taken. This is a major discussion point in the field. It has never been proven formally that there is a process of biological ageing in whole animals independent of, and unrelated to pathology. However, having said that, I would point out three bits of evidence that seems to say that there is such a phenomenon as biological ageing, which is genetically modulated. There exist both natural and induced variants (?mutants) in which the natural lifespan value is altered. Experimentally induced mutants of this type have been described in both Drosophila and in C. elegans (a nematode worm). And in humans there exists the human genetic disease called Werner's Syndrome. This has been quite clearly demonstrated to be due to an autosomal, recessive allele of a single genetic locus; and in these patients lifespan is approximately halved. In addition, there are a number of other human genetic progeroid (premature ageing) syndromes. Thirdly, there is a weak correlation between ageing of cells in vitro, and human lifespan. More convincingly, Rohme has established that there is a very good correlation between in vitro lifespan and either the mean or maximum lifespans of a wide range of animal species. This almost certainly is genetically modulated because Pereira-Smith and Smith at Houston have unequivocally shown that in vitro lifespan of human fibroblasts is dependent on four genetic complementation groups. These bits of evidence seem very compelling to the notion that there there is a genetically influenced phenotype of biological ageing, independent of pathology and damage and accident. Of course, this evidence DOES NOT say that pathologym, damage and accident do not cause morbidity and mortlaity; it is clear that they do. But it seems that there are also genetic elemnets that are relevant. The definition of ageing therefore, is probably best given for whole animal organisms as the increasing loss of physiological function that leads to morbidity and mortality; this loss of function is brought about by an interacting set of exogenous and endogenous circumstances and properties. Complex - YES! Vague - very!!!! But I think both helpful and correct. it provides a framework for investigation; this framework says that one needs to look to exogenous and endogenous causes of disease as well as to endogenous explanations for loss of physiological function with time. I hope this stimulates some alternative interpretations! Sydney Shall. ************************************************************************** ************************************************************************** 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: +44.273.67.83.33 E-Mail: Janet: BAFA1@uk.ac.sussex.central Elsewhere: BAFA1@central.sussex.ac.uk EARN/BITNET: BAFA1%sussex.central@ukacrl ******************************************************************************* ******************************************************************************* From owner-ageing@net.bio.net Mon Jun 14 23:00:00 1993 Path: biosci!vigyan.ernet.in!mbu!barani From: mbu!barani@vigyan.ernet.in Newsgroups: bionet.molbio.ageing Subject: Energetics and Ageing Message-ID: <9306160447.AA28108@iisc.ernet.in> Date: 16 Jun 93 04:47:08 GMT Sender: daemon@net.bio.net Distribution: bionet Lines: 43 On the question of quantification of the ageing process (continuing from Sydney Shall's Million Dollar Question ..What is Ageing..) An idea can be borrowed from ecology. The ecological systems are considered from a point of view of energy flow through the system and ecological materials are also classified based on their calorific value. In a similar way, it is possible to quantify ageing depending on a cell's ability to perform work or convert chemical potential energy into heat. The rate of energy transfer in a cell is directly proportional to its ability to function and hence its age. This definition leads to a possibility that different parts of a living system age at different rates. Wild Thought! : Is it possible that Werner's syndrome is a result of body cells ageing at a much faster rate than the brain cells and on the other hand, the Alzheimer's disease is one in which the brain cells decay much faster than the body cells ? The rate of energy transfer in a cell can be worked out more rigorously and given a mathematical basis. There is a distant link to mtDNA theory of ageing too! S.Baranidharan Molecular Biophysics Unit Indian Institute of Science Bangalore 560 012 India. barani@mbu.iisc.ernet.in ================================================================ | This box is dedicated to the memory of those | | who spent their lifetime worrying about the | | AGE OLD PROBLEM OF THE OLD AGE PROBLEM | ================================================================ From owner-ageing@net.bio.net Tue Jun 15 23:00:00 1993 Path: biosci!agate!howland.reston.ans.net!usc!elroy.jpl.nasa.gov!news.claremont.edu!nntp-server.caltech.edu!ashley From: ashley@cco.caltech.edu (Allen M. Ashley) Newsgroups: bionet.molbio.ageing Subject: Fixing an Earlier Botch? Message-ID: <1vlu6hINN5d0@gap.caltech.edu> Date: 16 Jun 93 01:49:05 GMT Distribution: usa Organization: California Institute of Technology, Pasadena Lines: 14 NNTP-Posting-Host: alumni.caltech.edu I would like to do non-commercial research on the net: to do author and key word search in a number of areas, and be able to read the text of articles. I understand that there are EXPENSIVE subscription services that provide this capability, but I would like find something without charge. If anyone can direct me to such services I would appreciate a response by Email. Thank you for reading this posting. Allen Ashley==> ashley@alumni@caltech.edu From owner-ageing@net.bio.net Tue Jun 15 23:00:00 1993 Path: biosci!IFCSUN1.IFISIOL.UNAM.MX!rarredon From: rarredon@IFCSUN1.IFISIOL.UNAM.MX (Raul Arredondo) Newsgroups: bionet.molbio.ageing Subject: Request for references Message-ID: <9306161951.AA19287@ifcsun1.ifisiol.unam.mx> Date: 16 Jun 93 19:51:27 GMT Sender: daemon@net.bio.net Distribution: bionet Lines: 9 Dear Colleagues: I should greatly appreciate if someone could help us by sending specific references regarding ageing on different phyla (i.e. fungi, protoctist, monera, plantae, etc). Reviews would be highly useful. Thank you in advance. Raul Arredondo-Peter From owner-ageing@net.bio.net Thu Jun 17 23:00:00 1993 Path: biosci!parc!decwrl!decwrl!sdd.hp.com!caen!batcomputer!munnari.oz.au!uniwa!newsman!csuvax1!washer From: washer@csuvax1.csu.murdoch.edu.au (Stewart Washer) Newsgroups: bionet.molbio.ageing Subject: Human growth hormone Message-ID: <1vtic8INNl9e@newsman.csu.murdoch.edu.au> Date: 18 Jun 93 23:16:24 GMT Lines: 7 NNTP-Posting-Host: csuvax1.murdoch.edu.au Does anyone know of any references regarding the effect of Human growth hormone (somatotropin) on ageing ? If so please email me at washer@csuvax1.murdoch.edu.au. Thanking you Stewart Washer From owner-ageing@net.bio.net Thu Jun 17 23:00:00 1993 Path: biosci!daresbury!daresbury!news From: CS@abc.univie.ac.at ("Christoph Schller") Newsgroups: bionet.molbio.ageing Subject: Mitochondrial DNA isolation Message-ID: <1993Jun18.092607.6282@gserv1.dl.ac.uk> Date: 18 Jun 93 11:26:58 GMT Sender: list-admin@daresbury.ac.uk Distribution: bionet Lines: 8 Original-To: ageing@uk.ac.daresbury Priority: normal X-Mailer: Pegasus Mail v2.3 (R5). Dear Netters Does anyone have a protocol to isolate mt-DNA from tissue (rat brain)? How to estimate nuclear DNA contamination? We want to analyse oxidative damage. Christoph Schueller. In der Kuerze liegt die Wuerze. From owner-ageing@net.bio.net Thu Jun 17 23:00:00 1993 Path: biosci!uwm.edu!cs.utexas.edu!sdd.hp.com!col.hp.com!csn!shaman.nexagen.com!shaman.nexagen.com!not-for-mail From: cordell@shaman.nexagen.com (Bruce Cordell) Newsgroups: bionet.molbio.ageing Subject: Re: Human growth hormone Message-ID: <1vt3h6INNb1d@shaman.nexagen.com> Date: 18 Jun 93 19:03:02 GMT References: <1vtic8INNl9e@newsman.csu.murdoch.edu.au> Organization: NeXagen.com Lines: 23 NNTP-Posting-Host: shaman.nexagen.com washer@csuvax1.csu.murdoch.edu.au (Stewart Washer) writes: >Does anyone know of any references regarding the effect of Human growth hormone (somatotropin) on ageing ? >If so please email me at washer@csuvax1.murdoch.edu.au. > Thanking you > Stewart Washer Two or three years ago a read an article in The New England Journal of Medicine about a study conducted with HGH in 60-80yr old subjects. The results seemed fascinating to me, but I have lost the reference. If anyone is aware of this article, pleas email me with the details. The above poster would probably also be very interested in this information. Thanks! ___________________________________________________________________________ GOD IS NO WHERE Bruce Robert Cordell GOD IS NOW HERE cordell@shaman.nexagen.com ___________________________________________________________________________ From owner-ageing@net.bio.net Sun Jun 20 23:00:00 1993 Path: biosci!POSSUM.MURDOCH.EDU.AU!cummins From: cummins@POSSUM.MURDOCH.EDU.AU (Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Hypophysectomy and ageing Message-ID: Date: 21 Jun 93 00:38:20 GMT Sender: news@net.bio.net Distribution: bionet Lines: 12 I've been told that hypophysectomy coupled with moderate diet in rats retards ageing. I'm trying to get the original source of this report, that apparently came out in an endocrinological journal in the 1930s. Can anyone help with this? Dr Jim Cummins +61-9-360 2668 School of Veterinary Studies FAX =61-9-310 4144 Murdoch University cummins@possum.murdoch.edu.au Murdoch, Western Australia 6015 From owner-ageing@net.bio.net Sun Jun 20 23:00:00 1993 Path: biosci!daresbury!daresbury!news From: brack@urz.unibas.ch (Christine Brack) Newsgroups: bionet.molbio.ageing Subject: hypophysectomy and aging Message-ID: <1993Jun21.080723.1144@gserv1.dl.ac.uk> Date: 21 Jun 93 08:11:23 GMT Sender: list-admin@daresbury.ac.uk Distribution: bionet Lines: 10 Content-Identifier: 477 Original-To: ageing@uk.ac.daresbury Conversion: Prohibited Dr. Cummins is looking for the original report on hypophysectomy. low calory diet and aging. A paper by Pierpaoli & Yi (Aging 37, 171-175, 1990) might help you to get to this reference. They mention a paper by McCay et al. J. Nutr. 18, 1-13, 1939. Dr. Christine Brack Biozentrum University Basel Switzerland Brack@urz.unibas.ch From owner-ageing@net.bio.net Mon Jun 21 23:00:00 1993 Path: biosci!uwm.edu!ux1.cso.uiuc.edu!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr From: jwhitesi@ACAD.BRYANT.EDU (Jennifer A Whiteside) Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet Subject: Budget Cuts in Rhode Island (fwd) Message-ID: Date: 22 Jun 93 19:11:54 GMT Sender: Geriatric Health Care Discussion Group Reply-To: Geriatric Health Care Discussion Group Lines: 25 Xref: biosci bionet.molbio.ageing:439 To: IN%"NEWSMGR@muvms6.wvnet.edu" "Marshall University" CC: Return-path: <@UBVM.CC.BUFFALO.EDU:owner-gerinet@UBVM.CC.BUFFALO.EDU> Return-path: jwhitesi <@UBVM.CC.BUFFALO.EDU:jwhitesi@ACAD.BRYANT.EDU> To: Marshall University MIME-version: 1.0 Content-type: TEXT/PLAIN; charset=US-ASCII Content-transfer-encoding: 7BIT X-To: GERINET@UBVM.cc.buffalo.edu I am a 20 year old RI resident hoping to make my future in the area of social work, particularly with the elderly. I am currently doing an internship in a hospice here and I have become aware that I am going to face many problems. A few weeks ago, our governor proposed his budget plan for the next fiscal year. It includes an increase in spending for education and a big multi-million dollar decrease in spending for health care--more importantly nursing homes. Now, since this came out every health care center has rallied against it. They've held town meeting, written letters, made phone calls, etc. Everyone has been involved to stop this, including the residents of these places. Yet, the state still insists that this budget plan is needed. It has already passed in the House, what will happen if it passes the Senate? One nursing home has already closed because of this and another is announcing it's plan to close as well. This means that 400 people will need to be relocated to the 90 or so beds that are left in the state. I understand that Connecticut went through this same thing recently. However, they were able to reverse the proposal and even ended up getting more money from the state. What I really asking is, How can we stop this? If anyone has been through a similar situation, I'd really be interested in hearing about how you delt with it and any possible suggestions you might have. Thank-you for your time. Jennifer Whiteside Bryant College jwhitesi@acad.bryant.edu From owner-ageing@net.bio.net Thu Jun 24 23:00:00 1993 Path: biosci!agate!dog.ee.lbl.gov!network.ucsd.edu!sdcc12!jeeves!rabani From: rabani@jeeves.ucsd.edu (Ely Rabani) Newsgroups: bionet.molbio.ageing Subject: Exercise, free radicals, radon & repair Message-ID: <51210@sdcc12.ucsd.edu> Date: 25 Jun 93 03:00:35 GMT Sender: news@sdcc12.ucsd.edu Organization: University of California, San Diego Lines: 112 Nntp-Posting-Host: jeeves.ucsd.edu Newsgroups: sci.life-extension Subject: Re: Effect of exercise on longevity (was: Re: Transcendental Meditation slows/reverses biomarkers?) Summary: Expires: References: <1993Jun18.195111.21776@midway.uchicago.edu> <208j2g$o6e@uniwa.uwa.edu.au> <68730@mimsy.umd.edu> A couple of points: Exercise produces free radicals. This shouldn't be too surprising to anyone, since we know that energy utilization increases during exercise, that initially this by way of glycogen anabolism (to glucose, released to blood, taken up by cells) and that glucose is metabolized (eventually) by mitochondria. Fat anabolism (later in exercise) also occurs in mitochondria. Mitochondria, as readers of this group probably know, pump out lots of radicals as a result of their synthesis of ATP. Now, we know that free radicals dammage both proteins and DNA, and that dammage of both is associated with aging. (Draw your own causal arrows....) But it's not quite so simple, since repair of this dammage occurs at response regulated levels. Two observations: A few years ago, a Sweedish study found that low levels of Radon were associated with a longevity _increase_ of a few years. We know that inhaling Radon exposes the organism to decay products that form free radicals. Do we conclude that free radicals promote longevity? Not exactly. The researchers speculated (if I recall) that this effect was due to the induction of free radical scavengin systems and/or repair mechanisms by low levels of free radicals. If this is the case, it's easy to see how these responses, once induced, scavenge/repair the Radon induced effects and then some, such that the steady state of free-radical dammage is actually lower than ambient (non-scavenge/repair) levels. Another point they made was that satiety/appetite mechanisms may involve the monitoring of free-radical levels, such that the Radon exposure could have resulted in lower caloric intake. The free radicals released into the blood upon eating are suspected by some to be the basis for the effects of CR: less calories-->less radicals. This would explain the observations that anti-oxidants don't have much lifespan effects on CRed rats, and that the effects of CR and antioxidants are roughly as large. (If anyone has followed research on that last point, please post a summary.) [as i was rereading this text, i decided to look for that ref. couldn't find it on medline, but i did find this: Search request: F KW RADON AND KW INCREASE Search result: 31 citations in the Medline database Display: SHO AB 1 1. Yamaoka K; Komoto Y; Suzuka I; Edamatsu R; Mori A. Effects of radon inhalation on biological function--lipid peroxide level, superoxide dismutase activity, and membrane fluidity. Archives of Biochemistry and Biophysics, 1993 Apr, 302(1):37-41. (UI: 93228362) Abstract: We administered radon (Rn) to rabbits by inhalation and examined changes in the lipid peroxide (TBARS) level, superoxide dismutase (SOD) activity, and membrane fluidity in various organs to clarify the therapeutic effects of Rn. The lipid peroxide level of the brain was significantly decreased immediately after Rn inhalation for 90 min in both the low concentration group (about 7-10 kBq/liter) and the high concentration group (about 14-18 kBq/liter) as compared with that in the control group. It further decreased in the low concentration group but slightly recovered in the high concentration group 2 h after inhalation. The lipid peroxide level of the lung showed no change immediately after inhalation but decreased significantly in both groups 2 h after inhalation. With regard to SOD activity in the brain and lung, only that in the brain showed significant increase in the high concentration group immediately after inhalation; no other change was observed. Membrane fluidity, especially the fluidity of membrane protein, was significantly increased in the brains of both groups immediately after inhalation, and that 2 h after inhalation in the lung was significantly increased in both groups. These findings suggest that the inhalation of Rn at Rn springs contributes to the prevention of brain disorders related to peroxidation reactions by promoting these physiologic changes. It is, of course, worth pointing out that inhaling radon is still not a great idea, since it does cause lung and other cancers. This is the difference between simple life expectancy and quality of life comparissons. ] Another study, before World War II, found that rats exposed to low levels of radiation also lived longer. This was refered to as the hormetic effect. If I remember correctly, these rats also displayed reduced ad libitum appetite. This (if memory serves) was the impetus to look at the effects of CR on longevity. Some speculation: Whatever the effects of exercise on lifespan (can anyone produce numbers?) we do know that it is nonetheless good for you, in particular reducing heart attacks and strokes, keeping body-fat down and increasing blood-flow to the brain (lack of oxygen to the brain may be an important component in Alzheimers...so if you want to live long....) The obvious solution for anyone concerned about any potential effects of exercise should load up on anti-oxidants (good for you anyway) and just do it. Unless of course this is just a rationalization to not exercise, in which case you need to find a new one (Also, on the lifespan bit, were incidental effects, like being hit by cars while jogging, or for that matter, sucking up exhaust fumes while jogging, taken into account??? The latter might not be trivial, since [we are told] living in LA is the equivalent of smoking two packs a day.) ---- Ely. From owner-ageing@net.bio.net Thu Jun 24 23:00:00 1993 Path: biosci!POSSUM.MURDOCH.EDU.AU!cummins From: cummins@POSSUM.MURDOCH.EDU.AU (Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Re: Exercise, free radicals, radon & repair Message-ID: Date: 25 Jun 93 05:24:44 GMT References: <9306250324.AA15621@net.bio.net> Sender: daemon@net.bio.net Distribution: bionet Lines: 17 Exercise also prevents obesity and reduces the energy intake: energy stored ration. Dietary restriction is known to retard ageing: maybe there's a link? Incidentally, although free radicals are commonly portrayed as villains they actually play important roles as second messengers at very low concentrations. H2O2 is now known to be a co-factor in the sperm acrosome reaction even though at high concentrations it's extremely toxic. NO, CO are also important. Damage comes when free radicals spin out of control. Dr Jim Cummins +61-9-360 2668 School of Veterinary Studies FAX =61-9-310 4144 Murdoch University cummins@possum.murdoch.edu.au Murdoch, Western Australia 6015 From owner-ageing@net.bio.net Thu Jun 24 23:00:00 1993 Path: biosci!daresbury!buzz.bmc.uu.se!corax.udac.uu.se!sunic!isgate!krafla!php From: php@rhi.hi.is (Petur Henry Petersen) Newsgroups: bionet.molbio.ageing Subject: 1 april? Message-ID: <7206@krafla.rhi.hi.is> Date: 25 Jun 93 14:25:02 GMT Sender: usenet@rhi.hi.is Lines: 15 Nntp-Posting-Host: hengill.rhi.hi.is There was this extraordinary report in Nature the first of April concerning age-research. I simply cant find that number in our library now (sic) so i cant qouite it but... It was about some miracle-protein extracted from carp. Was this true and if so does anyone have comments? Or am i an april-fool? p.henry deptm.biology U.iceland ps: If this text looks funny it is caused by my computer not my twisted mind... From owner-ageing@net.bio.net Thu Jun 24 23:00:00 1993 Path: biosci!daresbury!doc.ic.ac.uk!uknet!pipex!zaphod.crihan.fr!usenet From: PODO@cgmvax.cgm.cnrs-gif.fr (PODO) Newsgroups: bionet.molbio.ageing Subject: Re: Request for references Message-ID: <20f2u3$qsv@zaphod.crihan.fr> Date: 25 Jun 93 14:43:15 GMT References: <9306161951.AA19287@ifcsun1.ifisiol.unam.mx> Organization: CENTRE DE GENETIQUE MOLECULAIRE Lines: 15 NNTP-Posting-Host: 157.136.20.1 X-News-Reader: VMS NEWS 1.24 In-Reply-To: rarredon@IFCSUN1.IFISIOL.UNAM.MX's message of 16 Jun 93 19:51:27 GMT In <9306161951.AA19287@ifcsun1.ifisiol.unam.mx> rarredon@IFCSUN1.IFISIOL.UNAM.MX writes: > > Dear Colleagues: > I should greatly appreciate if someone could help us by sending > specific references regarding ageing on different phyla (i.e. > fungi, protoctist, monera, plantae, etc). Reviews would be highly > useful. > We would like to suggest: C. E. FINCH Longevity, Senescence and the genome 1990 The university of chicago press ISBN 0-226-24888-7 This is a very comprehensive book about senesence in every phyla From owner-ageing@net.bio.net Fri Jun 25 23:00:00 1993 Path: biosci!NETCOM.COM!wick From: wick@NETCOM.COM (Potter Wickware) Newsgroups: bionet.molbio.ageing Subject: Re: 1 april? Message-ID: Date: 26 Jun 93 03:12:25 GMT References: <9306251457.AA17901@net.bio.net> Sender: daemon@net.bio.net Distribution: bionet Lines: 27 Me too! The citation I looked for was the review by Obispo in Adv Gerontol 6:1-39 (1990). But that journal ceased publication some years ago. Next step would be to check other gerontology journals for that volume and date, on the chance that the citation got scrambled. Or else contact the author Robin Weiss, if anyone has an e-mail for him. On 25 Jun 1993, Petur Henry Petersen wrote: > > There was this extraordinary report in Nature the first of > April concerning age-research. I simply cant find that number in > our library now (sic) so i cant qouite it but... > > It was about some miracle-protein extracted from carp. > > Was this true and if so does anyone have comments? Or am i > an april-fool? > > p.henry > deptm.biology > U.iceland > > ps: If this text looks funny it is caused by my computer not my twisted mind... > From owner-ageing@net.bio.net Fri Jun 25 23:00:00 1993 Path: biosci!uwm.edu!ux1.cso.uiuc.edu!howland.reston.ans.net!math.ohio-state.edu!magnus.acs.ohio-state.edu!cis.ohio-state.edu!news.sei.cmu.edu!fs7.ece.cmu.edu!crabapple.srv.cs.cmu.edu!tsf From: tsf@CS.CMU.EDU (Timothy Freeman) Newsgroups: bionet.molbio.ageing Subject: Re: 1 april? Message-ID: Date: 26 Jun 93 17:25:47 GMT References: <9306251457.AA17901@net.bio.net> Sender: news@cs.cmu.edu (Usenet News System) Distribution: bionet Organization: Carnegie Mellon University Lines: 32 In-Reply-To: wick@NETCOM.COM's message of 26 Jun 93 03:12:25 GMT Originator: tsf@U.ERGO.CS.CMU.EDU Nntp-Posting-Host: u.ergo.cs.cmu.edu In article wick@NETCOM.COM (Potter Wickware) writes: On 25 Jun 1993, Petur Henry Petersen wrote: > > There was this extraordinary report in Nature the first of > April concerning age-research. ... > > Was this true and if so does anyone have comments? Or am i > an april-fool? Me too! The citation I looked for was the review by Obispo in Adv Gerontol 6:1-39 (1990). But that journal ceased publication some years ago. Next step would be to check other gerontology journals for that volume and date, on the chance that the citation got scrambled. Or else contact the author Robin Weiss, if anyone has an e-mail for him. It was a joke. Thomas Donaldson on the cryonics mailing list was really excited about it for a little while before he figured this out. Mail to kqb@whscad1.att.com with the subject line "CRYOMSG 2128 2129" will get you copies of what he said. (I don't have his article in front of me and I don't remember the citation, so there could conceivably be two astonishing pieces of alledged ageing research that came out that day, only one of which was a joke. But I doubt it.) -- Tim Freeman When they took the fourth amendment, I was silent because I don't deal drugs. When they took the sixth amendment, I kept quiet because I know I'm innocent. When they took the second amendment, I said nothing because I don't own a gun. Now they've come for the first amendment, and I can't say anything at all. From owner-ageing@net.bio.net Sat Jun 26 23:00:00 1993 Path: biosci!NETCOM.COM!wick From: wick@NETCOM.COM (Potter Wickware) Newsgroups: bionet.molbio.ageing Subject: Re: 1 april? Message-ID: Date: 27 Jun 93 02:25:57 GMT References: <9306261731.AA00746@net.bio.net> Sender: daemon@net.bio.net Distribution: bionet Lines: 41 Well. I feel totally humiliated for falling for this. Thanks for setting me straight, Tim. On 26 Jun 1993, Timothy Freeman wrote: > In article wick@NETCOM.COM (Potter Wickware) writes: > > On 25 Jun 1993, Petur Henry Petersen wrote: > > > > > There was this extraordinary report in Nature the first of > > April concerning age-research. ... > > > > Was this true and if so does anyone have comments? Or am i > > an april-fool? > > Me too! The citation I looked for was the review by Obispo in Adv > Gerontol 6:1-39 (1990). But that journal ceased publication some years > ago. Next step would be to check other gerontology journals for that > volume and date, on the chance that the citation got scrambled. Or else > contact the author Robin Weiss, if anyone has an e-mail for him. > > It was a joke. Thomas Donaldson on the cryonics mailing list was > really excited about it for a little while before he figured this out. > Mail to kqb@whscad1.att.com with the subject line "CRYOMSG 2128 2129" > will get you copies of what he said. > > (I don't have his article in front of me and I don't remember the > citation, so there could conceivably be two astonishing pieces of > alledged ageing research that came out that day, only one of which was > a joke. But I doubt it.) > -- > Tim Freeman > When they took the fourth amendment, I was silent because I don't deal drugs. > When they took the sixth amendment, I kept quiet because I know I'm innocent. > When they took the second amendment, I said nothing because I don't own a gun. > Now they've come for the first amendment, and I can't say anything at all. > From owner-ageing@net.bio.net Sun Jun 27 23:00:00 1993 Path: biosci!agate!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr From: gdfb@TROI.CC.ROCHESTER.EDU (Brian Goldfarb) Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet Subject: Medical/HealthCare Hypermedia Exhibit (fwd) Message-ID: <9306281217.AA22821@troi.cc.rochester.edu> Date: 28 Jun 93 12:17:02 GMT Sender: Geriatric Health Care Discussion Group Reply-To: Geriatric Health Care Discussion Group Lines: 50 Xref: biosci bionet.molbio.ageing:447 To: IN%"NEWSMGR@muvms6.wvnet.edu" "Marshall University" CC: Return-path: <@UBVM.CC.BUFFALO.EDU:owner-gerinet@UBVM.CC.BUFFALO.EDU> Return-path: gdfb<@UBVM.CC.BUFFALO.EDU,@VM.CC.ROCHESTER.EDU:gdfb@TROI.CC.ROCHESTER.EDU> To: Marshall University Content-transfer-encoding: 7BIT X-Delivery-Notice: SMTP MAIL FROM does not correspond to sender. X-Mailer: ELM [version 2.3 PL11] X-To: EPID-L@QUCDN.BITNET X-cc: EMFLDS-L@UBVM.BITNET, FAM-MED@GACVAX1.BITNET, FAM-MED@GAC.EDU,FET-NET@HEARN.BITNET, FIT-L@ETSUADMN.BITNET, GENDER@RPIECS.BITNET,GERINET@UBVM.BITNET Forwarded message: From gdfb Mon Jun 28 08:10:00 1993 From: Brian Goldfarb Message-Id: <9306281209.AA22698@troi.cc.rochester.edu> Subject: Medical/HealthCare Hypermedia Exhibit To: gdfb (Brian Goldfarb) Date: Mon, 28 Jun 93 8:09:58 EDT Cc: @vm.cc.rochester.edu:COMSERV@RPIECS, @vm.cc.rochester.edu:DRUGABUS@UMAB, @vm.cc.rochester.edu:DTEP-L@UAMB, @vm.cc.rochester.edu:AIDS_INTL@RUTVM1, @vm.cc.rochester.edu:BIOMED-L@CGILL1, CCMEDH-L@tamvm1.tamu.edu, @vm.cc.rochester.edu:CLGSG-L@RICEVM1, @vm.cc.roch X-Mailer: ELM [version 2.3 PL11] Call for health-care or medical related hypermedia: The Media Center at Visual Studies Workshop in Rochester, New York is presently curating an exhibit of interactive media arts that take up issues related to health care and medicine. We are looking for hypermedia for the Macintosh computer (including Hypercard or Supercard stacks, Macromind Director movies or other interactive media). We are interested in both artistic and educational works dealing with such topics as public health, medical imaging, health care reform, AIDS, etc. We are especially interested in programs directed at non-medical professionals-(patients, affected communities, etc. ) The exhibit "Digital Check-up" will run from September 10 - December 6, 1993 in the Viewing/Listening Room of the Visual Studies Workshop Gallery. Pia Cseri-Briones Brian Goldfarb & Mona Jiminez Please send information or disks ASAP (deadline: July 14th) to US Mail: Digital Check-up c/o Brian Goldfarb 380 Wellington Avenue Rochester, New York 14619 (716) 436-8059 or Email (Internet) gdfb@troi.cc.rochester.edu (Please Email directly to the above address rather than to the discussion list address as we are not currently subscribed) From owner-ageing@net.bio.net Sun Jun 27 23:00:00 1993 Path: biosci!uwm.edu!ux1.cso.uiuc.edu!howland.reston.ans.net!noc.near.net!uunet!mcsun!uknet!comlab.ox.ac.uk!oxuniv!oxpath!rpgrant From: rpgrant@molbiol.ox.ac.uk Newsgroups: bionet.molbio.ageing Subject: Re: 1 april? Message-ID: <1993Jun28.163402.1@molbiol.ox.ac.uk> Date: 28 Jun 93 15:34:02 GMT References: <9306251457.AA17901@net.bio.net> Distribution: bionet Organization: Oxford University Molecular Biology Data Centre Lines: 19 Nntp-Posting-Host: heatly Nntp-Posting-User: rhubner > Me too! The citation I looked for was the review by Obispo in Adv > Gerontol 6:1-39 (1990). But that journal ceased publication some years [..] > > On 25 Jun 1993, Petur Henry Petersen wrote: > >> >> There was this extraordinary report in Nature the first of >> April concerning age-research. I simply cant find that number in >> our library now (sic) so i cant qouite it but... [...] Try in last week's Nature - 24th June '93. All is explained in the letters section... :) -- Richard P. Grant <>< rpgrant@molbiol.ox.ac.uk Sir William Dunn School of Pathology Fax. +44 865 275556 University of Oxford, UK. Tel. +44 865 275565 "It's easy when you know how" From owner-ageing@net.bio.net Tue Jun 29 23:00:00 1993 Path: biosci!NETCOM.COM!wick From: wick@NETCOM.COM (Potter Wickware) Newsgroups: bionet.molbio.ageing Subject: Re: 1 april? Message-ID: Date: 30 Jun 93 01:35:46 GMT References: <9306281635.AA00547@net.bio.net> Sender: daemon@net.bio.net Distribution: bionet Lines: 28 Thanks. I wonder how many people fell for this. Snd if any of them fell as hard as I did. On 28 Jun 1993 rpgrant@molbiol.ox.ac.uk wrote: > > Me too! The citation I looked for was the review by Obispo in Adv > > Gerontol 6:1-39 (1990). But that journal ceased publication some years > [..] > > > > On 25 Jun 1993, Petur Henry Petersen wrote: > > > >> > >> There was this extraordinary report in Nature the first of > >> April concerning age-research. I simply cant find that number in > >> our library now (sic) so i cant qouite it but... > [...] > Try in last week's Nature - 24th June '93. All is explained in the > letters section... :) > -- > Richard P. Grant <>< rpgrant@molbiol.ox.ac.uk > Sir William Dunn School of Pathology Fax. +44 865 275556 > University of Oxford, UK. Tel. +44 865 275565 > > "It's easy when you know how" > From owner-ageing@net.bio.net Wed Jun 30 23:00:00 1993 Path: biosci!NET.BIO.NET!kristoff From: kristoff@NET.BIO.NET (David Kristofferson) Newsgroups: bionet.molbio.ageing Subject: IMPORTANT BIOSCI INFORMATION Message-ID: <9307010900.AA29889@net.bio.net> Date: 1 Jul 93 09:00:03 GMT Sender: kristoff@net.bio.net Distribution: bionet Lines: 143 Three important items follow: BIOSCI archive searching by e-mail, the BIOSCI FAQ, and the BIOSCI User Address Directory form. If you have not yet listed yourself in our e-mail address directory, please take a few minutes to complete and return the form below. If your address information has changed since you listed yourself, please send us an updated form. Sincerely, Dave Kristofferson BIOSCI/bionet Manager kristoff@net.bio.net **** SEARCHING BIOSCI ARCHIVES WITH WAISMAIL **** E-mail users can search the BIOSCI archives by using our waismail e-mail server. 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Below is the address form that we would like each reader of the BIOSCI/bionet newsgroups to complete and return if you would like to be listed in our database. The database will serve as a directory that will enable biologists, who are currently using (or even just reading) the BIOSCI newsgroups, to look up e-mail addresses and other information about our users. The address database will be indexed for WAIS and waismail access (waismail is our WAIS e-mail server, more below) and will also be available for access via other gopher sites if they wish to permit it. The raw unindexed data will be available for FTP from net.bio.net and is atomized sufficiently to allow import into your local RDBMS should you so desire. Please carefully follow the instructions for completing the form below and return it to either of the following two addresses (whichever is more convenient for you). Thanks in advance for taking the time to complete and return the form. Addresses for returning forms Location Network ----------------------------- -------- ------- biovote@net.bio.net U.S.A. Internet/BITNET biovote@daresbury.ac.uk U.K. JANET MAKING SURE THAT YOUR INFORMATION IS CURRENT This notice will be mailed bimonthly to each newsgroup. You should check our WAIS source or waismail e-mail server from time-to-time to see if your address information is still up-to-date. Send the message help to waismail@net.bio.net for instructions on using waismail. Leave the Subject: line in your message blank. (Note as of 5 May 93 - the address database will be updated nightly and will go on-line soon after we have collected and processed the initial rush of data). IMPORTANT INSTRUCTIONS - PLEASE READ CAREFULLY Please enter all responses after the : on each line, leaving one (1) blank space after the : (i.e., before the start of your text). Please do NOT extend your responses past the end of each line (80 characters) or alter any of the field identifiers such as "first name: ". Several lines are provided at the end of the form for comments, but, please adhere to the line length restriction. On the date: line, please enter the date in the DD-MM-YY format, e.g., 05-05-93 for 5 May 1993. This line will tell others when the information was last updated. Please be sure to include the 0's for single digit days or months, e.g., 05-05-93, not 5-5-93. Note that the "e-mail network: " line below is for specifying, e.g., "Internet," "BITNET," "EARN," "JANET," or whatever other network that your computer may be on. If you are uncertain about any field, please feel free to leave it blank, but please DO NOT DELETE the field identifier from the form! In the first field below, "New information or Update ...", please enter "N" if this is the first time that you have registered in the directory or "U" if you are correcting a listing that you sent to us previously. Thanks again for your cooperation! --------------- please cut here and return portion below --------------- New information or Update to old record (enter N or U): date (DD-MM-YY): first name: middle initial: family name: job title: e-mail address: e-mail network: phone number: FAX number: institution: address1: address2: address3: city: state/province: country: postal code: research interest: research interest: comment: comment: comment: comment: comment: From owner-ageing@net.bio.net Wed Jun 30 23:00:00 1993 Path: biosci!agate!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr From: samajane@ATHENA.MIT.EDU (Samantha Scolamiero) Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet Subject: Message-ID: <9306301241.AA29016@alfredo> Date: 30 Jun 93 12:41:40 GMT Sender: Geriatric Health Care Discussion Group Reply-To: Geriatric Health Care Discussion Group Lines: 64 Xref: biosci bionet.molbio.ageing:451 To: IN%"NEWSMGR@muvms6.wvnet.edu" "Marshall University" CC: Subj: Return-path: <@UBVM.CC.BUFFALO.EDU:owner-gerinet@UBVM.CC.BUFFALO.EDU> Return-path: samajane<@UBVM.CC.BUFFALO.EDU,@MITVMA.MIT.EDU:samajane@ATHENA.MIT.EDU> To: Marshall University Content-transfer-encoding: 7BIT X-To: gerinet%ubvm.bitnet@mitvma.mit.edu ***** W E L C O M E T O B R A I N T M R ***** =============================================================================== The BRAINTMR list is a forum to discuss topics related to all types of brain tumors whether benign or malignant. It is my hope that information and experiences will be shared among brain tumor patients, their supporters, all kinds of medical professionals, and researchers who study brain tumor growth/treatment. To increase communication and networking in this medium it would be beneficial to include WHERE YOU WORK, YOUR POSITION OR SPECIALTY if you are a medical professional or researcher, TUMOR TYPE if you are a patient. (It would be a good idea to include this with each post since new people will be joining the list all the time and may not know you yet.) =============================================================================== PLEASE HELP ADVERTISE THIS LIST! Feel Free to forward this message. If you have not already you may subscribe by sending a message to: LISTSERV@MITVMA.MIT.EDU (the text of the message should read: SUBSCRIBE BRAINTMR YOURFIRSTNAME YOURLASTNAME ============================================================================== To distribute a message to the list, address it to: BRAINTMR@MITVMA.MIT.EDU ============================================================================== Right now the list will not send you a copy of anything you post, it assumes you will have already made your own copy. To AUTOMATICALLY RECEIVE COPIES of your posts you must first send the following message to: LISTSERV@MITVMA.MIT.EDU (the text of the message should read: SET BRAINTMR REPRO ============================================================================== The list is set up to send you a confirmation that your post has been successfully distributed to BRAINTMR. At the moment the confirmation reads: "Statistics for BRAINTMR mailing (Brain Tumor Research/Support): -> Only local users and domain-style recipients on the list." This is not what it's supposed to say and we're working to correct it. If you do not want a confirmation, change the settings as indicated in the message you received from the listerver stating your subscription was accepted. =============================================================================== If you would like to be included in a database of subscribers please send DIRECTLY TO ME: SAMAJANE@ATHENA.MIT (NOT TO THE LIST) whatever information you are comfortable with including: NAME, HOME/WORK ADDRESS(ES), HOME/WORK PHONE(S), POSITION, SPECIALTY OR BRAIN TUMOR INTEREST, BRAIN TUMOR TYPE (if applicable) SYMPTOMS leading to diagnosis & TREATMENT (if applicable) **If you are a patient please indicate if you would like CONTACT WITH OTHERS WHO HAVE YOUR TUMOR TYPE. **I would also be interested in HOW YOU DISCOVERED BRAINTMR. =============================================================================== If you have problems, please do not hesitate to contact me directly. Also, if you feel this letter of introduction could be improved in any way I'd be happy to hear from you. Sincerely, Samantha Scolamiero, brain tumor patient (epidermoid) and list owner samajane@athena.mit.edu 182 Redington Street home phone: 617/593-5095 Swampscott, MA 01907-2135 U.S.A.