From owner-ageing@net.bio.net Sun Mar 02 22:00:00 1997
Path: biosci!internet!biosci!not-for-mail
From: biohelp (BIOSCI Administrator)
Newsgroups: bionet.molbio.ageing
Subject: BIOSCI/bionet miniFAQ & Fundraiser
Date: 3 Mar 1997 02:00:12 -0800
Organization: BIOSCI International Newsgroups for Molecular Biology
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(LAST REVISION: 30-JUL-95)

This BIOSCI "miniFAQ" is designed to answer the questions that come up
the *most frequently*.  The main BIOSCI FAQ (Frequently Asked
Questions) is accessible on the World Wide Web at URL
http://www.bio.net/.

If you can not find an answer to your question in this or other
documentation, the BIOSCI technical support staff answers e-mail
queries sent to

		       biosci-help@net.bio.net

We can only answer questions about the use of the newsgroups and
mailing lists.  We unfortunately do not have the staff to do Internet
information searches or answer scientific questions.  Please post
those to the appropriate BIOSCI/bionet newsgroups.


	Contents:
	--------
	0) BIOSCI NEEDS YOUR SUPPORT!!

	1) Using the WWW to access the BIOSCI/bionet newsgroups.

	2) What to do about "spams," i.e., junk mail, ads, etc.

	3) Examples of subscribing and unsubscribing to the mailing lists.

	4) The BIOSCI user address and research interest directory.


0) BIOSCI NEEDS YOUR SUPPORT!!
------------------------------
BIOSCI's government funding has been expended, and we are now
operating solely from advertising revenue that we have raised from our
Web site at http://www.bio.net/.  We need just a few minutes of your
time to help us serve you.

You can do two important things which will take very little time for
you individually and will immensely help us continue to help you.

First, please use our WWW system at http://www.bio.net/ to access the
archives.  You can post or reply to messages via your Web browser as
described in item #1 below.  Your usage helps attract sponsors. If you
contact any of our sponsors, please be sure to thank them for
supporting BIOSCI. It is critical for them to get this feedback if
they are to continue their sponsorship for the long term.

Second, if you work for a company or organization that provides
products or services of interest to the biology community, please pass
this message on to your marketing or marketing communications
department or other appropriate group.  Please ask them to help
support BIOSCI by sponsoring our Web site and explain the uses and
benefits of the system to the biology community. If they are
interested, they can then contact us for further information at our
tech support address, biosci-help@net.bio.net.


1) Using the WWW to access the BIOSCI/bionet newsgroups.
--------------------------------------------------------
As of 10 December 1995, all BIOSCI/bionet full newsgroups are
accessible through the World Wide Web (WWW) at URL http://www.bio.net.
One can read and reply publicly or privately to both recent postings
and archived messages through one's Web browser if it is configured
properly to send e-mail.  Each newsgroup is equipped with its own WAIS
index.  The main BIOSCI home page also has access to the BIO-JOURNALS
Table of Contents database WAIS index and the BIOSCI user address
database described in another item further below.


2) What to do about "spams," i.e., junk mail, ads, etc.
-------------------------------------------------------
BIOSCI is a set of parallel USENET newsgroups (the "bionet" groups),
mailing lists, and a hypermail archive at URL http://www.bio.net/.
The same postings are distributed on all media (except for a small
number of mailing-list-only groups at net.bio.net).  Unfortunately it
is becoming a despicable practice on the Internet (by a few people out
to make a fast buck) to do automated mass postings to thousands of
newsgroups and mailing lists.  These attempts to grab free advertising
are refered to as "spams" in the usual, somewhat boneheaded, net
terminology.  USENET is more susceptible to this practice, and many
spams originate on the USENET groups and then are passed on to the
mailing lists.  However, spammers also get lists of mailing addresses
and hit these too, so neither medium is immune.

What should you do personally if you get junk mail?
---------------------------------------------------
Just delete it and move on without reading it further.  Filing a
protest is becoming increasingly useless because spammers are often
disguising the addresses where the messages are sent from.  Unless you
really understand Internet mail systems, your attempt at protest by
sending replies to the message will often end up being sent to the
address of an innocent person that the spammer is victimizing.

What can BIOSCI/bionet do to protect its newsgroups?
----------------------------------------------------
The only solution currently available is to moderate the newsgroup.
If this newsgroup is already moderated, then you are in good shape.
Moderation protects the USENET distribution from about 95% of the
spams that are being sent to date and protects the mailing lists
completely.  Moderation means, however, that someone has to take the
time to review each message before it goes out.  We have set up
software here that simply allows the moderator to forward to an
address at net.bio.net messages that (s)he wishes to have distributed.
This takes no more time than that needed to read the message and pass
it on, say about 1 min. per message.

Most newsgroups currently have a discussion leader who is responsible
for their newsgroup.  The discussions leaders and their e-mail
addresses are listed in the BIOSCI Information Sheet which is
available on the Web at http://www.bio.net/.  If a newsgroup is being
hit with too many junk postings, please contact the discussion leader
for that group and see if there is interest in moderating the group.
Please do not assume that by simply posting a complaint to the
newsgroup itself, anyone on the BIOSCI staff will act on your
complaint.  With close to 100 newsgroups to run, the BIOSCI staff has
to rely on the discussion leaders of each newsgroup to report problems
directly to us at biosci-help@net.bio.net.

We will moderate any of our newsgroups if the discussion leader tells
us that the readership of the group wishes to do so and if a moderator
is willing to do the work.  For most BIOSCI/bionet groups, this
entails only a few minutes of work each day.

Moderating a newsgroup will resolve probably 95% of the junk postings
on the USENET distribution.  Unfortunately there are easy ways for
determined spammers to override the moderation mechanism on USENET,
but we can protect our e-mail subscribers from unwanted postings if
the newsgroup is moderated.  You can also access our newsgroups over
the WWW at URL http://www.bio.net.  While this Web interface will not
stop spammers from trying to post to the groups, this will give you
yet another way, besides using USENET news, to keep the junk out of
your personal mail files.  For those of you with local USENET news
systems, the Web interface will also give you faster access to new
newsgroups and recent postings.


3) Examples of subscribing and unsubscribing to the mailing lists.
------------------------------------------------------------------
PLEASE NOTE: The BIOSCI management does NOT act on
subscription/unsubscription requests that are posted improperly to the
newsgroups and mailing lists.  People who do this only bother everyone
on the lists to no avail.  Please be sure to follow the proper
procedures below.

Gory details are in the BIOSCI Information sheets on the Web at
http://www.bio.net.  Below we give an example utilizing the
METHODS-AND-REAGENTS list at both of our two BIOSCI sites:

Users in the Americas and Pacific Rim countries who use the BIOSCI
------------------------------------------------------------------
node at computer net.bio.net:
----------------------------

A) Determine the "listname" which is the <=8 character mail address
                                         ^^^^^^^^^^^^^
   for the group.  These can be found in the BIOSCI Info. Sheet.  For
   the METHODS-AND-REAGENTS group the mailing address is
   methods@net.bio.net.  The listname is the portion of the address to
   the left of the @ sign, i.e., "methods".  The listname is used with
   the "subscribe" and "unsubscribe" commands illustrated below.

B) Mail all commands in the body of a mail message addressed to
   biosci-server@net.bio.net.  Do NOT send commands to the newsgroup
   posting addresses!  Leave the Subject: line blank, any text on it
   will be ignored.

C) In the body of your message put one or more of the following
   commands with an "end" command on the last line, e.g.,

   subscribe methods
   unsubscribe methods
   end

   Do NOT put your e-mail address or other text on these lines.  The
   server only allows you to cancel your subscription if the address
   on your mail header matches the address on our mailing list.
   Please ask for help at biosci-help@net.bio.net if your address has
   changed, e.g., if you know you are on the list but the server tells
   you that you are not a member.


Users in Europe, Africa, and Central Asia who use the BIOSCI node at
--------------------------------------------------------------------
computer daresbury.ac.uk (also known as dl.ac.uk):
-------------------------------------------------

To subscribe and unsubscribe to/from the BIOSCI lists, you need to
specify the full USENET newsgroup name with "bionet-news." prepended.
The USENET newsgroup names are listed in the BIOSCI Information sheet
on the Web at http://www.bio.net/.  For the METHODS-AND-REAGENTS list
the USENET newsgroup name is bionet.molbio.methds-reagnts, thus the
appropriate commands are

    sub bionet-news.bionet.molbio.methds-reagnts

    unsub bionet-news.bionet.molbio.methds-reagnts

These commands are included in a message addressed to mxt@dl.ac.uk,
NOT to the newsgroup mailing addresses.  As usual, include the text in
the body of the message as text on the Subject: line is ignored.

To unsubscribe from all the lists at the UK node, use

    unsub bionet-news

Please note that if the address in the list is different than the one
in your mail message header, you will not be able to unsubscribe by
this method. If you have problems, please mail biosci@daresbury.ac.uk.


4) The BIOSCI user address and research interest directory.
-----------------------------------------------------------
Please take this opportunity to add your name, address, and research
interest information to the BIOSCI User Address Database if you have
not already done so.

You can fill out the address form directly through our Web page at URL
http://www.bio.net/adrform.html.

The address database is reindexed nightly for WWW access (the URL is
http://www.bio.net/).  If you are not directly on the Internet but can
reach it by e-mail, please use our waismail server to access the user
directory.  waismail use is described above.  You can also request a
user address form by e-mail from biosci-help@net.bio.net.

Please check your database entry from time-to-time to see if your
address information is still up-to-date.  Because of our limited
personnel resources, we ask that you resubmit a *complete* form to
revise your entry; we only replace complete entries and do not have
resources to edit old forms.

				Sincerely,

				Dave Kristofferson
				BIOSCI/bionet Manager

				biosci-help@net.bio.net

From owner-ageing@net.bio.net Mon Mar 03 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!uwm.edu!newsfeeds.sol.net!europa.clark.net!news.msfc.nasa.gov!info.uah.edu!te6000.otc.lsu.edu!sp115.ocs.lsu.edu!grant
From: grant@bit.csc.lsu.edu (Kevin Paul Grant)
Newsgroups: bionet.molbio.ageing
Subject: Roslin sheep/genetics/aging questions
Date: 4 Mar 1997 11:10:47 GMT
Organization: Department of Computer Science, LSU, Baton Rouge
Lines: 84
Message-ID: <5fgvvn$h6m@sp115.ocs.lsu.edu>
NNTP-Posting-Host: bit.csc.lsu.edu

 
Forgive me if the material below shows a horrible ignorance of
basic biochemistry.  I have no training in the area.
 
 
The genetic material used in the sheep cloning experiments so
recently in the news was taken from cells from adult sheep. The
procedure resulted in what appears to be another, normal sheep. 
This gives rise to some interesting questions:
 
  1. If aging is due to cumulative damage in DNA wouldn't a
     cloning using DNA from the mammeries (the donor site,
     according to the CNN story) of an adult sheep *not*
     result in a normal, healthy clone sheep?
 
  2. Are there cells ("stem" cells?) in a sheep's mammeries
     that are not susceptible to such cumulative damage and
     that were, in fact, used to get the needed DNA for
     these experiments?
 
  3. Perhaps the DNA used *was* age-damaged but something about 
     the cloning process or some natural process that takes    
     place during the development of the fetus reverses the    
     damage?
 
 
Now if I may drift slightly for just a moment, my understanding
is that:
 
  1. The genes in DNA are covered by molecules that can prevent 
     some of them from doing anything.
 
  2. Every cell in the body has the same DNA but that what makes
     the cells different is that each type of cell has its own   
     specific combination of "uncovered" genes that are able to    
     operate.
 
  3. At different times the set of "uncovered" genes in a cell  
     can change.
 
  4. All of this (and a lot more) is what comes under the heading
     of "gene expression" in genetics textbooks.
 
 
Now the following question arises:
 
  Has "naked" (completely lacking in any covering molecules) 
  DNA from a person ever been checked to see if it is the DNA 
  itself that accumulates age-related damage?  Or is it possible
  that it is the stuff that covers the various genes that gets
  damaged and it is the symptoms of *this* damage that are at
  least partially responsible for aging?
 
 
Perhaps the DNA in sex cells (as they exist in normal fertilization)
is completely "uncovered" and some part of the cloning (or fetal
development) process can completely "uncover" covered DNA, removing
the damaged covering material and thus allowing "adult" DNA to be
used for cloning purposes without resulting in a damaged end-product.
 
If any of this is reasonable, then perhaps a lot of what I've seen
bandied about concerning telomere length and DNA damage is not as
critical to the aging process as it would seem and restoring proper
gene-expression would be a more profitable avenue to pursue regarding
anti-aging.  If this is reasonable, is there any material available
about this sort of thing?  Has anyone ever tried such an approach and
if so what were the results? 
 
 
None of what I'm writing is new, I'm sure.  My interest here is more
along the lines of getting the answers to some questions like:
 
  1. What are the stupid mistakes in what I've written?
 
  2. Can anyone give me further information along the lines of  
     what I've written (at least the parts that aren't stupid)?
 
  3. Does the successful use of "adult" DNA in the "Roslin" sheep
     tell us anything about cumulative damage to genetic material
     as a partial explanation of the symptoms of aging?"
 
 
Thanks,
Kevin

From owner-ageing@net.bio.net Tue Mar 04 22:00:00 1997
Path: biosci!OLINET.ISF.KIEV.UA!gerund
From: gerund@OLINET.ISF.KIEV.UA (Vadim Chromiak)
Newsgroups: bionet.molbio.ageing
Subject: Quest fo Dr.Kirkwood's email
Date: 4 Mar 1997 22:58:24 -0800
Organization: Research Center for Radiology, Kiev, Ukraine
Lines: 15
Sender: daemon@net.bio.net
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Message-ID: <331D9E4A.5C05@olinet.isf.kiev.ua>
Reply-To: gerund@olinet.isf.kiev.ua
NNTP-Posting-Host: net.bio.net

Hello to all,

Can anybody send me the e-mail address of Prof.Kirkwood.
Some people in the Institute of Gerontology of Ukraine
are very interested in receiving his address urgently in order to 
propose him a colabourative research project. 

Please, respond to "direct@geront.freenet.kiev.ua" (for Dr.Muradian)
or to "gerund@olinet.isf.kiev.ua"(for Dr.Muradian)

Many thanks in advance!

Vadim Chromyak,
Inst. Gerontology,
Kiev, Ukraine

From owner-ageing@net.bio.net Tue Mar 04 22:00:00 1997
Newsgroups: bionet.molbio.ageing
Path: biosci!rutgers.rutgers.edu!news.sgi.com!howland.erols.net!cam-news-hub1.bbnplanet.com!cpk-news-hub1.bbnplanet.com!news.bbnplanet.com!news.sprintlink.net!news-peer.sprintlink.net!news-pull.sprintlink.net!news.sprintlink.net!news-stk-3.sprintlink.net!NEWS!not-for-mail
From: "Joseph Cannon" <JCannon@icdc.com>
Subject: DHEA and athletic performance question
Message-ID: <01bc28ca$dd6f6060$6d1b29cf@JCannon>
Date: Tue, 04 Mar 1997 17:38:03 GMT
X-Newsreader: Microsoft Internet News 4.70.1155
Lines: 11

I have read that DHEA works some of its reported benefits via inhibition of
glucose -6- phosphat dehydrogenase, which is needed in a nutshell for ATP
resynthesis. if this is true, would using DHEA effect athletic
performance??? please reply via email. any respnonse is greately
appreciated
-- 
Joseph Patrick Cannon
BS chemistry and Biology
MS Exercise Physiology (May 1997)
CSCS



From owner-ageing@net.bio.net Tue Mar 04 22:00:00 1997
Path: biosci!agate!howland.erols.net!usenet.kornet.nm.kr!newsfeed.dacom.co.kr!usenet.dacom.co.kr!not-for-mail
From: Hang-Jun Chang <iam@chollian.dacom.co.kr>
Newsgroups: bionet.molbio.ageing
Subject: Re: Roslin sheep/genetics/aging questions
Date: Wed, 05 Mar 1997 23:44:33 +0900
Organization: Dansan Public Health Center
Lines: 40
Message-ID: <331D86D1.A97@chollian.dacom.co.kr>
References: <5fgvvn$h6m@sp115.ocs.lsu.edu>
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To: Kevin Paul Grant <grant@bit.csc.lsu.edu>
CC: iam@chollian.dacom.co.kr

Kevin Paul Grant wrote:
> 
> 
> 
>   Has "naked" (completely lacking in any covering molecules)
>   DNA from a person ever been checked to see if it is the DNA
>   itself that accumulates age-related damage?  Or is it possible
>   that it is the stuff that covers the various genes that gets
>   damaged and it is the symptoms of *this* damage that are at
>   least partially responsible for aging?
> 
> 
> Perhaps the DNA in sex cells (as they exist in normal fertilization)
> is completely "uncovered" and some part of the cloning (or fetal
> development) process can completely "uncover" covered DNA, removing
> the damaged covering material and thus allowing "adult" DNA to be
> used for cloning purposes without resulting in a damaged end-product.
> 

What a great idea it is! 
Kevin's idea can be summaried as follows:
The cause of aging is in the altered expression of genes like a 
developmental process, rather than in accumulated damages to genes 
themselves. Should a certain damage be involved in the aging process, it 
may be in the molecules to regulate the gene expression.
Thus, Aging may occurs as a result of altered expressions of genes 
by such accumulated damages.

I want to suggest that DNA methylation holds some answers to your
questions.
Although I don't know much about it, as far as I know, DNA methylation
patterns change as a cell differentiates, or ages.
Perhaps DNA methylation appeares to be involved in transcription 
regulation. I remember the journal Cell has several good reviews on it.
I hope that this discussion goes on.
Is there anyboy to comment it? I am really excited by this great post.


Best regards
Hang-Jun Jang

From owner-ageing@net.bio.net Tue Mar 04 22:00:00 1997
Path: biosci!CIS.OHIO-STATE.EDU!jj
From: jj@CIS.OHIO-STATE.EDU (John Josephson)
Newsgroups: bionet.molbio.ageing
Subject: re: aging questions
Date: 5 Mar 1997 12:48:03 -0800
Organization: LAIR, CIS, The Ohio State University
Lines: 32
Sender: daemon@net.bio.net
Distribution: world
Message-ID: <331D8E0F.72AE@cis.ohio-state.edu>
References: <331D86D1.A97@chollian.dacom.co.kr>
NNTP-Posting-Host: net.bio.net

> ... .
> I want to suggest that DNA methylation holds some answers to your
> questions.
> Although I don't know much about it, as far as I know, DNA methylation
> patterns change as a cell differentiates, or ages.
> Perhaps DNA methylation appeares to be involved in transcription
> regulation. I remember the journal Cell has several good reviews on it.
> I hope that this discussion goes on.
> Is there anyboy to comment it? I am really excited by this great post.
> 
> Best regards
> Hang-Jun Jang

Richard Cutler has proposed what he calls the "disdifferentiation
hypothesis," basically, that a big cause of the disfunctions of aging
may be that differentiated cells tend to loose their specificity over
time so that, for example, neurons tend to make more muscle proteins,
livers make more skin proteins, etc.  That they do so is supposedly an
experimental fact; what is in question is whether that is indeed a deep
cause of the manifestations of aging, or whether it is more an effect
than a cause.  (Sorry, I can't give references right now.)  Presumably,
too, one main way that the differentiation of cells is maintained is by
methylation of DNA.  (Though I think that methylation is supposedly used
to do some imprinting across generations, i.e., for some genes it matter
whether you got the gene from your mother or father, and that the
mechanism for this sex imprinting is methylation of DNA. So perhaps just
putting the nucleus of an adult cell into an egg is not enough to remove
all methylation.)

 .. jj



From owner-ageing@net.bio.net Wed Mar 05 22:00:00 1997
Newsgroups: bionet.molbio.ageing
Path: biosci!rutgers.rutgers.edu!news.sgi.com!howland.erols.net!cam-news-hub1.bbnplanet.com!cpk-news-hub1.bbnplanet.com!news.bbnplanet.com!cam-news-feed2.bbnplanet.com!shore!mv!mv.mv.com!katel
From: katel@mv.mv.com (Katharine Lindner)
Subject: Re: Roslin sheep/genetics/aging questions
Organization: MV Communications, Inc.
Message-ID: <E6Lw67.DyM@mv.mv.com>
References: <5fgvvn$h6m@sp115.ocs.lsu.edu> <331D86D1.A97@chollian.dacom.co.kr>
X-Nntp-Posting-Host: mv.mv.com
Date: Thu, 6 Mar 1997 05:20:30 GMT
Lines: 48

Hang-Jun Chang <iam@chollian.dacom.co.kr> writes:

>Kevin Paul Grant wrote:
>> 
>> 
>> 
>>   Has "naked" (completely lacking in any covering molecules)
>>   DNA from a person ever been checked to see if it is the DNA
>>   itself that accumulates age-related damage?  Or is it possible
>>   that it is the stuff that covers the various genes that gets
>>   damaged and it is the symptoms of *this* damage that are at
>>   least partially responsible for aging?
>> 
>> 
>> Perhaps the DNA in sex cells (as they exist in normal fertilization)
>> is completely "uncovered" and some part of the cloning (or fetal
>> development) process can completely "uncover" covered DNA, removing
>> the damaged covering material and thus allowing "adult" DNA to be
>> used for cloning purposes without resulting in a damaged end-product.
>> 

>What a great idea it is! 
>Kevin's idea can be summaried as follows:
>The cause of aging is in the altered expression of genes like a 
>developmental process, rather than in accumulated damages to genes 
>themselves. Should a certain damage be involved in the aging process, it 
>may be in the molecules to regulate the gene expression.
>Thus, Aging may occurs as a result of altered expressions of genes 
>by such accumulated damages.

>I want to suggest that DNA methylation holds some answers to your
>questions.
>Although I don't know much about it, as far as I know, DNA methylation
>patterns change as a cell differentiates, or ages.
>Perhaps DNA methylation appeares to be involved in transcription 
>regulation. I remember the journal Cell has several good reviews on it.
>I hope that this discussion goes on.
>Is there anyboy to comment it? I am really excited by this great post.


  Another possibility is that DNA in some cells is healthy and damaged
in others.  With a full organism the damage is averaged, but maybe in a
single cell its likely to be either dead or reasonably healthy.

  Yet another speculation.

                                            Kate


From owner-ageing@net.bio.net Wed Mar 05 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!uwm.edu!newsfeeds.sol.net!europa.clark.net!cpk-news-hub1.bbnplanet.com!su-news-hub1.bbnplanet.com!news.bbnplanet.com!news.pbi.net!news.PBI.net!nitrogen-c.themall.net!ptp105-218.themall.net
From: JULIO KARWOSKI <xman4321@themall.net>
Newsgroups: bionet.molbio.ageing
Subject: Re: aging questions
Date: Wed, 05 Mar 1997 23:32:38 -0800
Organization: Pacific Bell Internet Services
Lines: 71
Message-ID: <331E7316.554D@themall.net>
References: <331D86D1.A97@chollian.dacom.co.kr> <331D8E0F.72AE@cis.ohio-state.edu>
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John Josephson wrote:
> 
> > ... .
> > I want to suggest that DNA methylation holds some answers to your
> > questions.
> > Although I don't know much about it, as far as I know, DNA methylation
> > patterns change as a cell differentiates, or ages.
> > Perhaps DNA methylation appeares to be involved in transcription
> > regulation. I remember the journal Cell has several good reviews on it.
> > I hope that this discussion goes on.
> > Is there anyboy to comment it? I am really excited by this great post.
> >
> > Best regards
> > Hang-Jun Jang
> 
> Richard Cutler has proposed what he calls the "disdifferentiation
> hypothesis," basically, that a big cause of the disfunctions of aging
> may be that differentiated cells tend to loose their specificity over
> time so that, for example, neurons tend to make more muscle proteins,
> livers make more skin proteins, etc.  That they do so is supposedly an
> experimental fact; what is in question is whether that is indeed a deep
> cause of the manifestations of aging, or whether it is more an effect
> than a cause.  (Sorry, I can't give references right now.)  Presumably,
> too, one main way that the differentiation of cells is maintained is by
> methylation of DNA.  (Though I think that methylation is supposedly used
> to do some imprinting across generations, i.e., for some genes it matter
> whether you got the gene from your mother or father, and that the
> mechanism for this sex imprinting is methylation of DNA. So perhaps just
> putting the nucleus of an adult cell into an egg is not enough to remove
> all methylation.)
> 
>  .. jj

Hello Mr. J.J. and Mr Han Juang:

I was somewhat surprised and pleased that somebody brought the methylation 
hypothesis to explain the cloning process. From what I read, these British 
researchers had to fertilize about 300 cells to obtain one successful 
fertilization. It appears that the DNA of the unsuccessful attempts was 
damaged in some way. Methylation is one of the major mechanisms for gene 
silencing and I am surprised that it is given so little publicity by those
involved in aging research. The genetic "imprinting" as Mr J.J. well points
out is according to some researchers an inherited pattern of distribution 
of methyl groups along the DNA strand. In addition to maintaining the 
expression or silencing of the appropriate genes, there is a loss of methyl 
groups with each cell division, and also due to random damage in 
postmitotic cells. This loss of methyl groups {C-H3} will cause some 
unwanted genes to be expressed, and according to several authorities will 
cause the appearance of scenesence. To me this theory is quite conclusive.
There could be still a more basic mecanism for cellular aging but these 
researchers are definitely on the right track. The books I would recommend
for anyone to read on the cutting edge on aging research are:

               genes and aging, by M.S. Kanungo
               understanding ageing, by Robin Holliday

They give a comprehensive review of the different theories and focus an 
what is the most logical cause of aging at the cellular level, the inherent 
failure of maintenance mechanisms of the cell. For example, methylase does 
not repair the missing methyl groups perfectly, therefore, eventually the 
cell will have unwanted active genes. J.R.Smith from the University of 
Texas has, without mentioning methylation as a cause, discovered that 
unwanted proteins are expressed in aging cells. He has identified these 
proteins and his results have been confirmed by a different route by 
other researchers. They only focussed their research on those proteins
which interfered with cell division. Their studies were done by cell fusion
techniques. If anybody is interested in more information or the articles 
I have, please post. J.R. Smith also has a home page with useful information.

cordially,
               Julio Karwoski

From owner-ageing@net.bio.net Wed Mar 05 22:00:00 1997
Path: biosci!daresbury!lyra.csx.cam.ac.uk!hgmp.mrc.ac.uk!gmorley
From: gmorley@hgmp.mrc.ac.uk (Mr. G. Morley)
Newsgroups: bionet.molbio.ageing
Subject: Re: Sheep genetics ageing
Date: 6 Mar 1997 14:04:36 GMT
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Another possibility is that the aging process is linked
to the number of normal mitochondria the individual possess
per cell..... the nucleus of the adult cell was transplanted
into the denucleated egg of another sheep - the mitochondria
of which should all be fully functioning.
Also telomerases might be active in the early embryo which
are switched of in the adult (?) lengthening the telomeres
and thus extending the division rate of the cell (?)
But these (previous to this reply)are interesting speculations 
and they go to show that
the cloning has already stimulated scientific discussion as well
as, alas,  the more excitable members of the general
population.



From owner-ageing@net.bio.net Thu Mar 06 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!uwm.edu!newsfeeds.sol.net!news.maxwell.syr.edu!worldnet.att.net!howland.erols.net!torn!n1tor.istar!tor.istar!east.istar!news
From: Webmaster <oxylite@gtn.net>
Newsgroups: bionet.molbio.ageing
Subject: Tempur-Pedic
Date: 7 Mar 1997 15:30:22 GMT
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for the space program.  Because of its pressure relieving properties the
Tempur-Pedic mattress effectively relieves bodily pains caused or made
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Test made at the Institution for Clinical and Physiological Research,
Lillhagen Hospital, Gothenburg, Sweden, have demonstrated that subject
turned an average of 17 times per night compared to 80-100 times on a
conventional mattress.

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E-mail= oxylite@gtn.net

From owner-ageing@net.bio.net Sun Mar 09 22:00:00 1997
Path: biosci!daresbury!not-for-mail
From: mjfasmb <mjfasmb@fs1.ce.umist.ac.uk>
Newsgroups: bionet.molbio.ageing
Subject: (Fwd) Re: Sheep genetics ageing
Date: 10 Mar 1997 11:41:52 -0000
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In reply to Mr. G. Morley, I'd be surprised if the mitochondria play 
an important role in the ageing process.  My work with yeast (i'm 
afraid i work at the unglamorous end of the ageing field) implies 
that mitochondrial damage has very little effect on cellular 
senescence. 

Cheers
Gordon Barker



Another possibility is that the aging process is linked
to the number of normal mitochondria the individual possess
per cell..... the nucleus of the adult cell was transplanted
into the denucleated egg of another sheep - the mitochondria
of which should all be fully functioning.





From owner-ageing@net.bio.net Sun Mar 09 22:00:00 1997
Path: biosci!ALUMNI.UBC.CA!BRowley
From: BRowley@ALUMNI.UBC.CA (Longevity-Digest/Brian Rowley)
Newsgroups: bionet.molbio.ageing
Subject: English gerontologists
Date: 10 Mar 1997 15:05:11 -0800
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Those of you who are English gerontologists or graduate students studying
the biology of aging, please reply to this post. I will be in England
between April 28 and May 20, and would like to meet English gerontologists
and their graduate students to chat with them informally about their (past
or present) work. My purpose is purely educational; I'm not a job-seeker or
spy trying to swipe unpublished ideas. I am visiting my English grandparents
and wish to use the opportunity to hear about the work of as many English
gerontologists as are willing to talk to me.

        I am Brian Rowley (BS, MS). I am currently applying to Ph. D
programs at UCLA and UC Riverside to study the biology of aging (I'm being
purposely vague, here). I wasn't planning on doing my Ph. D in England, but
am interested in gaining contacts for possible future collaboration, and
most importantly, in getting up to date on a broad range of work :->

                                Regards,

                                Brian Rowley


From owner-ageing@net.bio.net Tue Mar 11 22:00:00 1997
Path: biosci!GNN.COM!DSchwa1234
From: DSchwa1234@GNN.COM (Douglas Schwartz)
Newsgroups: bionet.molbio.ageing
Subject: Re: (Fwd) Re: Sheep genetics ageing
Date: 11 Mar 1997 21:45:31 -0800
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>From:	mjfasmb <mjfasmb@fs1.ce.umist.ac.uk>
>
>In reply to Mr. G. Morley, I'd be surprised if the mitochondri
>a play 
>an important role in the ageing process.  My work with yeast (
>i'm 
>afraid i work at the unglamorous end of the ageing field) impl
>ies 
>that mitochondrial damage has very little effect on cellular 
>senescence. 
>
>Cheers
>Gordon Barker

Gordon,

Could you go into what sorts of things you find with senescent 
yeast?  And what (if any) methods of slowing their rate of aging are 
known.

Thanks,

--Doug Schwartz
dschwa1234@gnn.com


From owner-ageing@net.bio.net Tue Mar 11 22:00:00 1997
Path: biosci!daresbury!not-for-mail
From: mjfasmb <mjfasmb@fs1.ce.umist.ac.uk>
Newsgroups: bionet.molbio.ageing
Subject: Sheep don't make beer
Date: 12 Mar 1997 15:35:34 -0000
Organization: Dept. Chem Eng - UMIST (FS1)
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> Could you go into what sorts of things you find with senescent 
> yeast?  And what (if any) methods of slowing their rate of aging are 
> known.
> Thanks,
> 
> --Doug Schwartz
> dschwa1234@gnn.com

Hi Doug,
Blimey !  I'm not too sure where to begin...
I guess the most interesting result is that whilst you can shorten yeast 
lifespan by increasing oxidative damage (by deleting SOD1 for 
example),  senescing yeast only one division from arrest - which 
according to damage hypotheses are so knackered they are about to die 
from their mutational load - are still able to generate viable 
progeny.  These daughters, despite inheriting an almost lethally 
mutated set of cellular apparatus, can divide several times and in 
turn give rise to perfectly healthy daughter cells !

Sounds to me like cells just lose the ability to overide their 
cell-cycle checkpoints.  Perhaps each time a cell stalls in the cell 
cycle ('cos there aren't quite enough nutrients or maybe DNA damage 
has been detected), it doesn't quite reset the biological activity of 
its checkpoint-arrest signal.  These signals would accumulate as the 
cell got older, until such a time as they prevented further division 
- even if the cell was otherwise fairly healthy....
what do you think ?

As for methods of slowing ageing down in yeast - one of the easiest 
is to grow them on different carbon sources.  Strains I've handled 
seem to increase their replicative lifespans on ethanol (as opposed 
to glucose) and especially galactose.  I've tested other carbon 
sources too, and there doesn't appear to be any predictable pattern 
with, say, fermentable versus non-fermentable  sources .

Altering the expression levels of genes like LAG1 + 2, RAS2 (Jazwinski's group) 
and PHB1 seem able to extend yeast lifespan.  Guarente's lab isolated 
a whole bunch of lifespan-extending genes which they called 
UTH1, 2, etc  (for youth).  I think their screen was based upon 
starvation tolerance.  They found some pretty interesting genes with 
the screen - like SIR4 and HTR1 !

Cheers
Gordon

From owner-ageing@net.bio.net Fri Mar 14 22:00:00 1997
Path: biosci!IUNHAW1.IUN.INDIANA.EDU!TSTABLER
From: TSTABLER@IUNHAW1.IUN.INDIANA.EDU ("Tim Stabler")
Newsgroups: bionet.molbio.ageing
Subject: Re: Meeting
Date: 15 Mar 1997 09:38:20 -0800
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The Society for In Vitro Biology (formerly the Tissue Culture 
Association)will be holding its 1997 Congress on In Vitro Biology in 
Washington, DC at the REnaissance Hotel, June 14-18, 1997.  Main 
areas of interest incklude vertebrate, invertebrate, toxicology and 
plant.

As a member of the Planning Committee, I can say the abstracts we 
reviewed for the meeting look to be excellent.  The hotel is elegant 
and isa located about two blocks from museums and about a 15 walk 
from the White House.

The program for the meeting is available at:

                 http://www.sivb.org
                 
You can Email the Society at:  sivb@sivb.org

Although the abstract deadline is past, abstracts are still being 
accepted as "Hot Topics" to be published in a separate journal 
available at the meeting.  I believe the deadline for these is April 
15.

If you have any questions, feel free to contact the Society or myself.



Timothy A. Stabler, Ph.D.
Department of Biology
Indiana University Northwest
Gary, IN 46408

(219)980-6718
FAX: (219)980-7125

From owner-ageing@net.bio.net Sat Mar 15 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!gatech!csulb.edu!hammer.uoregon.edu!news-peer.gsl.net!news.gsl.net!cpk-news-hub1.bbnplanet.com!cam-news-hub1.bbnplanet.com!news.bbnplanet.com!howland.erols.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!news.campus.mci.net!n-f-m
From: "Jan Coetzee" <coetzee_jv@news.campus.mci.net>
Newsgroups: bionet.molbio.ageing
Subject: Is Hayflick's theory universal?
Date: 15 Mar 1997 21:05:05 GMT
Organization: CampusMCI
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I am trying to find publications on Hayflick studies that has been done on
different animals such as dogs, horses and turtles in order to see if his
hypothesis is true for species other than man. If these studies has been
done and there is a linear relationship between the age limit of different
animals and limited cell division then his theory is universal. If not then
his ideas are given to much emphasis in aging research

Jan (John) Coetzee

From owner-ageing@net.bio.net Mon Mar 17 22:00:00 1997
Path: biosci!worldnet.att.net!grendle
From: grendle@worldnet.att.net (jim and barbara burkhart)
Newsgroups: bionet.molbio.ageing
Subject: implications of dolly
Date: 17 Mar 1997 19:09:46 -0800
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The cloning of the sheep has certainly opened a number of questions 
about the regulation of lifespan and the critical aging signal. The 
possibilty importance of methylation was mentioned. Alternate 
methylation patterns in maternal and paternal gametes have been 
suggested as critical for development but the cloning of the sheep 
clearly doesn't require gamete methylation programing. The suggestion of 
methylation as important to ageing is likewise defeated by the sheep. In 
both cases the presumed crucial methylation is a property of the "old" 
nucleus but development apparently proceeds normally. I believe that 
implicates the programming of the egg as critical.  
Does the ageing signal reside in the nucleus? If the ageing "clock" is 
nuclear, DNA damage or telomere lenth have been proposed, then Dolly is 
a problem. Perhaps the successful fusion contains not the odd undamaged 
nucleus but a nucleus that has lost genes critical to sensing ageing. It 
will be interesting to see if clones have an elevated cancer incidence.

From owner-ageing@net.bio.net Mon Mar 17 22:00:00 1997
Path: biosci!daresbury!not-for-mail
From: rattan@kemi.aau.dk (Suresh Rattan)
Newsgroups: bionet.molbio.ageing
Subject: Scientific hierarchy/humor
Date: 18 Mar 1997 09:23:56 -0000
Lines: 28
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Message-ID: <5glmvc$343@mserv1.dl.ac.uk>
Original-To: ageing@dl.ac.uk

All those scientists who study living systems are supposed to be
"biologists". Yet, there is an intrinsic intellectual hierarchy which is
mainly due to the changing fashions. It appears that for the last several
years:

        Clinicians think that they are physiologists;
        Physiologists think that they are anatomists;
        Anatomists think that they are cell biologists;
        Cell biologists think that they are biochemists;
        Biochemists think that they are molecular biologists;
        Molecular biologists think that they are God;
        and what about God?
        Well, God does not think !!!

        (Got it????)...

Suresh Rattan

Dr. Suresh I.S. Rattan, PhD; DSc
Laboratory of Cellular Ageing
Department of Chemistry
Aarhus University
DK-8000 Aarhus - C
Denmark

(Phone: +45 8942 3956; Fax: +45 8619 6199)



From owner-ageing@net.bio.net Mon Mar 17 22:00:00 1997
Path: biosci!daresbury!not-for-mail
From: mjfasmb <mjfasmb@fs1.ce.umist.ac.uk>
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: 18 Mar 1997 17:13:34 -0000
Organization: Dept. Chem Eng - UMIST (FS1)
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> Date:          Tue, 18 Mar 1997 13:24:41 GMT
Re: implications of dolly

Surely patterns of transcription can be stably maintained without 
having to invoke some change in the methylation state of the DNA ?
Such patterns might, given the right environmental cues, alter to 
assume a new expression-pattern (attractor ?), during progression 
from embryo to adult,  but needn't be the product of physically altering
the DNA.  Resetting to some basal / default expression pattern either 
through mating or electric shock (I seem to remember that's what the 
Rosalin people did) would then suffice to produce a viable clone...

MGB
x 

> I disagree with your dismissal of methylation's role in
> aging: DNA methylation patterns are reset during early
> embryogenesis. In fact, the Dolly experiment supports a
> methylation theory of aging (changes irreversible in adult
> cells but reversible in embryonal cells) over a mutational
> theory of aging (changes irreversible no matter what).
> Incidentally, there is some data suggesting that this may be
> true for some cancers as well.
> Jean-Pierre Issa
> 
> grendle@worldnet.att.net (jim and barbara burkhart) wrote:

From owner-ageing@net.bio.net Mon Mar 17 22:00:00 1997
Path: biosci!daresbury!lyra.csx.cam.ac.uk!hgmp.mrc.ac.uk!gmorley
From: gmorley@hgmp.mrc.ac.uk (Mr. G. Morley)
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: 18 Mar 1997 16:18:31 GMT
Organization: MRC Human Genome Resource Centre
Lines: 54
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NNTP-Posting-Host: tin.hgmp.mrc.ac.uk

grendle@worldnet.att.net (jim and barbara burkhart) wrote:

>>The cloning of the sheep has certainly opened a number of questions 
>>about the regulation of lifespan and the critical aging signal. The 
>>possibilty importance of methylation was mentioned. Alternate 
>>methylation patterns in maternal and paternal gametes have been 
>>suggested as critical for development but the cloning of the sheep 
>>clearly doesn't require gamete methylation programing. The suggestion of 
>>methylation as important to ageing is likewise defeated by the sheep. In 
>>both cases the presumed crucial methylation is a property of the "old" 
>>nucleus but development apparently proceeds normally. I believe that 
>>implicates the programming of the egg as critical.  
>>Does the ageing signal reside in the nucleus? If the ageing "clock" is 
>>nuclear, DNA damage or telomere lenth have been proposed, then Dolly is 
>>a problem. Perhaps the successful fusion contains not the odd undamaged 
>>nucleus but a nucleus that has lost genes critical to sensing ageing. It 
>>will be interesting to see if clones have an elevated cancer incidence.

Jean-Pierre Issa wrote:
>I disagree with your dismissal of methylation's role in
>aging: DNA methylation patterns are reset during early
>embryogenesis. In fact, the Dolly experiment supports a
>methylation theory of aging (changes irreversible in adult
>cells but reversible in embryonal cells) over a mutational
>theory of aging (changes irreversible no matter what).
>Incidentally, there is some data suggesting that this may be
>true for some cancers as well.
>Jean-Pierre Issa

I may be wrong but what I think jim and barbara burkhart were
reffering to was the aspect that imprinting can play in 
development... I don't think all DNA Methylation patterns are
removed following miosis - the damaged gene which causes
Angelman syndrome in females ,(I think!) is the same as that
which causes Prauder-Willie (spelling?) syndrome...
I may well be wrong (as my memory is not the best) but the differences
in phenotype are determined by whether the gene is inhereted from
the father or the mother..(via I think differences in parent methylation 
patterns.
I could well be wrong but I think there are other cases (such as an
offspring inheriting for eg. two chromosome 11's from the father and
none from the mother) where the offsprings phenotype is affected(?)
 The second possibility is that I am talking complete b****ks..
I would be interested if anyone out there could make some sense
of this post and the relevance of methylation/demethylation in
embryogenisis vs aging?
Cheers!
Gary Morley
gmorley@rpms.ac.uk






From owner-ageing@net.bio.net Mon Mar 17 22:00:00 1997
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From: "mjfasmb,mjfasmb@fs1.ce.umist.ac.uk"@invivo.edu
Reply-To: "mjfasmb,mjfasmb@fs1.ce.umist.ac.uk"@invivo.edu
Newsgroups: bionet.molbio.ageing
Distribution: world
Subject: implications of dolly
Date: Tue, 18 Mar 1997 17:13:34 GMT
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> Date:          Tue, 18 Mar 1997 13:24:41 GMT
Re: implications of dolly

Surely patterns of transcription can be stably maintained without 
having to invoke some change in the methylation state of the DNA ?
Such patterns might, given the right environmental cues, alter to 
assume a new expression-pattern (attractor ?), during progression 
from embryo to adult,  but needn't be the product of physically altering
the DNA.  Resetting to some basal / default expression pattern either 
through mating or electric shock (I seem to remember that's what the 
Rosalin people did) would then suffice to produce a viable clone...

MGB
x 

> I disagree with your dismissal of methylation's role in
> aging: DNA methylation patterns are reset during early
> embryogenesis. In fact, the Dolly experiment supports a
> methylation theory of aging (changes irreversible in adult
> cells but reversible in embryonal cells) over a mutational
> theory of aging (changes irreversible no matter what).
> Incidentally, there is some data suggesting that this may be
> true for some cancers as well.
> Jean-Pierre Issa
> 
> grendle@worldnet.att.net (jim and barbara burkhart) wrote:

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From: mjfasmb <mjfasmb@fs1.ce.umist.ac.uk>
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: 18 Mar 1997 17:13:34 -0000
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-- end **** Sent by inVivo. The BBS of Life Sciences, Paris, France, 
******** mailto://info@invivo.edu ****** http://www.invivo.net *****


From owner-ageing@net.bio.net Mon Mar 17 22:00:00 1997
Path: biosci!ALUMNI.UBC.CA!BRowley
From: BRowley@ALUMNI.UBC.CA (Longevity-Digest/Brian Rowley)
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: 18 Mar 1997 12:13:54 -0800
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mjfasmb <mjfasmb@fs1.ce.umist.ac.uk> wrote:

>Surely patterns of transcription can be stably maintained without 
>having to invoke some change in the methylation state of the DNA ?
>Such patterns might, given the right environmental cues, alter to 
>assume a new expression-pattern (attractor ?), during progression 
>from embryo to adult,  but needn't be the product of physically altering
>the DNA.  Resetting to some basal / default expression pattern either 
>through mating or electric shock (I seem to remember that's what the 
>Rosalin people did) would then suffice to produce a viable clone...
>
>MGB
>x 

        Your arguments make a lot of sense. I'd like to know, though, were
Dolly's telomeres (or Hayflick divisions) restored to those of a newborn
lamb? It would be easy to find that out; just compare number of remaining
divisions (and length of telomeres) of sheep progenitor with that of lamb
clone. If the telomeres and remaining divisions were restored by cloning
that would imply that rejuvenation of adult cells is possible.
Brian Rowley


From owner-ageing@net.bio.net Mon Mar 17 22:00:00 1997
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From: jpissa@welchlink.welch.jhu.edu
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: Tue, 18 Mar 1997 13:24:41 GMT
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I disagree with your dismissal of methylation's role in
aging: DNA methylation patterns are reset during early
embryogenesis. In fact, the Dolly experiment supports a
methylation theory of aging (changes irreversible in adult
cells but reversible in embryonal cells) over a mutational
theory of aging (changes irreversible no matter what).
Incidentally, there is some data suggesting that this may be
true for some cancers as well.
Jean-Pierre Issa

grendle@worldnet.att.net (jim and barbara burkhart) wrote:

>The cloning of the sheep has certainly opened a number of questions 
>about the regulation of lifespan and the critical aging signal. The 
>possibilty importance of methylation was mentioned. Alternate 
>methylation patterns in maternal and paternal gametes have been 
>suggested as critical for development but the cloning of the sheep 
>clearly doesn't require gamete methylation programing. The suggestion of 
>methylation as important to ageing is likewise defeated by the sheep. In 
>both cases the presumed crucial methylation is a property of the "old" 
>nucleus but development apparently proceeds normally. I believe that 
>implicates the programming of the egg as critical.  
>Does the ageing signal reside in the nucleus? If the ageing "clock" is 
>nuclear, DNA damage or telomere lenth have been proposed, then Dolly is 
>a problem. Perhaps the successful fusion contains not the odd undamaged 
>nucleus but a nucleus that has lost genes critical to sensing ageing. It 
>will be interesting to see if clones have an elevated cancer incidence.


From owner-ageing@net.bio.net Tue Mar 18 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!news.sgi.com!news.maxwell.syr.edu!cpk-news-hub1.bbnplanet.com!news.bbnplanet.com!newsfeed.internetmci.com!news.campus.mci.net!n-f-m
From: "Jan Coetzee" <coetzee_jv@news.campus.mci.net>
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: 18 Mar 1997 17:47:30 GMT
Organization: CampusMCI
Lines: 8
Message-ID: <01bc33c4$7421a5a0$2e1166ce@coetzee_jv>
References: <332DC71E.59AF@worldnet.att.net>
NNTP-Posting-Host: s17-pm07.atlanta.campus.mci.net
X-Newsreader: Microsoft Internet News 4.70.1157


I think dolly is going to change the direction of aging research for the
better.
It is time to through out old theories and bring in new ones!

Jan (John) Ph.D..

coetzee_jv@peachnet.campus.mci.net

From owner-ageing@net.bio.net Tue Mar 18 22:00:00 1997
Path: biosci!OLINET.ISF.KIEV.UA!gerund
From: gerund@OLINET.ISF.KIEV.UA (Vadim Chromiak)
Newsgroups: bionet.molbio.ageing
Subject: IP address of "www.aeiveos.com"
Date: 18 Mar 1997 22:01:12 -0800
Organization: Research Center for Radiology, Kiev, Ukraine
Lines: 11
Sender: daemon@net.bio.net
Distribution: world
Message-ID: <333009AD.55D9@olinet.isf.kiev.ua>
Reply-To: gerund@olinet.isf.kiev.ua
NNTP-Posting-Host: net.bio.net

Dear Group,

Who can give me an IP address of "Aeiveos".
My Name server can't translate "www.aeiveos.com". 
The same is true for "Life Extension Foundation". 
A typical response is " <www.lef.org> doesn't have a DNS Entry".

Thanks in advance,

Vadim.


From owner-ageing@net.bio.net Tue Mar 18 22:00:00 1997
Path: biosci!newshost.lanl.gov!usenet
From: Brian Foley <btf@t10.lanl.gov>
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: Wed, 19 Mar 1997 11:56:26 -0700
Organization: HIV Database
Lines: 31
Message-ID: <333036DA.56A1@t10.lanl.gov>
References: <332DC71E.59AF@worldnet.att.net>
NNTP-Posting-Host: idiotype.lanl.gov
Mime-Version: 1.0
Content-Type: text/plain; charset=us-ascii
Content-Transfer-Encoding: 7bit
X-Mailer: Mozilla 3.01 (X11; U; SunOS 5.5.1 sun4m)

The Dolly Lamb ah...

 Mary had a little lamb,
 its fleece was slightly grey,
 It didn't have a father,
 just some borrowed DNA.

 It sort of had a mother, 
 though the ovum was on loan, 
 It was not so much a lambkin, 
 as a little lamby clone.

 And soon it had a fellow clone, 
 and soon it had some more,
 They followed her to school one day, 
 all cramming through the door.

 It made the children laugh and sing, 
 the teachers found it droll,
 There were too many lamby clones, 
 for Mary to control.

 No other could control the sheep, 
 since their programs didn't vary, 
 So the scientists resolved it all, 
 by simply cloning Mary.

 But now they feel quite sheepish, 
 those scientists unwary, 
 One problem solved, but what to do, 
 with Mary, Mary, Mary...

From owner-ageing@net.bio.net Tue Mar 18 22:00:00 1997
Path: biosci!bcm.tmc.edu!cs.utexas.edu!howland.erols.net!worldnet.att.net!news.maxwell.syr.edu!mindspring!news.mindspring.com!usenet
From: lockshin@mindspring.com (Richard A. Lockshin)
Newsgroups: bionet.molbio.ageing
Subject: NYC Cell Death meeting April 2 corrections
Date: Wed, 19 Mar 1997 20:05:08 GMT
Organization: MindSpring Enterprises, Inc.
Lines: 23
Message-ID: <5gph8r$n6u@camel0.mindspring.com>
Reply-To: lockshin@mindspring.com
NNTP-Posting-Host: ip72.an11-new-york4.ny.pub-ip.psi.net
X-Server-Date: 19 Mar 1997 20:11:07 GMT
X-Newsreader: Forte Free Agent 1.0.82

The Cell Death Society will meet on Wednesday, April 1, 1997 at
Rockefeller University, 1230 York Avenue, Weiss Research 
Building (Room 301). This month's speakers will be: 1) Karen Newell,
University of Vermont Coll. of Med., "Evidence for the 
involvement of Fas and Fas-L in multidrug resistance"; 2) Stuart
Horowitz, Winthrop-University Hospital SUNY Stony Brook, 
"Oxidative cell death and lung injury." To help us plan for pizza and
number of attendees, we ask that you call Dr. Zakeri's lab 
(718) 997-3429 and let them know the number of people coming for
pizza, talk, and if you need parking. RSVP by Tuesday, April 
1, 1997. 

NOTE: WE NEED FOR SUBSCRIBERS YOUR COMPLETE MAILING ADDRESS, PHONE AND
FAX NUMBERS, AND EMAIL 
ADDRESS. 
If you want to be on our list, register at our site
(http://celldeath-apoptosis.org)

Richard A. Lockshin
(lockshin@mindspring.com;lockshin@sjumusic.stjohns.edu)
check out Cell Death Soc web page: 
http://rdz.stjohns.edu/~lockshin/index.html


From owner-ageing@net.bio.net Tue Mar 18 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!gatech!arclight.uoregon.edu!news.sprintlink.net!news-peer.sprintlink.net!news.maxwell.syr.edu!mindspring!news.mindspring.com!usenet
From: lockshin@mindspring.com (Richard A. Lockshin)
Newsgroups: bionet.molbio.ageing
Subject: NYC CELL DEATH: WED APRIL 2
Date: Wed, 19 Mar 1997 20:12:36 GMT
Organization: MindSpring Enterprises, Inc.
Lines: 23
Message-ID: <5gphmr$n6u@camel0.mindspring.com>
Reply-To: lockshin@mindspring.com
NNTP-Posting-Host: ip72.an11-new-york4.ny.pub-ip.psi.net
X-Server-Date: 19 Mar 1997 20:18:35 GMT
X-Newsreader: Forte Free Agent 1.0.82

The Cell Death Society will meet on Wednesday, April 2, 1997 at
Rockefeller University, 1230 York Avenue, Weiss Research 
Building (Room 301). This month's speakers will be: 1) Karen Newell,
University of Vermont Coll. of Med., "Evidence for the 
involvement of Fas and Fas-L in multidrug resistance"; 2) Stuart
Horowitz, Winthrop-University Hospital SUNY Stony Brook, 
"Oxidative cell death and lung injury." To help us plan for pizza and
number of attendees, we ask that you call Dr. Zakeri's lab 
(718) 997-3429 and let them know the number of people coming for
pizza, talk, and if you need parking. RSVP by Tuesday, April 
1, 1997. 

NOTE: WE NEED FOR SUBSCRIBERS YOUR COMPLETE MAILING ADDRESS, PHONE AND
FAX NUMBERS, AND EMAIL 
ADDRESS. 
IF YOU WANT TO BE ON THE MAILING LIST, SUBSCRIBE AT 
HTTP:\\WWW.CELLDEATH-APOPTOSIS.ORG

Richard A. Lockshin
(lockshin@mindspring.com;lockshin@sjumusic.stjohns.edu)
check out Cell Death Soc web page: 
http://rdz.stjohns.edu/~lockshin/index.html


From owner-ageing@net.bio.net Tue Mar 18 22:00:00 1997
Path: biosci!ABULAFIA.ST.HMC.EDU!kkalafus
From: kkalafus@ABULAFIA.ST.HMC.EDU (Ken)
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: 19 Mar 1997 15:33:53 -0800
Organization: BIOSCI International Newsgroups for Molecular Biology
Lines: 41
Sender: daemon@net.bio.net
Distribution: world
Message-ID: <199703192339.PAA03214@abulafia.st.hmc.edu>
NNTP-Posting-Host: net.bio.net

Certainly the cloning of Dolly has some interesting implications for aging
theory, but keep in mind:

1.  The cell population used as the source of DNA in the cloning experiment
was mixed (not all the same cell type).  According to the science paper in
which cloning was reported, the experimenters could not rule out the
possibility that Dolly arose from a stem cell -- if this is the case, the
cloning experiment does not tell us much about the reversibility of cellular
changes associated with aging because a stem cell would presumably be
protected from having undergone these changes in the first place.

2.  Dolly's progenitor was only 6 years old when the cells were harvested.
A sheep can live to about 30 years.  Even if the source of DNA was a normal,
terminally differentiated somatic cell, further information is needed before
we can conclude that a molecular clock was reset at the time of Dolly's
conception.  It would be much more convincing if Dolly lived the maximum
sheep lifespan, or even better, if Dolly were herself cloned at some
advanced age.

Of course, the strength of evidence for reseting Dolly's molecular clock
largely depends on what sort of molecular clock you're talking about.  The
ability of a terminally differentiated cell to replicate itself the
incredible number of times required to create an entire organism would argue
very convincingly that a clock which counts divisions has been reset.

Another thing to keep in mind is that the fusion of a normal cell with a
denucleated egg results in an embryo which has the mitochondrea from a
normal egg.  This makes it impossible to rule out that aging has something
to do with damage to mitochondrea.  Can anyone think of a way to permanently
inactivate the mitochondrea in the denucleated egg, without causing other
significant damage?  Perhaps cyanide?


This definitely has the potential to tell us some interesting things about
the aging process.  It would be unfortunate if the current negative public
opinions of cloning leads to a blanket ban on cloning research.

---
Ken Kalafus



From owner-ageing@net.bio.net Wed Mar 19 22:00:00 1997
Path: biosci!EARTHLINK.NET!AlexYCChiu
From: AlexYCChiu@EARTHLINK.NET ("Alex Chiu")
Newsgroups: bionet.molbio.ageing
Subject: (none)
Date: 20 Mar 1997 02:30:12 -0800
Organization: BIOSCI International Newsgroups for Molecular Biology
Lines: 34
Sender: daemon@net.bio.net
Distribution: world
Message-ID: <199703201029.CAA15577@lithuania.it.earthlink.net>
NNTP-Posting-Host: net.bio.net

Please visit http://home.earthlink.net/~alexycchiu/
I have invented The Eternal Life Device which allows
you to keep your body physically young forever as long 
as you use the device every night during sleep.NEW INVENTION ALLOWS HUMANS
TO LIVE FOREVER

     http://home.earthlink.net/~alexycchiu

ACCORDING TO ALEX CHIU, PEOPLE CAN STAY YOUNG AND LIVE FOREVER BY USING HIS
NEW INVENTION 'THE ETERNAL LIFE RINGS' OR 'THE ETERNAL LIFE FOOT BRACES'. 
The Eternal Life Rings are rings to be worn on both small fingers of a user
during sleep.  The Eternal Life Foot Braces are to be worn on all fingers
of both feet of a user during sleep.  Both devices consist simply magnets
and braces which hold magnets onto the fingers of the user.

Mr. Alex Chiu claims that the magnetic devices, the finger rings or the
foot braces, both are believed to allow the user to stay young physically
forever or to become younger!  The inventor explained that the magnetic
pole on the right small finger or on the right foot is opposite to the
poles of the magnets on the left small finger or of the left foot. With a
different pole on each side of the human body, blood circulation and
electric current of the body are propelled.  The speeded up blood
circulation and electric current generate faster metabolism in order to
fight aging process.  The mentioned devices invented by Alex Chiu are
believed to be able to alter aging or to keep the users young physically as
long as the users wear them every night during sleep.  The devices also
cure many handicapnesses and deseases.  

Mr.Alex Chiu is an inventor who is mainly specialized in effects on human
health by magnetic forces.  For interested party, please email  
alexycchiu@earthlink.net   Check out my web site 
http://home.earthlink.net/~alexycchiu
  tel 415 585 3825


From owner-ageing@net.bio.net Wed Mar 19 22:00:00 1997
Path: biosci!EARTHLINK.NET!AlexYCChiu
From: AlexYCChiu@EARTHLINK.NET ("Alex Chiu")
Newsgroups: bionet.molbio.ageing
Subject: (none)
Date: 20 Mar 1997 01:39:32 -0800
Organization: BIOSCI International Newsgroups for Molecular Biology
Lines: 34
Sender: daemon@net.bio.net
Distribution: world
Message-ID: <199703200940.BAA25553@spain.it.earthlink.net>
NNTP-Posting-Host: net.bio.net

Please visit http://home.earthlink.net/~alexycchiu/
I have invented The Eternal Life Device which allows
you to keep your body physically young forever as long 
as you use the device every night during sleep.
NEW INVENTION ALLOWS HUMANS TO LIVE FOREVER

     www.swiftsite.com/eternal

ACCORDING TO ALEX CHIU, PEOPLE CAN STAY YOUNG AND LIVE FOREVER BY USING HIS
NEW INVENTION 'THE ETERNAL LIFE RINGS' OR 'THE ETERNAL LIFE FOOT BRACES'. 
The Eternal Life Rings are rings to be worn on both small fingers of a user
during sleep.  The Eternal Life Foot Braces are to be worn on all fingers
of both feet of a user during sleep.  Both devices consist simply magnets
and braces which hold magnets onto the fingers of the user.

Mr. Alex Chiu claims that the magnetic devices, the finger rings or the
foot braces, both are believed to allow the user to stay young physically
forever or to become younger!  The inventor explained that the magnetic
pole on the right small finger or on the right foot is opposite to the
poles of the magnets on the left small finger or of the left foot. With a
different pole on each side of the human body, blood circulation and
electric current of the body are propelled.  The speeded up blood
circulation and electric current generate faster metabolism in order to
fight aging process.  The mentioned devices invented by Alex Chiu are
believed to be able to alter aging or to keep the users young physically as
long as the users wear them every night during sleep.  The devices also
cure many handicapnesses and deseases.  

Mr.Alex Chiu is an inventor who is mainly specialized in effects on human
health by magnetic forces.  For interested party, please email  
alexycchiu@earthlink.net   Check out my web site  www.swiftsite.com/eternal
  tel 415 585 3825



From owner-ageing@net.bio.net Wed Mar 19 22:00:00 1997
Path: biosci!agate!spool.mu.edu!uwm.edu!newsfeeds.sol.net!news.maxwell.syr.edu!cpk-news-hub1.bbnplanet.com!news.bbnplanet.com!newsfeed.internetmci.com!news.campus.mci.net!n-f-m
From: "Jan Coetzee" <coetzee_jv@news.campus.mci.net>
Newsgroups: bionet.molbio.ageing
Subject: To the moderator of this group
Date: 20 Mar 1997 17:36:35 GMT
Organization: CampusMCI
Lines: 4
Message-ID: <01bc3555$43463c60$291166ce@coetzee_jv>
References: <5gph8r$n6u@camel0.mindspring.com>
NNTP-Posting-Host: s12-pm07.atlanta.campus.mci.net
X-Newsreader: Microsoft Internet News 4.70.1157


How can I post to this group?

coetzee_jv@peachnet.campus.mci.net

From owner-ageing@net.bio.net Wed Mar 19 22:00:00 1997
Path: biosci!EARTHLINK.NET!AlexYCChiu
From: AlexYCChiu@EARTHLINK.NET ("Alex Chiu")
Newsgroups: bionet.molbio.ageing
Subject: (none)
Date: 20 Mar 1997 02:27:04 -0800
Organization: BIOSCI International Newsgroups for Molecular Biology
Lines: 34
Sender: daemon@net.bio.net
Distribution: world
Message-ID: <199703201026.CAA29932@sweden.it.earthlink.net>
NNTP-Posting-Host: net.bio.net

Please visit http://home.earthlink.net/~alexycchiu/
I have invented The Eternal Life Device which allows
you to keep your body physically young forever as long 
as you use the device every night during sleep.NEW INVENTION ALLOWS HUMANS
TO LIVE FOREVER

     http://home.earthlink.net/~alexycchiu

ACCORDING TO ALEX CHIU, PEOPLE CAN STAY YOUNG AND LIVE FOREVER BY USING HIS
NEW INVENTION 'THE ETERNAL LIFE RINGS' OR 'THE ETERNAL LIFE FOOT BRACES'. 
The Eternal Life Rings are rings to be worn on both small fingers of a user
during sleep.  The Eternal Life Foot Braces are to be worn on all fingers
of both feet of a user during sleep.  Both devices consist simply magnets
and braces which hold magnets onto the fingers of the user.

Mr. Alex Chiu claims that the magnetic devices, the finger rings or the
foot braces, both are believed to allow the user to stay young physically
forever or to become younger!  The inventor explained that the magnetic
pole on the right small finger or on the right foot is opposite to the
poles of the magnets on the left small finger or of the left foot. With a
different pole on each side of the human body, blood circulation and
electric current of the body are propelled.  The speeded up blood
circulation and electric current generate faster metabolism in order to
fight aging process.  The mentioned devices invented by Alex Chiu are
believed to be able to alter aging or to keep the users young physically as
long as the users wear them every night during sleep.  The devices also
cure many handicapnesses and deseases.  

Mr.Alex Chiu is an inventor who is mainly specialized in effects on human
health by magnetic forces.  For interested party, please email  
alexycchiu@earthlink.net   Check out my web site 
http://home.earthlink.net/~alexycchiu
  tel 415 585 3825


From owner-ageing@net.bio.net Wed Mar 19 22:00:00 1997
Path: biosci!EARTHLINK.NET!AlexYCChiu
From: AlexYCChiu@EARTHLINK.NET ("Alex Chiu")
Newsgroups: bionet.molbio.ageing
Subject: (none)
Date: 20 Mar 1997 01:45:12 -0800
Organization: BIOSCI International Newsgroups for Molecular Biology
Lines: 34
Sender: daemon@net.bio.net
Distribution: world
Message-ID: <199703200946.BAA25736@spain.it.earthlink.net>
NNTP-Posting-Host: net.bio.net

Please visit http://home.earthlink.net/~alexycchiu/
I have invented The Eternal Life Device which allows
you to keep your body physically young forever as long 
as you use the device every night during sleep.
NEW INVENTION ALLOWS HUMANS TO LIVE FOREVER

     www.swiftsite.com/eternal

ACCORDING TO ALEX CHIU, PEOPLE CAN STAY YOUNG AND LIVE FOREVER BY USING HIS
NEW INVENTION 'THE ETERNAL LIFE RINGS' OR 'THE ETERNAL LIFE FOOT BRACES'. 
The Eternal Life Rings are rings to be worn on both small fingers of a user
during sleep.  The Eternal Life Foot Braces are to be worn on all fingers
of both feet of a user during sleep.  Both devices consist simply magnets
and braces which hold magnets onto the fingers of the user.

Mr. Alex Chiu claims that the magnetic devices, the finger rings or the
foot braces, both are believed to allow the user to stay young physically
forever or to become younger!  The inventor explained that the magnetic
pole on the right small finger or on the right foot is opposite to the
poles of the magnets on the left small finger or of the left foot. With a
different pole on each side of the human body, blood circulation and
electric current of the body are propelled.  The speeded up blood
circulation and electric current generate faster metabolism in order to
fight aging process.  The mentioned devices invented by Alex Chiu are
believed to be able to alter aging or to keep the users young physically as
long as the users wear them every night during sleep.  The devices also
cure many handicapnesses and deseases.  

Mr.Alex Chiu is an inventor who is mainly specialized in effects on human
health by magnetic forces.  For interested party, please email  
alexycchiu@earthlink.net   Check out my web site  www.swiftsite.com/eternal
  tel 415 585 3825



From owner-ageing@net.bio.net Wed Mar 19 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!gatech!howland.erols.net!cam-news-hub1.bbnplanet.com!su-news-hub1.bbnplanet.com!news.bbnplanet.com!news.alt.net!newspost1.alt.net!usenet
From: biochemist@biochemist.com (Michael Almeida)
Newsgroups: bionet.molbio.ageing
Subject: Biochemist.com
Date: Thu, 20 Mar 1997 17:41:34 GMT
Organization: Biochemist.com
Lines: 22
Message-ID: <333176c0.70460953@news.alt.net>
X-Newsreader: Forte Agent .99d/32.182

Fellow Scientists,

Biochemsit.com is a new site dedicated to Biochemistry and Molecular
Biology.  It is run and maintained by a stundent of MSU majoring in
Biochemistry.

The site has:
1) Online live chat room dedicated to scientific discusions
2) A message board where individuals can post question for opions
related to the sciences
3) Refernces to all the commercial databases on the Internet
4) A place where individuals can post their finding/research FREE of 	
           charge

Please visit the site and and make comments on what you would like
added!!!

					thanks,
				Michael ALmeida	

http://www.biochemist.com
biochemist@biochemist.com

From owner-ageing@net.bio.net Wed Mar 19 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!news.sgi.com!news.maxwell.syr.edu!ix.netcom.com!compuserve.com!news.production.compuserve.com!news
From: Ming Soo <110025.1742@CompuServe.COM>
Newsgroups: bionet.microbiology,bionet.molbio.ageing,bionet.molbio.bio-matrix
Subject: ..,WE ARE ACCEPTING NEW WRITERS
Date: 19 Mar 1997 22:26:06 GMT
Organization: teehoo
Lines: 19
Message-ID: <5gpp5u$g0n$1@mhafc.production.compuserve.com>
Xref: biosci bionet.microbiology:9364 bionet.molbio.ageing:3275 bionet.molbio.bio-matrix:878

We**are now accepting new & previously published* 
writers for publication. We have 3 offices/ 2 in *New York /
the other in *Florida**. For ALL fiction & nonfiction/ 
send brief digest/ first chapter/ include a self 
addressed, stamped envelope: *S.A.S.E.*
Poetry: send 3 poems/ *S.A.S.E.
Short Stories: send brief *synopsis/ 3 pages/ *S.A.S.E.
Do not send complete manuscript* unless invited to do so.

*We are also accepting screenplays for TV/ Movies/
Please follow guidelines as for fiction and nonfiction.
>*NYC AGENCY==
>*33-29 58 Street==
>*Woodside, NY 11377=-
>*(718)651-8145==



 

From owner-ageing@net.bio.net Wed Mar 19 22:00:00 1997
Path: biosci!IMB.IMB.AC.RU!koudin
From: koudin@IMB.IMB.AC.RU ("Alexei R. Koudinov")
Newsgroups: bionet.molbio.ageing
Subject: MBF / 2 MOLGMI / RGMY
Date: 20 Mar 1997 14:09:03 -0800
Organization: BIOSCI International Newsgroups for Molecular Biology
Lines: 26
Sender: daemon@net.bio.net
Distribution: world
Message-ID: <3.0.16.19970321000322.351f8d64@imb.imb.ac.ru>
NNTP-Posting-Host: net.bio.net

        =C0 =EF=EE=F7=E5=EC=F3 =E1=FB, =E3=EE=F1=EF=EE=E4=E0, =ED=E0=EC =ED=
=E5 =EE=E1=FA=E5=E4=E8=ED=E8=F2=FC=F1=FF =E8 =ED=E5 =EF=EE=E7=ED=E0=EA=EE=EC=
=E8=F2=FC=F1=FF --
=F0=F3=F1=F1=EA=EE=EC=F3 =F1=EE=EE=E1=F9=E5=F1=F2=E2=F3 =F1=E8=F5 =F0=E5=F1=
=F3=F0=F1=EE=E2 ? =CC=EE=E9 =F1=EF=E5=F6=E8=E0=EB=FC=ED=FB=E9 =E8=ED=F2=E5=
=F0=E5=F1 -- =F1=EE=E1=F0=E0=F2=FC
=E2=FB=EF=F3=F1=EA=ED=E8=EA=EE=E2 =CC=E5=E4=E8=EA=EE-=C1=E8=EE=EB=EE=E3=E8=
=F7=E5=F1=EA=EE=E3=EE =D4=E0=EA=F3=EB=FC=F2=E5=F2=E0 =D0=EE=F1=F1=E8=E9=F1=
=EA=EE=E3=EE
=C3=EE=F1.=CC=E5=E4.=D3=ED=E8=E2=E5=F0=F1=E8=F2=E5=F2=E0, =E1=FB=E2=F8=E5=E3=
=EE 2=EE=E3=EE =CC=EE=F1=EA=EE=E2=F1=EA=EE=E3=EE =CE=F0=E4=E5=ED=E0 =CB=E5=
=ED=E8=ED=E0 =CC=E5=E4.=C8=ED=F1=F2=E8=F2=F3=F2=E0.
=CF=EE=EB=E5=E7=ED=FB=E5 references =E1=F3=E4=F3=F2 =F1 =F0=E0=E4=EE=F1=F2=
=FC=FE =EF=F0=E8=ED=FF=F2=FB.

        =C2=E0=F8 =C0. =CC=C1=D4-92.
_____________________________

        A pochemu by, gospoda, nam ne ob'edinit'sia  i ne poznakomit'sia --
russkomu soobshestvu sich resursov ? Moi special'nii interes -- sobrat
vypusknikov Mediko-Biologiheskogo Fakulteta Rossijskogo
Gos.Med.Universiteta, byvshego 2ogo Moskovskogo Ordena Lenina
Med.Instituta. Poleznye references budut s radost'iy i blagodarnost'iy
priniati.

        Vaw A. MBF-92.

From owner-ageing@net.bio.net Wed Mar 19 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!gatech!howland.erols.net!worldnet.att.net!news.alt.net!newspost1.alt.net!usenet
From: biochemist@biochemist.com (Michael Almeida)
Newsgroups: bionet.molbio.ageing
Subject: Biochemist.com
Date: Thu, 20 Mar 1997 17:41:37 GMT
Organization: Biochemist.com
Lines: 22
Message-ID: <333176cf.70476019@news.alt.net>
X-Newsreader: Forte Agent .99d/32.182

Fellow Scientists,

Biochemsit.com is a new site dedicated to Biochemistry and Molecular
Biology.  It is run and maintained by a stundent of MSU majoring in
Biochemistry.

The site has:
1) Online live chat room dedicated to scientific discusions
2) A message board where individuals can post question for opions
related to the sciences
3) Refernces to all the commercial databases on the Internet
4) A place where individuals can post their finding/research FREE of 	
           charge

Please visit the site and and make comments on what you would like
added!!!

					thanks,
				Michael ALmeida	

http://www.biochemist.com
biochemist@biochemist.com

From owner-ageing@net.bio.net Thu Mar 20 22:00:00 1997
Path: biosci!ksc-bg.murmansk.su!peterk
From: peterk@ksc-bg.murmansk.su ("P. A. Kaschoulin")
Newsgroups: bionet.molbio.ageing
Subject: describe needs
Date: 21 Mar 1997 03:44:45 -0800
Organization: Polar-Alpine Botanical Garden-Institute
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SUBSCRIBE



From owner-ageing@net.bio.net Sat Mar 22 22:00:00 1997
Path: biosci!webtv.net!uunet!in2.uu.net!199.94.215.18!cam-news-hub1.bbnplanet.com!news.bbnplanet.com!howland.erols.net!usc!chi-news.cic.net!cougar.olivet.edu!usenet
From: IRST <survey@eggbeater.olivet.edu>
Newsgroups: bionet.molbio.ageing
Subject: IRST Needs your help.
Date: Tue, 18 Mar 1997 22:21:01 -0600
Organization: Olivet Nazarene University
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Dear Internet User,
  By now you've probably heard about the current issues pertaining to
free speech and the regulation of Internet related materials. We, The
Internet Regulatory Survey Team (IRST), are conducting a survey/study
pertaining to these issues and are interested in your opinions.

  We are sending along a small 16 question survey that should take no
more than five minutes of your time to complete. We ask for your
participation in this study and provide us with your information.
Your response will be completely anonymous.  If you'd prefer to
 visit our Web site and fill out the form there the address is:
http://eggbeater.olivet.edu/~survey/

Thank You in advance for your time!

-----------------------------------------------
  Internet Regulatory Survey

1. What service do you use to access the Internet?
    AOL
    Compuserve
    MSN
    Netcom
    Local Internet Service Provider (ISP)
    College or University LAN
    Other

2. How many times do you use Email during the week?
    0-5   6-10    11-15   16-20    20+

3. How many hours during the week do you spend on the Internet?
    0-5   6-10    11-15   16-20    20+

4. How long have you been using the Internet?
    1-6 months      7-12 months      1-2 years       2-3 years
    3+ years

5. How would you rate yourself as an Internet user?
    Beginner
    Intermediate
    Advanced
    Expert

For questions 6-11 please indicate the level of agreement or
disagreement for each.
SA=Strongly Agree   A=Agree   N=Neutral   D=Disagree
SD=Strongly Disagree

6. The government should be allowed to regulate the Internet in
general.
   SA   A   N   D   SD

7. How do you feel about laws governing material displayed on web
sites?
   SA   A   N   D   SD

8. How do you feel about Internet service providers censoring email?
   SA   A   N   D   SD

9. A web site should be able to contain any information it wants no
matter how vulgar, obscene, or derogatory it may be.
   SA   A   N   D   SD

10. Web sites should display a warning if they contain any material
that may be questionable or offensive to others.
   SA   A   N   D   SD

11. All web sites should register their site with an Internet Censor
Rating (ICR) company and display a censor rating, much like that used
in television.
   SA   A   N   D   SD

12. Gender: Male / Female

13. Age:

14. Country: __________________

15. Religious affiliation:
     Catholic
     Protestant
     Jewish
     Islamic
     Hindu
     Buddhist
     Other
     None

16. Political party:
     (U.S. Residents)
     Democrat
     Republican
     Independent
     Libertarian
     Other
     None

     (Non-US Residents)
     List political party name: _______________
-------------------------------------------------

We thank you for participation and encourage you to send us your
comments and suggestions. Visit our Web site for more info

Internet Regulatory Survey Team (IRST)
WEB:   http://eggbeater.olivet.edu/~survey/
EMAIL: survey@eggbeater.olivet.edu


From owner-ageing@net.bio.net Sun Mar 23 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!gatech!csulb.edu!newshub.csu.net!news.ironhorse.com!nntp.portal.ca!news.bc.net!rover.ucs.ualberta.ca!news.ucalgary.ca!srv1.freenet.calgary.ab.ca!hewitt
From: Duane Hewitt <hewitt@freenet.calgary.ab.ca>
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: Sun, 23 Mar 1997 16:57:48 -0700
Organization: Calgary Free-Net
Lines: 29
Message-ID: <Pine.A32.3.93.970323165157.87258D-100000@srv1.freenet.calgary.ab.ca>
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To: Longevity-Digest/Brian Rowley <BRowley@ALUMNI.UBC.CA>
In-Reply-To: <199703182014.MAA04074@unixg.ubc.ca>

On 18 Mar 1997, Longevity-Digest/Brian Rowley wrote:

>         Your arguments make a lot of sense. I'd like to know, though, were
> Dolly's telomeres (or Hayflick divisions) restored to those of a newborn
> lamb? It would be easy to find that out; just compare number of remaining
> divisions (and length of telomeres) of sheep progenitor with that of lamb
> clone. If the telomeres and remaining divisions were restored by cloning
> that would imply that rejuvenation of adult cells is possible.
> Brian Rowley

There seem to be two possibilities:

1) The early embryo has some telomerase activity which restores the
telomeres. This would mean that adult cells could be rejuvenated in their
telomeres.


2) The cell that the successful clone was derived from had long telomeres
and that was why it was able to be cloned. Some stem cells in adults have
detectable telomerase activity and it is quite possible that the cell that
Dolly arose from was one of these and therefore is a relatively "rare"
occurence.

Duane Hewitt

Immortality, Inc.
http://immortality.org



From owner-ageing@net.bio.net Sun Mar 23 22:00:00 1997
Path: biosci!agate!spool.mu.edu!uwm.edu!cs.utexas.edu!swrinde!howland.erols.net!newsxfer3.itd.umich.edu!newsfeed.internetmci.com!news.campus.mci.net!n-f-m
From: "Jan Coetzee" <coetzee_jv@news.campus.mci.net>
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: 24 Mar 1997 01:24:01 GMT
Organization: CampusMCI
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Message-ID: <01bc37f2$0ccff5a0$4e1166ce@coetzee_jv>
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Duane Hewitt  writes:



"There seem to be two possibilities:

1) The early embryo has some telomerase activity which restores the
telomeres. This would mean that adult cells could be rejuvenated in their
telomeres.


2) The cell that the successful clone was derived from had long telomeres
and that was why it was able to be cloned. Some stem cells in adults have
detectable telomerase activity and it is quite possible that the cell that
Dolly arose from was one of these and therefore is a relatively "rare"
occurence."

There is a third possibility!

Telomeres may have nothing to do with cell division in these particular
cells.  The telomere hypotheses is not universally true.

Jan(John)


From owner-ageing@net.bio.net Sun Mar 23 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!gatech!csulb.edu!hammer.uoregon.edu!news.ironhorse.com!nntp.portal.ca!van-bc!n1van.istar!van.istar!west.istar!ott.istar!istar.net!tor.istar!east.istar!news1.istar.ca!news
From: jpuderer@magi.com (James Puderer)
Newsgroups: bionet.molbio.ageing
Subject: Re: implications of dolly
Date: 24 Mar 1997 04:06:49 GMT
Organization: iSTAR Internet Incorporated
Lines: 47
Message-ID: <5h4ukp$goc@news.istar.ca>
References: <199703182014.MAA04074@unixg.ubc.ca> <Pine.A32.3.93.970323165157.87258D-100000@srv1.freenet.calgary.ab.ca> <01bc37f2$0ccff5a0$4e1166ce@coetzee_jv>
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"Jan Coetzee" <coetzee_jv@news.campus.mci.net> wrote:

>Duane Hewitt  writes:



>"There seem to be two possibilities:

>1) The early embryo has some telomerase activity which restores the
>telomeres. This would mean that adult cells could be rejuvenated in their
>telomeres.


>2) The cell that the successful clone was derived from had long telomeres
>and that was why it was able to be cloned. Some stem cells in adults have
>detectable telomerase activity and it is quite possible that the cell that
>Dolly arose from was one of these and therefore is a relatively "rare"
>occurence."

>There is a third possibility!

>Telomeres may have nothing to do with cell division in these particular
>cells.  The telomere hypotheses is not universally true.

As far as I know there is an awful lot of evidence pointing to
telemeres being genetic clocks.  It will be interesting to see what
effects the possibility of shortened telomeres has on Dolly.

In order to determine if telomeres do in fact play an important role
in the aging process it may be important to know if the adult genetic
material used to clone Dolly, was at anytime subject to telomerase
activity.

Which comes to my question.  Does anyone know if female gametes are
telomerase active?  Sperm are apparantly telomarase active and it
would make sence for ova to be telomarase active as well.  Also, if
the adult genetic material was in fact subject to telomarase activity
how much would this telomarase activity extend to telomeres?

It seems likely that even if the adult genetic material was subject to
telomarase activity Dolly's telomeres will probably not be as long as
telomeres occuring in an uncloned lamb, but then I'm just speculating.

Regards,
James Puderer.



From owner-ageing@net.bio.net Sun Mar 23 22:00:00 1997
Path: biosci!ihnp4.ucsd.edu!munnari.OZ.AU!news.ecn.uoknor.edu!feed1.news.erols.com!cpk-news-hub1.bbnplanet.com!news.bbnplanet.com!newsxfer3.itd.umich.edu!portc01.blue.aol.com!audrey01.news.aol.com!not-for-mail
From: djx1@aol.com (DJX1)
Newsgroups: bionet.molbio.ageing
Subject: Re: (none)
Date: 24 Mar 1997 15:19:54 GMT
Organization: AOL http://www.aol.com
Lines: 13
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Hahahahahahhahahahahahahahahahahha!

HHHAhaahahahahaahhahahahahahhahahhah!!
Hahahahahahhaahah

Hahahahh....


Whew!  I needed a good laugh.

Thanks, Alex.

DX

From owner-ageing@net.bio.net Sun Mar 23 22:00:00 1997
Path: biosci!daresbury!not-for-mail
From: mjfasmb <mjfasmb@fs1.ce.umist.ac.uk>
Newsgroups: bionet.molbio.ageing
Subject: Sheep stuff...
Date: 24 Mar 1997 20:53:03 -0000
Organization: Dept. Chem Eng - UMIST (FS1)
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Original-To: ageing@dl.ac.uk


> Hi Brian,
 
> >         Your arguments make a lot of sense. I'd like to know, though, were
> > Dolly's telomeres (or Hayflick divisions) restored to those of a newborn
> > lamb? It would be easy to find that out; just compare number of remaining
> > divisions (and length of telomeres) of sheep progenitor with that of lamb
> > clone. If the telomeres and remaining divisions were restored by cloning
> > that would imply that rejuvenation of adult cells is possible.
> > Brian Rowley
> 
> Interesting question.  I sincerely hope someone is 
> planning / attempting to find out how many P.D. Dolly's cells are 
> capable of.  The length of her telomeres would be easy enough to 
> ascertain.  Don't know if  Dolly's `mother' is still alive, or 
> whether tissue samples taken at the same time as the `Dolly-biopsy' 
> were frozen, but if would be nice to find out if there is a 
> difference in telomere length between mother and clone cells.
> 
> My guess is that in response to some maternal factor, or as a result 
> of manipulations to Dolly's original adult nucleus, some basal 
> embryonic expression pattern was re-established - including 
> expression of telomerase.  There does appear to be a telomere length 
monitoring pathway (recent Nature paper) in cells capable of 
expressing telomerase  - I imagine it would correct for any 
shortening detected...
> (?)
> MGB 

From owner-ageing@net.bio.net Tue Mar 25 22:00:00 1997
Path: biosci!BIOLOGY.LSA.UMICH.EDU!ijohn
From: ijohn@BIOLOGY.LSA.UMICH.EDU (Isaac John)
Newsgroups: bionet.molbio.ageing
Subject: (none)
Date: 26 Mar 1997 09:47:07 -0800
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unsubscribe



From owner-ageing@net.bio.net Fri Mar 28 22:00:00 1997
Path: biosci!agate!howland.erols.net!ix.netcom.com!enews.sgi.com!news.corp.sgi.com!news.sgi.com!news-out.internetmci.com!newsfeed.internetmci.com!news.campus.mci.net!n-f-m
From: "Jan Coetzee" <coetzee_jv@news.campus.mci.net>
Newsgroups: bionet.molbio.ageing
Subject: evolution and aging
Date: 28 Mar 1997 22:06:43 GMT
Organization: CampusMCI
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Has it occurred to anyone that aging may be the consequences of "evolution"
taking place in the body. For example take hair follicles. Assume that
every one are born with two kinds of follicles. Normal and gray pigmented.
With time subtle changes in the bodies chemistry cause the gray pigment
follicles to dominate.  Finally you end up with gray hair. If this is true
for most cells in the body this idea could explain aging.

Jan(John)

From owner-ageing@net.bio.net Fri Mar 28 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!uwm.edu!cs.utexas.edu!news.tamu.edu!news
From: Dawn <DawnC@bigfoot.com>
Newsgroups: bionet.molbio.ageing
Subject: Re: evolution and aging
Date: Sat, 29 Mar 1997 09:19:56 -0600
Organization: Texas A&M Univ., College of Medicine, Dept of Medical Biochemistry and Genetics
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Jan Coetzee wrote:
> 
> Has it occurred to anyone that aging may be the consequences of "evolution"
> taking place in the body. For example take hair follicles. Assume that
> every one are born with two kinds of follicles. Normal and gray pigmented.
> With time subtle changes in the bodies chemistry cause the gray pigment
> follicles to dominate.  Finally you end up with gray hair. If this is true
> for most cells in the body this idea could explain aging.
> 
> Jan(John)

While many people have proposed an evolutionary significace to aging
(may be an anti-cancer mechanism, etc.), THAT is not why we get grey
hair (i.e., we are not born with two kinds of hair follicles and one
begins to dominate.)
-- 
-Dawn-
Time is the best teacher. Unfortunately, it kills all of its students.
     Visit: http://members.aol.com/CappSci
     Animal Lovers check out http://members.tripod.com/~DawnC

From owner-ageing@net.bio.net Sat Mar 29 22:00:00 1997
Path: biosci!rutgers.rutgers.edu!gatech!www.nntp.primenet.com!nntp.primenet.com!newsfeed.nacamar.de!cpk-news-hub1.bbnplanet.com!news.bbnplanet.com!newsxfer3.itd.umich.edu!newsfeed.internetmci.com!news.campus.mci.net!n-f-m
From: "Jan Coetzee" <coetzee_jv@news.campus.mci.net>
Newsgroups: bionet.molbio.ageing
Subject: Re: evolution and aging
Date: 30 Mar 1997 02:41:19 GMT
Organization: CampusMCI
Lines: 6
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Some times a young person have an occasional gray hair. How do you know we
are not born with more than one kind of follicle? Babies (white) are often
born with blond hair just to lose the hair color later on. What about
animals. Some have white coats in the Winter.

Jan(John)

From owner-ageing@net.bio.net Mon Mar 31 23:00:00 1997
Path: biosci!TENET.EDU!dashley
From: dashley@TENET.EDU (Don Ashley)
Newsgroups: bionet.molbio.ageing
Subject: Senior numbers
Date: 1 Apr 1997 03:38:30 -0800
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from the newsgroup:

   
  FACTS YOU SHOULD KNOW ABOUT RETIREMENT
  
   
   Did you know that over 100 years ago, the first retirement act was
   established? In Germany, General Otto Von Bismarck set the age of
   retirement at 65. Back then, only two percent of the population lived
   to retire!
   
   Nowadays, the fastest-growing segment of the population is age 80 and
   over--we'll be enjoying retirement for 15 or more years, not just two
   or three. Retirement definitely isn't what it use to be!
   
   Whether we devote that time to our families, travel, hobbies or second
   careers, we all want to be able to live out those years in comfort and
   with the knowledge that we have enough for our needs.
   
   A longer retirement is both the good news and the bad news. It is
   fortunate to live a longer, healthier life, but where will the income
   come from when we're ready to retire? An average American in 1992,
   with an average household income of $35,000, received only 40% of his
   or her income from Social Security. The rest came from personal
   assets, private pensions, earnings and other sources.
   
   Sources of Retirement Income
   40% Social Security
   10% Private Pensions
   9% Government Employee Pensions
   17% Earnings
   21% Personal Assets
   3% Other
   100% Total
   
   Source: Social Security Administration, 1992.
   
   As the table indicates, you can expect to have to earn at least 38%
   (earnings and personal assets) of your retirement income from personal
   assets, private pensions, earnings and other sources.
   
   According to a 1993 Department of Labor Survey, of every 1000 people
       age 65, the following situations exist:
       
     * 450 are dependent on their relatives.
     * 280 rely entirely on public charity, welfare or Social Security.
     * 220 must continue to work.
     * 50 have enough money to meet their needs.
     * Of these 50, only ten have enough money to provide the financial
       independence that retirement should bring.
       
  YOU MAY SPEND A THIRD OF YOUR LIFE IN RETIREMENT
  
   Workers are retiring earlier. Longer life spans and earlier, healthier
   retirements mean you may end up spending 15, 20, even 25 or more years
   in retirement. It also means that there is more danger than ever of
   out-living your income.
   
  INFLATION
  
   Another important reason you need to plan and save for retirement is
   inflation. Inflation simply means that the cost of goods and services
   generally rises over time, as shown by the Consumer Price Index (CPI).
   This measurement of inflation is stated as a yearly percentage and,
   according to the Department of Labor, has averaged approximately 5.4%
   from 1965 through 1994.
   
          For example, a loaf of bread costing $1.00 today would cost
          $1.05 a year from now. In 20 years, that same loaf of bread
          would cost about $2.86, assuming that inflation continues to
          average 5.4%. In other words, your money will not go as far in
          the future as it does today.
          

