From owner-ageing@net.bio.net Thu Jan 02 22:00:00 1997 Path: biosci!UMABNET.AB.UMD.EDU!aandreye From: aandreye@UMABNET.AB.UMD.EDU ("Alexander Y. Andreyev") Newsgroups: bionet.molbio.ageing Subject: Seminars on Ageing in USA by Drs.Gavrilovs Date: 3 Jan 1997 03:32:56 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 94 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net THE SCHEDULE OF SEMINARS BY DRS.LEONID AND NATALIA GAVRILOV Jan 3-4 - Boulder Creek, CA. Contact person: Dr.Rollin McCraty Institute of HeartMath 14700 West Park Ave. Boulder Creek, CA 95006 phone: 408-338-8727 fax: 408-338-1182 E-mail: ihmlab@heartmath.org Jan 5-10 - Ventura, CA. Doubletree Hotel. The Gordon Research Conference on the Biology of Aging Contact: Dr.Leonid and Natalia Gavrilov Doubletree Hotel 2055 Harbor Boulevard, Ventura, CA 93001 USA Tel.: 805-643-6000 Fax: 805-643-7137 Jan 11-14 - Athens, Georgia. Contact person: Dr.Leonard W.Poon Univ.of Georgia Gerontology Center Athens Ga. 30602 phone: 706-542-3954 fax: 706-542-4805 E-mail: Lpoon@uga.cc.uga.edu Jan 15-17 - Ames, Iowa. Contact person: Dr.Peter Martin Dept.of Human Development and Family Studies Iowa State University 209 CD Building Ames, IA 50011 phone: 515-294-5186 fax: 515-294-1765 E-mail: pxmartin@iastate.edu Jan 18-20 - Baltimore, MD Contact person: Dr.Alex Andreyev 3 Dalecrest Ct., apt.102 Timonium, MD 21093 USA phone: 410-560-7167 E-mail: aandreye@umabnet.ab.umd.edu Jan 21-23 - Chicago, Illinois Contact person: Dr.Brian Charlesworth Department of Ecology and Evolution University of Chicago tel.773-702-8942 fax: 773-702-9740 tel.(home): 773-642-1446 E-mail: bcworth@pondside.uchicago.edu Jan 24 - Madison, Wisconsin Contact person: Kay Smith (administrator) Institute on Aging 2245 Medical Sciences Center l300 University Avenue Madison, WI 53706 phone:608-262-1818 fax: 608-263-6211 phone (direct): 608-263-6404 E-mail: smithk@ssc.wisc.edu 2nd contact person: Dr.James Crow phone (home): 608-233-6709 phone (office): 608-263-4438 fax: 608-262-2976 E-mail: jfcrow@facstaff.wisc.edu ********************************THE END****************************** From owner-ageing@net.bio.net Thu Jan 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 Jan 1997 02:00:42 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 239 Sender: daemon@net.bio.net Distribution: world Message-ID: <199701031000.CAA24345@net.bio.net> NNTP-Posting-Host: net.bio.net (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 Thu Jan 02 22:00:00 1997 Path: biosci!rutgers!iag.net!news.magicnet.net!feed1.news.erols.com!worldnet.att.net!ix.netcom.com!news From: ed111@ix.netcom.com(Ed) Newsgroups: bionet.molbio.ageing Subject: DHEA and Testicular Cancer? Date: 3 Jan 1997 08:36:05 GMT Organization: Netcom Lines: 15 Message-ID: <5aigdl$rk3@dfw-ixnews4.ix.netcom.com> NNTP-Posting-Host: whx-ca1-08.ix.netcom.com X-NETCOM-Date: Fri Jan 03 2:36:05 AM CST 1997 I am a middle-aged, healthy male. I recently found through a blood test that my DHEA is relatively low. So, based on what I've read, I thought it would be a good idea to take 50mg DHEA supplements per day. I also take vitamins. Well, wouldn't you know. I talked to a physician at a party, and he said that, even though DHEA may help to improve your immune response, and do some of the other wonderful things it is supposed to do, the main drawback is that DHEA can increase one's susceptibility to Testicular Carcinoma, since it is androgenic. Anyone have any thoughts on this, because it sure puts a damper on taking oral supplements of DHEA. Thanks, Ed. From owner-ageing@net.bio.net Thu Jan 02 22:00:00 1997 Path: biosci!BIOTOP.UMCS.LUBLIN.PL!TCHORZ From: TCHORZ@BIOTOP.UMCS.LUBLIN.PL ("Marek Tchorzewski") Newsgroups: bionet.molbio.ageing Subject: DNA software Date: 3 Jan 1997 03:54:31 -0800 Organization: Marie Curie-Sklodowska University Lines: 20 Sender: daemon@net.bio.net Distribution: world Message-ID: <1ABD4E9700B@biotop.umcs.lublin.pl> NNTP-Posting-Host: net.bio.net Dear Netters, First of all, Happy New Year 1997 to all of you !!! On the other hand, I need advice concerning programs for DNA and protein analysis. I am going to buy such program however I am not fully determined which program I should purchase. So far, I have seen DNAsis and DNAstar, however I am not sufficiently confident that these programs are reliable, and can provide me with the best options. So, could you advice me, which programs is actually the best on the market. Marek Tchorzewski PhD Univ. of Maria Curie-Sklodowska Dept. of Molecular Biology Lublin, Poland From owner-ageing@net.bio.net Sat Jan 04 22:00:00 1997 Newsgroups: bionet.molbio.ageing Path: biosci!agate!spool.mu.edu!uwm.edu!newsfeed.internetmci.com!howland.erols.net!feed1.news.erols.com!insync!news.azstarnet.com!news.sprintlink.net!news-ana-7.sprintlink.net!NEWS!not-for-mail From: "Joseph Cannon" Subject: I need a GOOD DHEA review article Message-ID: <01bbfb29$3b8196c0$a61b29cf@joe-s-computer> Date: Sun, 05 Jan 1997 16:04:49 GMT X-Newsreader: Microsoft Internet News 4.70.1155 Lines: 8 does anybody know where I can get my hands on a GOOD (i.e., from a reputable Journal) and current review article on DHEA? I write for a local health and fitness magazine here in Pa and everybody is asking me about DHEA. does anybody know if Journal of applied Physiology or Medicine and Science in Sports and Exercise has a review or some other reputable jorunal? Please Email me back any responses thanks Joe Cannon From owner-ageing@net.bio.net Sat Jan 04 22:00:00 1997 Path: biosci!GNN.COM!DSchwa1234 From: DSchwa1234@GNN.COM (Douglas Schwartz) Newsgroups: bionet.molbio.ageing Subject: Re: DHEA and Testicular Cancer? Date: 5 Jan 1997 07:14:45 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 28 Sender: daemon@net.bio.net Distribution: world Message-ID: <199701051514.KAA19926@mail-e2b.gnn.com> NNTP-Posting-Host: net.bio.net >From: ed111@ix.netcom.com (Ed) > >Well, wouldn't you know. I talked to a physician at a party, > and he >said that, even though DHEA may help to improve your immune > response, >and do some of the other wonderful things it is supposed to > do, the >main drawback is that DHEA can increase one's susceptibility > to >Testicular Carcinoma, since it is androgenic. I think taking DHEA is extremely unwise. It is thermogenic, so if it does have any life-extending abilities it first must overcome this tremendous hurdle (the lower the temp., the longer the life, & this is probably a logarithmic relationship). It speeds up the metabolism, causing many to feel younger, but this is precisely the last thing you want to do. I am sure that it will not only encourage testicular cancer, but probably all other types as well. Melatonin, on the other hand, both lowers temp. & is a great antioxidant. --Doug Schwartz dschwa1234@gnn.com From owner-ageing@net.bio.net Sat Jan 04 22:00:00 1997 Path: biosci!bcm.tmc.edu!cs.utexas.edu!howland.erols.net!news.bbnplanet.com!cam-news-hub1.bbnplanet.com!uunet!in2.uu.net!204.245.3.50!news.primenet.com!melsmi From: Melvin Smith Newsgroups: bionet.molbio.ageing Subject: Re: DHEA and Testicular Cancer? Date: 4 Jan 1997 20:04:01 -0700 Organization: Primenet (602)416-7000 Lines: 33 Message-ID: <5an5n1$30h@nnrp1.news.primenet.com> References: <5aigdl$rk3@dfw-ixnews4.ix.netcom.com> X-Posted-By: melsmi@206.165.5.107 (melsmi) Ed wrote: : said that, even though DHEA may help to improve your immune response, : and do some of the other wonderful things it is supposed to do, the : main drawback is that DHEA can increase one's susceptibility to : Testicular Carcinoma, since it is androgenic. Ed, I have BPH + high cholesterol (I'm 64), and I'm changing from someone who *never* took vitamins to one who is now looking at all recent developments. (I take by prescription Hytrin (for blood pressure) and Pavastatin (tradename Pravachol). My doctor says that the Hytrin should also help my nightly forays to the bathroom (3 times nitely). Recently (9 months ago), I started taking melatonin at nite, then several weeks ago, I started taking 25mg of DHEA in the morning. The results: ZIP !! Maybe I'm resistant to all those drugs, or maybe they are all neutralizing each other. Anyway, my blood pressure is still high, I have no libido, I assume that my cholesterol is high, AND I'm about to try buying some selenium to complete my set of daily pills to protect me against cancer (it probably won't work either !) -Mel Smith ps. And now I've got a goddammed abscessed tooth !! -- ------------------------------------------------------------------------------- melsmi __ __ ____ ___ ___ ____ melsmi@primenet.com /__)/__) / / / / /_ /\ / /_ / / / \ / / / / /__ / \/ /___ / ------------------------------------------------------------------------------- From owner-ageing@net.bio.net Tue Jan 07 22:00:00 1997 Path: biosci!agate!howland.erols.net!cam-news-hub1.bbnplanet.com!news.bbnplanet.com!cpk-news-hub1.bbnplanet.com!news.mindspring.com!usenet From: lockshin@mindspring.com (Richard A. Lockshin) Newsgroups: bionet.molbio.ageing Subject: Apoptosis mirror site Date: Wed, 08 Jan 1997 03:41:32 GMT Organization: MindSpring Enterprises, Inc. Lines: 14 Message-ID: <5av5h4$b14@camel0.mindspring.com> Reply-To: lockshin@mindspring.com NNTP-Posting-Host: ip62.garden-city.ny.pub-ip.psi.net X-Server-Date: 8 Jan 1997 03:49:56 GMT X-Newsreader: Forte Free Agent 1.0.82 We announce the opening of a mirror site for our Apoptosis web page. Its address is: http://www.celldeath-apoptosis.org We hope that this site will provide less down-time, and that eventually we will incorporate more functionality into the site. Your comments are solicited. lockshin@stjohns.edu lockshin@mindspring.com check out Apoptosis/Programmed Cell Death Web Page http://rdz.stjohns.edu/~lockshin/index.html From owner-ageing@net.bio.net Wed Jan 08 22:00:00 1997 Path: biosci!biosci!not-for-mail From: lockshin@mindspring.com (Richard A. Lockshin) Newsgroups: bionet.celegans,bionet.cellbiol,bionet.drosophila,bionet.general,bionet.immunology,bionet.molbio.ageing,bionet.neuroscience Subject: Apoptosis mirror site Date: 8 Jan 1997 22:48:07 -0800 Organization: MindSpring Enterprises, Inc. Lines: 15 Sender: daemon@net.bio.net Distribution: world Message-ID: <5av54n$b14@camel0.mindspring.com> Reply-To: lockshin@mindspring.com NNTP-Posting-Host: net.bio.net Xref: biosci bionet.celegans:1227 bionet.cellbiol:6376 bionet.drosophila:2765 bionet.general:25061 bionet.immunology:10605 bionet.molbio.ageing:3130 bionet.neuroscience:17612 We announce the opening of a mirror site for our Apoptosis web page. Its address is: http://www.celldeath-apoptosis.org We hope that this site will provide less down-time, and that eventually we will incorporate more functionality into the site. Your comments are solicited. lockshin@stjohns.edu lockshin@mindspring.com check out Apoptosis/Programmed Cell Death Web Page http://rdz.stjohns.edu/~lockshin/index.html From owner-ageing@net.bio.net Thu Jan 09 22:00:00 1997 Path: biosci!rutgers!gatech!csulb.edu!hammer.uoregon.edu!news-xfer.netaxs.com!news.bbnplanet.com!cam-news-hub1.bbnplanet.com!howland.erols.net!newsserver.jvnc.net!netnews.sbphrd.com!campbejr From: campbejr@phu989.mms.sbphrd.com (John R. Campbell) Newsgroups: bionet.molbio.ageing Subject: Re: DHEA and Testicular Cancer? Date: 10 Jan 1997 17:22:39 GMT Organization: SmithKline Beecham Pharmaceuticals Research & Development Lines: 48 Message-ID: References: <199701051514.KAA19926@mail-e2b.gnn.com> Reply-To: soup@jtan.com NNTP-Posting-Host: phu989.sbphrd.com X-Newsreader: slrn (0.8.5) On 5 Jan 1997 07:14:45 -0800, Douglas Schwartz wrote: >>From: ed111@ix.netcom.com (Ed) > >> >>Well, wouldn't you know. I talked to a physician at a party, and he >>said that, even though DHEA may help to improve your immune response, >>and do some of the other wonderful things it is supposed to do, the >>main drawback is that DHEA can increase one's susceptibility to >>Testicular Carcinoma, since it is androgenic. > >I think taking DHEA is extremely unwise. It is thermogenic, so if >it does have any life-extending abilities it first must overcome >this tremendous hurdle (the lower the temp., the longer the life, & >this is probably a logarithmic relationship). It speeds up the >metabolism, causing many to feel younger, but this is precisely the >last thing you want to do. I am sure that it will not only >encourage testicular cancer, but probably all other types as well. Actually, I was under the (perhaps mistaken) impression that a longer life *would* come from a higher metabolic rate- since this means that your normal immune system and cell division functions are operating normally. I suspect there's something interfering w/ the main metabolic program loop w/i the cell. >Melatonin, on the other hand, both lowers temp. & is a great >antioxidant. Sure, but when the metabolism drops a bit you lose too much functionality. You may hibernate better but is that really much of an advantage? I suspect the antioxidant behavior of melatonin is a side defect of the material, since I don't see how such a small quantity (normally secreted) could make any real difference; Somehow I doubt that the oxydizing radicals last all that long in the body; Something's gonna inherit it... Mind you, I'm no expert. -- John R. Campbell, Speaker to Machines, Resident Heckler soup@jtan.com "As a SysAdmin, yes, I CAN read your e-mail, but I DON'T get that bored!"-me Disclaimer: I'm just a consultant at the bottom of the food chain, so, if you're thinking I speak for anyone but myself, you must have more lawyers than sense. From owner-ageing@net.bio.net Thu Jan 09 22:00:00 1997 Path: biosci!ihnp4.ucsd.edu!munnari.OZ.AU!bunyip.cc.uq.oz.au!not-for-mail From: John.Harrison@mailbox.uq.oz.au Newsgroups: bionet.molbio.ageing Subject: Energy loss with mitochondrial mutation at 11778 (ND4)?? Date: Fri, 10 Jan 1997 19:50:17 GMT Organization: University of Queensland Lines: 3 Message-ID: <32d69ccf.4692682@news.uq.edu.au> NNTP-Posting-Host: sujharri.slip.cc.uq.oz.au X-Newsreader: Forte Free Agent 1.1/32.230 This causes Lebers hereditary optic neuropathy. What is the best way of "boosting" energy production via mitochondria with this mutation present in 100% of cells. From owner-ageing@net.bio.net Fri Jan 10 22:00:00 1997 Path: biosci!daresbury!nntp-trd.UNINETT.no!sn.no!hermod.uio.no!ifi.uio.no!nntp.uio.no!news.nacamar.de!news.icm.edu.pl!hammer.uoregon.edu!arclight.uoregon.edu!netnews.nwnet.net!news-hub.interserv.net!news.interserv.com!news From: phis@sprynet.com (James Howard) Newsgroups: bionet.molbio.ageing Subject: Re: DHEA and Testicular Cancer? Date: Fri, 10 Jan 1997 21:50:30 GMT Organization: InterServ News Service Lines: 7 Message-ID: <5b6d4n$iq5@lal.interserv.com> References: <199701051514.KAA19926@mail-e2b.gnn.com> NNTP-Posting-Host: dd70-203.compuserve.com X-Newsreader: Forte Free Agent 1.0.82 Actually, it is a combination of low DHEA and high testosterone that may be involved in cancer of the prostate. "DHEA levels in patients with prostatic cancer were significantly lower, and free testosterone significantly higher as those in an age-matched control group." Experimental and Clinical Endocrinology 1992; 99: 68 James Howard From owner-ageing@net.bio.net Mon Jan 13 22:00:00 1997 Path: biosci!bcm.tmc.edu!cs.utexas.edu!howland.erols.net!worldnet.att.net!arclight.uoregon.edu!news.bc.net!rover.ucs.ualberta.ca!mongol.sasknet.sk.ca!news@mongol.sasknet.sk.ca From: Asha Newsgroups: bionet.molbio.ageing Subject: Re: Energy loss with mitochondrial mutation at 11778 (ND4)?? Date: Mon, 13 Jan 1997 17:47:50 -0600 Organization: SaskNet News Distribution Lines: 32 Message-ID: <32DAC9A6.DB6@sk.sympatico.ca> References: <32d69ccf.4692682@news.uq.edu.au> NNTP-Posting-Host: vultee17.sk.sympatico.ca Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.02E-SYMPA (Win16; I) John.Harrison@mailbox.uq.oz.au wrote: > > This causes Lebers hereditary optic neuropathy. > What is the best way of "boosting" energy production via mitochondria > with this mutation present in 100% of cells. As the mutation at 11778 affects the ND4 gene of Complex I, and results in a decrease in oxidative phosphorylation, it follows that any treatment able to increase either the efficiency of oxidative phosphorylation or its rate in the affected cells should be able to delay the onset of the disease. It is possible to accomplish this in spite of the defect in Complex I. If we consider that the symptoms caused by the 11778 mutation are essentially due to a Complex I defect (ignoring environmental factors), and that ubiquinone is the rate-limiting compound of the activity of complex I, then increasing the concentration of ubiquinone within the mitochondrial inner membrane will cause an increase in the production of ATP. Addition of ubiquinone to the system should enhance the respiratory rate above the current physiological (diseased) state. The only problem with this treatment theoretically, is to determine whether exogenous administration of ubiquinone is effective in raising the concentration of ubiquinone in the mitochondria. Best Regards, -- Asha Pharma http://www.nethomes.com/asha From owner-ageing@net.bio.net Mon Jan 13 22:00:00 1997 Path: biosci!ONLINE.TMSK.RU!blk From: blk@ONLINE.TMSK.RU (Alive) Newsgroups: bionet.molbio.ageing Subject: test Date: 14 Jan 1997 11:06:31 -0800 Organization: Evolution Center of Planet Earth Lines: 6 Sender: daemon@net.bio.net Distribution: world Message-ID: <32DBD90A.7423@online.tmsk.ru> Reply-To: blk@online.tmsk.ru NNTP-Posting-Host: net.bio.net test -- Name: Alive Organization: Evolution Center of Planet Earth E-mail: blk@online.tmsk.ru Aphorism: "Object is process" From owner-ageing@net.bio.net Wed Jan 15 22:00:00 1997 Path: biosci!rutgers!news.sgi.com!mr.net!news.clark.net!noos.hooked.net!news.hooked.net!usenet From: Caligari Newsgroups: bionet.molbio.ageing Subject: Rejuvination ? Date: Wed, 08 Jan 1997 12:41:09 -0800 Organization: Latent Image Media Lines: 11 Message-ID: <32D40665.124A@hooked.net> NNTP-Posting-Host: sf3-ppp25.well.com Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 3.01 (Win95; I) I'm new to this forum (and a lay person). But I'm quite interested in genetic research and manipulation. From what I gather, our bodies except for sperm or eggs cells are somatic that multiply onely a given amount of times and stop. What work is being done currently on discovering the mechanism that regulates this process. And are there theories on scenarious for discovering genes that regulate this process and modifying or controlling them? For instance, if brain cells could be made to clone or regenrate themselves, would people lose their memories and individuality? -- Enric From owner-ageing@net.bio.net Wed Jan 15 22:00:00 1997 Newsgroups: bionet.molbio.ageing Path: biosci!bcm.tmc.edu!cs.utexas.edu!news.sprintlink.net!news-peer.sprintlink.net!NEWS!not-for-mail From: "Joseph Cannon" Subject: NEED INFO ON EARLOBE CREASE AND HEART ATTACKS ECT...... Message-ID: <01bc03d0$97df3580$8d1b29cf@joe-s-computer> Date: Thu, 16 Jan 1997 16:23:16 GMT X-Newsreader: Microsoft Internet News 4.70.1155 Lines: 10 Im looking for information substantuating the connection between having an earlobe crease and an increased incidence of atherosclerosis, heart attacks and strokes. the only reference I have for it is in Life Extension by Dirk Person (1984). does anybody have any more up to date info on this that either substantuates or refutes this phenomenon? -- Joseph Patrick Cannon BS chemistry and Biology MS Exercise Physiology (May 1997) CSCS From owner-ageing@net.bio.net Wed Jan 15 22:00:00 1997 Path: biosci!IMMORTALITY.ORG!duane From: duane@IMMORTALITY.ORG (Duane Hewitt) Newsgroups: bionet.molbio.ageing Subject: Rejuvenation ? Date: 16 Jan 1997 07:42:00 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 10 Sender: daemon@net.bio.net Distribution: world Message-ID: <32DE4C28.4844@immortality.org> NNTP-Posting-Host: net.bio.net If you want to know about the latest research in the field of ageing then I would you suggest that you check out http://immortality.org You can also look for research that involves telomerase which has been implicated in causing the difference between germ cells (sperm and egg) and somatic cells. Duane Hewitt From owner-ageing@net.bio.net Wed Jan 15 22:00:00 1997 Path: biosci!MSN.COM!RonBlue From: RonBlue@MSN.COM ("Ronald Blue") Newsgroups: bionet.molbio.ageing Subject: RE: Rejuvination ? Date: 15 Jan 1997 21:09:17 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 21 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net ---------- From: Caligari Sent: Wednesday, January 08, 1997 3:41 PM To: ageing@net.bio.net Subject: Rejuvination ? For instance, if brain cells could be made to clone or regenrate themselves, would people lose their memories and individuality? -- Enric >>>>>>>>>>>>>>>>>>>>>>>>>>>>>> Yes, they would lose memories and their individuality. If you want to know why check out http://www.aston.ac.uk/~batong/Neutronics and ask for an email copy of Correlational Opponent- Processing. Ron Blue From owner-ageing@net.bio.net Thu Jan 16 22:00:00 1997 Path: biosci!bcm.tmc.edu!news.msfc.nasa.gov!news.sgi.com!news.sprintlink.net!news-peer.sprintlink.net!uunet!in1.uu.net!192.80.63.252!delphi.com!usenet From: Lou Pagnucco Newsgroups: bionet.molbio.ageing Subject: Re: NEED INFO ON EARLOBE CREASE AND HEART ATTACKS ECT...... Date: Fri, 17 Jan 97 02:10:31 -0500 Organization: Delphi (info@delphi.com email, 800-695-4005 voice) Lines: 18 Message-ID: References: <01bc03d0$97df3580$8d1b29cf@joe-s-computer> NNTP-Posting-Host: bos1d.delphi.com X-To: "Joseph Cannon" "Joseph Cannon" writes: >Im looking for information substantuating the connection between having an >earlobe crease and an increased incidence of atherosclerosis, heart attacks >and strokes. the only reference I have for it is in Life Extension by Dirk >Person (1984). does anybody have any more up to date info on this that >either substantuates or refutes this phenomenon? >-- >Joseph Patrick Cannon >BS chemistry and Biology >MS Exercise Physiology (May 1997) > I read a report debunking the original paper. I can't remember where, but it seems to me that an ear crease is much more indicative of sleeping style than of a propensity toward heart disease. It is hard to take any of these uncorroborated claims rushed into print by our "publish or perish" news media. From owner-ageing@net.bio.net Thu Jan 16 22:00:00 1997 Path: biosci!daresbury!nntp-trd.UNINETT.no!sn.no!nntp.uio.no!news.maxwell.syr.edu!news.bbnplanet.com!cpk-news-hub1.bbnplanet.com!cpk-news-feed1.bbnplanet.com!news1.usf.edu!chuma!mmunoz1 From: "Mauricio Munoz (BIO)" Newsgroups: bionet.molbio.ageing Subject: Re: Superhormones Date: Fri, 17 Jan 1997 11:11:48 -0500 Organization: University of South Florida Lines: 6 Message-ID: References: <1996121011530675438@zetnet.co.uk> Reply-To: "Mauricio Munoz (BIO)" NNTP-Posting-Host: chuma.cas.usf.edu Mime-Version: 1.0 Content-Type: TEXT/PLAIN; charset=US-ASCII X-Sender: mmunoz1@chuma To: Michael Quarrinton In-Reply-To: <1996121011530675438@zetnet.co.uk> It is my understanding that DHEA is sold in any GNC around the country. In regards to your question about superhormones I don't know. Mauricio H. Munoz Moffitt Cancer Research Institute From owner-ageing@net.bio.net Fri Jan 17 22:00:00 1997 Path: biosci!TENET.EDU!dashley From: dashley@TENET.EDU (Don Ashley) Newsgroups: bionet.molbio.ageing Subject: RE: Rejuvination ? Date: 17 Jan 1997 20:22:25 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 19 Sender: daemon@net.bio.net Distribution: world Message-ID: References: NNTP-Posting-Host: net.bio.net Does this mean that if I can remember something from my childhood, those memory cells have been alive for 40 years? If not, how do the new memory cells take on the memory of the cells that die? > For instance, if brain cells could > be made to clone or regenrate themselves, would people lose their > memories and individuality? > > -- Enric > > >>>>>>>>>>>>>>>>>>>>>>>>>>>>>> > Yes, they would lose memories and their individuality. > If you want to know why check out http://www.aston.ac.uk/~batong/Neutronics > and ask for an email copy of Correlational Opponent- Processing. > Ron Blue > > > From owner-ageing@net.bio.net Fri Jan 17 22:00:00 1997 Path: biosci!bcm.tmc.edu!cs.utexas.edu!uwm.edu!newsfeeds.sol.net!news.maxwell.syr.edu!news.bc.net!unixg.ubc.ca!rover.ucs.ualberta.ca!mongol.sasknet.sk.ca!news@mongol.sasknet.sk.ca From: Asha Newsgroups: bionet.molbio.ageing,sci.bio.misc,sci.med.diseases.cancer,sci.med.immunology,sci.life-extension,sci.bio.technology,sci.med.nutrition,sci.med.pathology,sci.med.cardiology,sci.med,sci.med.pharmacy,alt.health,bionet.biology.cardiovascular,can.med.misc Subject: Theory of Aging and Disease - Please Comment Date: Fri, 17 Jan 1997 23:08:39 -0600 Organization: SaskNet News Distribution Lines: 251 Message-ID: <32E05AD7.35B8@sk.sympatico.ca> NNTP-Posting-Host: kamov46.sk.sympatico.ca Mime-Version: 1.0 Content-Type: text/plain; charset=iso-8859-1 Content-Transfer-Encoding: 8bit X-Mailer: Mozilla 2.02E-SYMPA (Win16; I) Xref: biosci bionet.molbio.ageing:3155 sci.bio.misc:7034 sci.med.diseases.cancer:15326 sci.med.immunology:8720 sci.life-extension:16477 sci.bio.technology:6816 sci.med.nutrition:57428 sci.med.pathology:4314 sci.med.cardiology:7492 sci.med:147644 sci.med.pharmacy:39696 bionet.biology.cardiovascular:1445 Hello, Please reply I am looking for comments or input on the following theory of aging. Anyone interested in further information on this topic or on Coenzyme Q10 can refer to our internet site at http://www.nethomes.com/asha Please mail your comments to asha@sk.sympatico.ca Ubiquinone is an essential electron and protein carrier in ATP synthesis in the mitochondrial inner membrane. Besides its well-established role in energy production in aerobic organisms, ubiquinone is required for transmembrane electron transport that activates signals in the cell which stimulate cell growth.[2] Ubiquinol, the reduced form of ubiquinone, acts as a lipophilic antioxidant, preventing initiation and/or propagation of free radicals and lipid peroxidation in biological membranes, and is the only known lipid soluble antioxidant that animal cells can synthesize de novo.[9] There is accumulating evidence that ubiquinone and possibly other components of the mevalonate pathway, such as dolichol and dolichyl phosphate, could be important in various disease and senescence mechanisms. The evidence relates to mitochondrial and cell energetics, accumulation of damage to DNA, cell signaling, saturation kinetics of mitochondrial enzymes, and clinical data. Aged cells contain partly altered mitochondria that are less able to fulfill their energy requirements so that a general lowering of homeostasis and increased susceptibility is obtained.[16,21] When oxidative phosphorylation decreases below an energetic threshold, disease symptoms appear and cell degeneration results if energy production decreases further.[16] Analysis of mitochondrial respiratory chain function and mitochondrial DNA deletion with aging has shown that between the ages of 20-30 and 60-90, there are large and significant decreases in the activities of Complexes I and IV, which decrease by 59% and 47% respectively.[1] Although deletions of mt DNA increase with age,[1] it is not certain whether this is in itself responsible for the decline in ATP production. At least one type of fatal mitochondrial disease due to mt DNA depletion has been shown to be under control of the nuclear genome.[3] It is possible that general lowered homeostasis due to a related process results in accumulation of errors in those regions of the nuclear genome that control mt DNA depletion. Evidence to support an accumulation of errors is that the repair of carcinogen-induced DNA damage is age dependent, and falls rapidly with increasing age.[5] Alteration and decline of respiratory chain enzyme activity decreases the maximal rate of ATP formation in old cells, forcing the cells to adapt to a declining availability of energy for biosynthesis and repair. A new equilibrium will be established for the particular level of energy that is available to the cell.[16] The concentration of ubiquinone falls with increasing age in all tissues analyzed in both humans, and rats.[14] As ubiquinone levels decrease dolichol levels increase, indicating a shift in the regulation of the related pathways of dolichol, ubiquinone, and cholesterol synthesis. Dolichol destabilizes model membranes and increases fluidity and permeability.[17] This shift in the pathway could alter the role of ubiquinone in signaling for cell growth, and a reduction of ubiquinone’s mitogenic properties could indirectly lead to accumulation of DNA damage and reduction of cell viability. Complex I activity shows a drastic decrease in activity in rats and humans, resulting from a defect in the complex. Levels of complex III activity and ubiquinone in the inner membrane of the mitochondria remain unaltered with increasing age in rats.[10] Ubiquinone is the rate-limiting compound of the activity of complexes I and III but not of complexes II and IV.[18] Therefore lowered ATP synthesis results both directly and indirectly from the shift in mevalonate regulation, and not from an actual lack of ubiquinone in the mitochondria. This regulation of the cell’s energy and developmental program could function as a type of feedback amplification, where a small shift in regulation is the direct cause of further shifts. If these shifts in regulation are major inducers of pathological conditions, then their specific mechanisms would explain the widely observed exponential increase of disease and disease related mortality. Under conditions in which the activities of the various complexes are sub-optimal, increasing the concentration of ubiquinone within the mitochondrial inner membrane will cause an increase in the production of ATP due to ubiquinone being the rate limiting compound for complex I. Ubiquinone concentration within the mitochondrial inner membrane can control the efficiency of oxidative phosphorylation, and addition of exogenous ubiquinone enhances respiratory turnover above the physiological rate but without reaching theoretical maximum velocity of the reaction.[4] Various ubiquinone homologs stimulate respiratory activities in isolated mitochondria.[15] In cultured myocardial cells, only long chain ubiquinone homologs stimulate the formation of ATP, homologs with shorter side chains are toxic.[6] Ubiquinone is currently being investigated as a treatment for various diseases, and is already in use as a safe and effective treatment for heart failure. Administration of ubiquinone improves contractility and ejection fraction in heart failure,[12] and can significantly increase myocardial function and work capacity in normal sedentary people and in patients with mitochondrial disease.[20] Potential therapeutic uses include arterial hypertension, mitochondrial myopathies, muscular dystrophies, angina pectoris, and periodontal diseases,[7] and preliminary results from case trials have yielded remarkable results in the treatment of breast cancer.[11] Statistical data support prediction of death within 6 months in hospitalized patients with low blood levels of ubiquinone,[13] and deficiency of ubiquinone is observed in several pathological conditions. The major degenerative diseases that are leading causes of mortality, increase at an exponential rate that is independent of various environmental factors recognized as being causal in the development of these diseases. Although different epidemiological sub-populations have different risks of succumbing to a particular degenerative disease, each population will experience a similar if not identical exponential increase in disease frequency. The dramatic increase of degenerative diseases seen with increasing age may be the results of a common mechanism. One underlying factor is the cause of the major disease of morbidity and mortality in humans. Research on the mevalonate pathway, primarily those branches leading to the synthesis of dolichol and ubiquinone, when analyzed statistically and linked to a novel theory of disease etiology, lead to the possibility that these branches are directly involved in the progression of the major degenerative diseases. I have compiled several charts using tissue lipid data taken from reference 14, combined these data with age specific death rates and analyzed the result statistically. There is a very strong statistical correlation between the increase in mortality (and of the incidence of degenerative disease) of human populations beginning at approximately age 20, and the shift in the regulation of the related pathways of ubiquinone, dolichol and cholesterol synthesis. When different tissues from human and rats of varying ages are analyzed for concentrations of cholesterol, dolichol , and dolichyl phosphate, and these results are regressed against expected age-specific rates of mortality, very high correlation coefficients are produced. These show that the regulation of the pathway is altered with age in both humans and rats, in the direction of increased cholesterol, dolichol, and dolichyl phosphate, and lowered ubiquinone. Furthermore, for seven different human tissues, the dolichol/ubiquinone ratio, when regressed against age specific death rates, produces correlation coefficients which range between r=0.9858 and r=0.999954. The one factor underlying morbidity and mortality in humans may be this alteration in the mevalonate pathway. It has been thoroughly established that caloric restriction can lengthen both mean and maximum life span in mammals, reduce the frequency of degenerative diseases, and delay their onset.[21] The dietary restriction model of senescence is likely interrelated to the alterations in regulation of the mevalonate pathway, and indeed may be explained by it. Dietary restriction leads to low blood glucose levels, which in turn stimulate the release of glucagon. Glucagon has a range of effects on different pathways, including the mevalonate pathway.[22] Increased glucagon levels inhibit glycolysis by lowering the level of the intermediate fructose-2,6-bisphosphate, which is an inhibitor of fructose-1,6-phosphatase and an activator of phosphofructokinase-1. Glucagon also inhibits pyruvate kinase, so that pyruvate is prevented from entering the citric acid cycle, and the resulting accumulation of phosphoenol pyruvate favors gluconeogenesis.[22] As long as caloric restriction is not too severe, and is maintained over long period of time, there should be no increase in acetyl-CoA due to fatty acid metabolism, and there would not be an increase in the level of precursors of the mevalonate pathway. In addition, an increased level of glucagon itself is sufficient to inhibit HMG-CoA reductase,[22] and thereby would actually decrease the level of mevalonate. Mevalonate is at a major control point in this pathway, and is converted into farnesyl pyrophosphate, common precursor to the cholesterol, ubiquinone, and dolichol synthetic pathways. Due to the differential Km of squalene synthase, cis-prenyl transferase, and trans-prenyl transferase, a decreased level of the substrate farnesyl pyrophosphate would lead to a shift in the production of the three end products, and to a shift in the dolichol/ubiquinone ratio. This shift in regulation resulting from dietary restriction could explain the unique effectiveness of dietary restriction as a method of retarding the actuarial rate of aging and of extending mean and maximum life span in mammals. Arin Elliott Asha Pharma Co. http://www.nethomes.com/asha References 1. Cooper, J. Analyses of mitochondrial respiratory chain function and mitochondrial DNA deletion in human skeletal muscle: effect of ageing. Journal of Neurological Science (1992) 113(1): 91-8. 2. Sun, I. Requirement for coenzyme Q in plasma membrane electron transport. Proc-Natl-Acad-Sci-USA (1992) 89: 11126-30. 3. Bodnar, A. Nuclear complementation restores mt DNA levels in cultured cells from a patient with mt DNA depletion. American Journal of Human Genetics. (1993) 53(3): 663-9. 4. Battino, M. Coenzyme Q can control the efficiency of oxidative phosphorylation. International Journal of Tissue Reactions. (1990) 12(3); 137- 44. 5. Ball, S. DNA damage and repair in female C57BL/10 mice of different ages injected with the carcinogen benzo(a)pyrene-trans-7,8-diol. Mutation Research. (1989) 219(4): 241-6. 6. Kishi, T. Cardiostimulatory action of coenzyme Q homologs on cultured myocardial cells and their biochemical mechanisms. Clinical Investigator (1993) 71: S71-5. 7. Mortensen, S. Perspectives on therapy of cardiovascular disease with coenzyme Q (ubiquinone). Clinical Investigator (1993) 71: S116-23. 8. Crane, F. The essential functions of coenzyme Q. Clinical Investigator (1993) 71: S55-9. 9. Ernster, L. Ubiquinol: an endogenous antioxidant in aerobic organisms. Clinical Investigator (1993) 71: S60-5. 10. Lenaz, G. The function of coenzyme Q in mitochondria. Clinical Investigator (1993) 71: S66-70. 11. Lockwood, K. Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10. Biochemical and Biophysical Research Communications (1994) 199(3): 1504-8. 12. Rengo, F. Role of metabolic therapy in cardiovascular disease. Clinical Investigator (1993) 71: S124-8. 13. Jameson, S. Statistical data support prediction of death within 6 months on low levels of coenzyme Q10 and other entities. Clinical Investigator (1993) 71: S137-9. 14. Kalen, A. Age related changes in the lipid compositions of rat and human tissues. Lipids (1989) 24(7): 579-84. 15. Lenaz, G. Coenzyme Q saturation kinetics of mitochondrial enzymes: theory, experimental aspects and biomedical implications. Biomedical and Clinical Aspects of Coenzyme Q. (1991) 11-18. 16. Corbisier, P. Influence of the energetic pattern of mitochondria in cell ageing. Mechanisms of Ageing and Development (1993) 71: 47-58. 17. Appelkvist, E. Effects of inhibitors of hydroxymethylglutaryl coenzyme A reductase on coenzyme Q and dolichol biosynthesis. Clinical Investigator (1993) 71: S97-102. 18. Maurer, I. Positive correlation between aortic valve pressure gradient and mitochondrial respiratory chain capacity in hypertrophied human left ventricles. Clinical Investigator (1992) 70: 896-901. 19. Kanazawa, M. Coenzyme Q10 by fermentation. Biomedical and Clinical aspects of coenzyme Q volume 3. (1981) 31-42. 20. Zeppilli, P. Influence of coenzyme Q10 on physical work capacity in athletes, sedentary people and patients with mitochondrial disease. Biomedical and Clinical Aspects of Coenzyme Q volume 6 (1991) 541-5. 21. Walford, R. The Retardation of Aging and Disease by Dietary Restriction. (1986). 22. Lehninger, A. Principles of Biochemistry. (1993). From owner-ageing@net.bio.net Fri Jan 17 22:00:00 1997 Path: biosci!agate!spool.mu.edu!uwm.edu!newsfeeds.sol.net!news.maxwell.syr.edu!news.bc.net!rover.ucs.ualberta.ca!mongol.sasknet.sk.ca!news@mongol.sasknet.sk.ca From: Asha Newsgroups: bionet.molbio.ageing,sci.bio.misc,sci.med.diseases.cancer,sci.med.immunology,sci.life-extension,sci.bio.technology,sci.med.nutrition,sci.med.pathology,sci.med.cardiology,sci.med,sci.med.pharmacy,alt.health,bionet.biology.cardiovascular,can.med.misc Subject: Coenzyme Q10 Information Date: Sat, 18 Jan 1997 00:01:50 -0600 Organization: SaskNet News Distribution Lines: 19 Message-ID: <32E0674E.6CA6@sk.sympatico.ca> NNTP-Posting-Host: kamov42.sk.sympatico.ca Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.02E-SYMPA (Win16; I) Xref: biosci bionet.molbio.ageing:3156 sci.bio.misc:7036 sci.med.diseases.cancer:15327 sci.med.immunology:8723 sci.life-extension:16478 sci.bio.technology:6818 sci.med.nutrition:57440 sci.med.pathology:4316 sci.med.cardiology:7495 sci.med:147667 sci.med.pharmacy:39706 bionet.biology.cardiovascular:1446 We have a wide variety of information and references available on Coenzyme Q10. Please contact asha@sk.sympatico.ca to request additional information or to answer any questions you may have about Coenzyme Q10 or other antioxidants. http://www.nethomes.com/asha/heart.htm (heart disease) http://www.nethomes.com/asha/breast.htm (breast cancer) http://www.nethomes.com/asha/co10.htm (structural chemistry) Detailed references http://www.nethomes.com/asha/ref2.htm Ordering http://www.nethomes.com/asha/order1.htm Best Regards, -- Asha Pharma asha@sk.sympatico.ca From owner-ageing@net.bio.net Mon Jan 20 22:00:00 1997 Path: biosci!UMABNET.AB.UMD.EDU!aandreye From: aandreye@UMABNET.AB.UMD.EDU ("Alexander Y. Andreyev") Newsgroups: bionet.molbio.ageing Subject: Seminars on Aging and Longevity in USA by Drs.Gavrilov Date: 20 Jan 1997 18:14:24 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 87 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Here is the information about forthcoming seminars. The schedule of further seminars is under construction now and invitations for them are very much welcome. *********************************************************** THE SCHEDULE OF SEMINARS BY DRS.LEONID AND NATALIA GAVRILOV Jan 21-23 - Chicago, Illinois Quadrangle Club (1155 East 57th St., phone 773-702-2550, fax: 773-493-3792) Contact person: Dr.Brian Charlesworth Department of Ecology and Evolution University of Chicago tel.773-702-8942 fax: 773-702-9740 tel.(home): 773-642-1446 E-mail: bcworth@pondside.uchicago.edu Second contact person: Dr.Francie Margolin Center on Aging, Population Research Center NORC and University of Chicago 1155 East 60th Street Chicago IL 60637 Phone: 312-753-7586 Fax: 312-702-3788/753-7886 E-mail: frmar@cicero.spc.uchicago.edu Jan 24-25 - Madison, Wisconsin Ivy Inn, 2355 University Avenue, phone: 608-233-9717 Contact person: Kay Smith (administrator) Institute on Aging 2245 Medical Sciences Center l300 University Avenue Madison, WI 53706 phone:608-262-1818 fax: 608-263-6211 phone (direct): 608-263-6404 E-mail: smithk@ssc.wisc.edu 2nd contact person: Dr.James Crow phone (home): 608-233-6709 phone (office): 608-263-4438 fax: 608-262-2976 E-mail: jfcrow@facstaff.wisc.edu January 27-31 - Baltimore, Gerontology Research Center, NIA, NIH Contact person: Dr.Alex Andreyev 3 Dalecrest Ct., apt.102 Timonium, MD 21093 USA phone: 410-560-7167 E-mail: aandreye@umabnet.ab.umd.edu February 1-4 - Seattle, Aeiveos Sciences Group Contact person: Rajinder Kaul, Scientific Director E-mail: kaul@aeiveos.com ******************************THE END************************************* From owner-ageing@net.bio.net Wed Jan 22 22:00:00 1997 Path: biosci!HUSC.HARVARD.EDU!kaljuvee From: kaljuvee@HUSC.HARVARD.EDU (Jurgen Kaljuvee) Newsgroups: bionet.molbio.ageing Subject: Proliferative Theory of Rejuvenation Date: 22 Jan 1997 23:04:55 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 36 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net As I understood it, the main idea of Fossel's book 'Reversing Human Aging' was that ensuring near-infinite cell division will constitute a repair mechanism for cytoplasmic cellular damage. But how good is this mechanism? That is, can reactivating telomerase and bestowing somatic cells with near-infinite proliferative capacity ensure arresting or even reversing aging, as Fossel claims? True, cells that are particularly heavily damaged will be programmed to apoptosis and replaced by adjacent cells but how will the adjacent cells escape cumulative damage, in both DNA and cytoplasm (isomerization, free radicals etc)? Where is this source of undamaged cells? It seems that for Fossels theory to work we need a source of cells with fresh undamaged DNA but there is no such source unless we design additional, artificial repair mechanisms for the cell. To paraphrase, it seems that it would be difficult to escape the 'normal' pathology (i.e., pathology NOT associated with telomere shortening) and it seems that ensuring the proliferation of cells by reactivating telomerase will extend the lifespan BUT UNDER NO CIRCUMSTANCES STOP AGING OR REVERSE IT (as the title of the book suggests). Thus, using the language of mathematicians, ensuring infinite proliferative capacity is a necessary but not a sufficient condition for arresting aging (because telomere shortening is only one of many causes of aging). So the best we can do in the near future is to get rid of the component of aging associated with telomeres and that should increase the life span a little. I think we cannot yet say by how much, though Fossel predicted 400-500 years (how?). The only experimental evidence for this that I know of (Shay, Wright paper in EMBO) was, though pioneering, not really therapeutic. Is there new evidence out there? I would be happy to hear any comments. Jurgen Kaljuvee kaljuvee@fas.harvard.edu From owner-ageing@net.bio.net Wed Jan 22 22:00:00 1997 Path: biosci!rutgers!gatech!csulb.edu!hammer.uoregon.edu!leto!news.ou.edu!news.ecn.uoknor.edu!news.ysu.edu!odin.oar.net!malgudi.oar.net!nike.heidelberg.edu!NewsWatcher!user From: bhenders@nike.heidelberg.edu (Bethany Henderson) Newsgroups: bionet.molbio.ageing Subject: Progeria Date: Thu, 23 Jan 1997 14:52:05 -0400 Organization: Heidelberg College Lines: 6 Message-ID: NNTP-Posting-Host: 141.139.3.40 I am a college student at Heidelberg College. I would like any general or specific information on the subject of Progeria. Any information would be of great help. Thank you, Bethany Henderson From owner-ageing@net.bio.net Sat Jan 25 22:00:00 1997 Path: biosci!agate!howland.erols.net!newsxfer3.itd.umich.edu!portc01.blue.aol.com!newstf02.news.aol.com!audrey01.news.aol.com!not-for-mail From: djx1@aol.com (DJX1) Newsgroups: bionet.molbio.ageing Subject: Re: Proliferative Theory of Rejuvenation Date: 26 Jan 1997 01:44:18 GMT Organization: AOL http://www.aol.com Lines: 41 Message-ID: <19970126014401.UAA27994@ladder01.news.aol.com> References: NNTP-Posting-Host: ladder01.news.aol.com X-Admin: news@aol.com Hello Jurgen, Thank you for your considered post. You have obviously given this subject (reactivation of telomerase) at least as much thought as have I. I can't offer you anything new at this point in time, but I will be happy to send you some of the information I have gotten from various Web searches on Telomere related topics, and some useful addresses. As far as I can tell, reactivating Telomerase would only act to cease the decrease of telomere length, which would in turn cease cell loss and associated tissue weakening by atrition. This would, perhaps significantly, delay the onset of various opportunistic age-related diseases. In addition, a diet that is not supportive of the organism would still lead to eventual catastrophic system failure and death. The average american diet would kill an immortal in a century! The best Telomerease can hope to do is give us a significant boost, and if augmented by proper diet, exercise, and attitude, perhaps enough of a boost so that when the next breakthrough comes down the road, we'll still be "young" enough and healthy & strong enough, to be able to take advantage of that. If you are seriously researching Telomere and other life-extending information, I would be interested in sharing notes. I am a member of The Life Extension Foundation, which I have found to be of great value, despite their somewhat "commercial" feel at times; and I am actively on a life-extension program of my own design, which has resulted in a great deal more physical vitality and mental clarity and alertness. I'm only 33, but I feel better now than I did in my 20's. I'll be happy to share the details of the program if you're interested. I will send you the other Telomere information I have found (printed most of it to save H.D. space) if you want it as well. Be well! David Xanatos DJX1@aol.com From owner-ageing@net.bio.net Sun Jan 26 22:00:00 1997 Path: biosci!rutgers!news.sgi.com!su-news-hub1.bbnplanet.com!news.bbnplanet.com!cpk-news-hub1.bbnplanet.com!EU.net!uknet!usenet1.news.uk.psi.net!uknet!uknet!yama.mcc.ac.uk!news.york.ac.uk!news From: CHRISTOPHER SWAINSON Newsgroups: bionet.molbio.ageing Subject: They did not find the grail Date: 27 Jan 1997 13:39:23 GMT Organization: The University of York, UK Lines: 23 Message-ID: <5cib6b$5ru@netty.york.ac.uk> NNTP-Posting-Host: biolvig28.york.ac.uk Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 1.2N (Windows; I; 16bit) Ok heres an argument as to why the aging phenomena can not be slowed to any extensive degree. If a gene had occured in any multicelled organism which coded for eternal youth and eternal reproductive status it would quickly proliferate through out life in the same way that genes coding for sexual reproduction have proliferated. However as individual cells age they become worn out and cease to function as well as younger cells. Thus the organism as a whole ages. What nature has not evolved is an organism that keeps replacing all the older cells with new ones. However what nature has been able to do is to ensure that old, worn out organisms die after reproducing and raising offspring, by means of a built in stopclock, so as not to cause specific competition with offspring that are potentially capable of more reproduction. To put it another way genes coding for death have occured and proliferated. My argument therefor is, if you jam this stopclock the organism will still get old and die. Ok it may live a little longer but immortality is totally out of the question. Remember that if evolution was unable to find a way to make immortal organisms which can reproduce forever what chance do we stand? Chris Swainson (genetics undergraduate) From owner-ageing@net.bio.net Sun Jan 26 22:00:00 1997 Path: biosci!agate!howland.erols.net!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: My L.E. program Date: 27 Jan 1997 02:10:00 GMT Organization: AOL http://www.aol.com Lines: 64 Message-ID: <19970127020901.VAA03865@ladder01.news.aol.com> NNTP-Posting-Host: ladder01.news.aol.com X-Admin: news@aol.com Hello all, Several requests came in for the Life extension Program that I am using, so I'll post it here for anyone who is interested... My program (remember, I worked this out for me: 161 lb, 6' 0", age 33 years, excellent health, excellent exercise including hiking/walking min. 3 mi/day, karate training 3x/week, etc. "your results may vary" as they say...) 9 tablets (3am, 3noon, 3pm) "Life Extension Mix", available from Life extension foundation (800) 544-4440 1 capsule (am) "Life Extension Booster", also from LEF. 2 capsule (am, pm) CoQ10, with above, 50mg/capsule 500mg 2x/day interspaced between above, Inositol 500mg 2x/day, with Inositol, Choline Bitartrate 500mg 2x/day, with above, Acetyl-L-carnitine 100mg 2x/day, with above, phosphatidylserine 100mg 2x/day, with above, DMAE 120mg, 2x/day, with above, Ginkgo Biloba extract As soon as the shipment arrives, Iwill also be adding: Hydergine, 5mg, 2x/day Piracetam, 800mg, 2x/day (am, pm) and last, but not least, 3mg, 1x/day @ bedtime, Melatonin. This is the Xanatos Life Extension Personal Program (XLEPP). I and my wife both follow this routine. Note that DHEA is conspicuously absent from the mix- my verdict is still out on the benefit/risk analysis of that touted "fountain of youth drug", at least for men with prostate glands! :) Again, this is the program I developed for myself in conjunction with the research division of my corporation. This information is in no way intended to reflect any hint of suggestion. Each supplement must be evaluated individually by you for your own particular situations. Your doctor may not be familiar with these suplements- a search on the web and a call to LEF (800) 544-4440 will get you a massive amount of information on these and a host of other items which may be of even greater value to you. I hope I have been of assistance to you. Be well! David Xanatos DJX1@aol.com From owner-ageing@net.bio.net Sun Jan 26 22:00:00 1997 Newsgroups: bionet.molbio.ageing Path: biosci!agate!spool.mu.edu!news.sgi.com!su-news-hub1.bbnplanet.com!news.bbnplanet.com!cpk-news-hub1.bbnplanet.com!feed1.news.erols.com!insync!uunet!in2.uu.net!192.35.48.11!hearst.acc.Virginia.EDU!murdoch!avery.med.Virginia.EDU!dsc9w From: dsc9w@avery.med.Virginia.EDU (David Cassarino) Subject: Re: Proliferative Theory of Rejuvenation X-Nntp-Posting-Host: avery.med.virginia.edu Message-ID: Sender: usenet@murdoch.acc.Virginia.EDU Organization: uva References: <19970126014401.UAA27994@ladder01.news.aol.com> Date: Mon, 27 Jan 1997 01:36:14 GMT Lines: 22 The limitations to only focusing on the loss of telomerase in anti-aging therapy have been well-documented, and make it highly unlikely that activating this enzyme alone will have much benefit. An extremely powerful argument against upregulating telomerase activity at all is the fact that this is a characteristic found consistently in cancer cells, which need high telomerase activity to continuosly replicate their DNA. By stimulating abnormal telomerase activity in all our cells, we run the risk of transforming some of them (many cells in our body accumulate mutations during the normal aging process, and some become immortalized, but are eliminated before forming tumors; adding telomerase to these cells would allow them to replicate quicker and increase the changes of metastasis before the IS detects them) and giving ourselves cancer--and premature death, not immortality. -- David S. Cassarino "I wanted to live deep and suck out the MSTP, Neuroscience marrow of life...if it were sublime UVA School of Medicine to know it by experience." dsc9w@virginia.edu -Thoreau From owner-ageing@net.bio.net Tue Jan 28 22:00:00 1997 Path: biosci!INFAR.EPM.BR!SSMAILI.FARM From: SSMAILI.FARM@INFAR.EPM.BR ("Soraya Smaili") Newsgroups: bionet.molbio.ageing Subject: please, help Date: 29 Jan 1997 04:05:48 -0800 Organization: infar Lines: 2 Sender: daemon@net.bio.net Distribution: world Message-ID: <3E864770A1@infar.epm.br> NNTP-Posting-Host: net.bio.net How could I unsubscribe this list? Thank you very much. From owner-ageing@net.bio.net Tue Jan 28 22:00:00 1997 Path: biosci!MAIL.WALDONET.NET.MT!cbonnici From: cbonnici@MAIL.WALDONET.NET.MT (charles Bonnici) Newsgroups: bionet.molbio.ageing Subject: info Date: 29 Jan 1997 07:23:14 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 24 Sender: daemon@net.bio.net Distribution: world Message-ID: <32EFEABF.7B9B@waldonet.net.mt> NNTP-Posting-Host: net.bio.net Dear sir. I am currently reading for a masters degree in Gerontology and Geriatrics at the university of Malta. The subject of my thesis is “Nursing Attitudes towards mobility and safety in institutionalised elderly persons” Would you kindly forward me any relevant leterature about this subject. If you have any relevant information you can either write me on this address; Mr. Remigio Zammit. Dip. Ger. “Falcore” Plot 78 Ta’ l-Ahfar street, Kirkop ZRQ10. Malta. or on this E-mail address; cbonnici@waldonet.net.mt Thanking you in advance. Remigio Zammit. Dip. Ger. From owner-ageing@net.bio.net Wed Jan 29 22:00:00 1997 Path: biosci!bcm.tmc.edu!news.msfc.nasa.gov!newsfeed.internetmci.com!howland.erols.net!cam-news-hub1.bbnplanet.com!news.bbnplanet.com!cpk-news-hub1.bbnplanet.com!news.maxwell.syr.edu!news.bc.net!rover.ucs.ualberta.ca!mongol.sasknet.sk.ca!news@mongol.sasknet.sk.ca From: Asha Newsgroups: bionet.molbio.ageing,sci.med.diseases.cancer,sci.med.immunology,sci.life-extension,sci.bio.technology,sci.med.pathology,sci.med,sci.med.pharmacy Subject: Coenzyme Q10 Information Date: Thu, 30 Jan 1997 02:26:10 -0600 Organization: SaskNet News Distribution Lines: 18 Message-ID: <32F05B22.10F7@sk.sympatico.ca> NNTP-Posting-Host: amiot41.sk.sympatico.ca Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.02E-SYMPA (Win16; I) Xref: biosci bionet.molbio.ageing:3175 sci.med.diseases.cancer:15608 sci.med.immunology:8857 sci.life-extension:16551 sci.bio.technology:6889 sci.med.pathology:4463 sci.med:149136 sci.med.pharmacy:40456 We have a wide variety of information and references available on Coenzyme Q10. Please contact asha@sk.sympatico.ca to request additional information or to answer any questions you may have about Coenzyme Q10. http://www.nethomes.com/asha Detailed references archive http://www.nethomes.com/asha/ref2.htm Ordering http://www.nethomes.com/asha/order1.htm Best Regards, -- Asha Pharma asha@sk.sympatico.ca From owner-ageing@net.bio.net Thu Jan 30 22:00:00 1997 Path: biosci!immortality.org!duane From: duane@immortality.org (Duane Hewitt) Newsgroups: bionet.molbio.ageing Subject: Re: They did not find the grail Date: 31 Jan 1997 05:29:46 -0800 Organization: Immortality, Inc. Lines: 38 Sender: daemon@net.bio.net Distribution: world Message-ID: <32F1F39D.5A03@immortality.org> NNTP-Posting-Host: net.bio.net > Ok heres an argument as to why the aging phenomena can not be slowed to > any extensive degree. > If a gene had occured in any multicelled organism which coded for > eternal youth and eternal reproductive status it would quickly > proliferate through out life in the same way that genes coding for sexual > reproduction have proliferated. > However as individual cells age they become worn out and cease to > function as well as younger cells. Thus the organism as a whole ages. > What nature has not evolved is an organism that keeps replacing all the > older cells with new ones. However what nature has been able to do is to > ensure that old, worn out organisms die after reproducing and raising > offspring, by means of a built in stopclock, so as not to cause specific > competition with offspring that are potentially capable of more > reproduction. To put it another way genes coding for death have occured > and proliferated. > My argument therefor is, if you jam this stopclock the organism will > still get old and die. Ok it may live a little longer but immortality is > totally out of the question. Remember that if evolution was unable to > find a way to make immortal organisms which can reproduce forever what > chance do we stand? > > Chris Swainson (genetics undergraduate) This argument is flawed because the conditions under which multicellular organisms evolve favored those that reproduced quickly and in great number. This may have been done at the expense of later life (antagonistic pleitropy). The genes that cause aging were not selected for that purpose but were caused by the decreasing force of natural selection with age. I would suggest that you read _The Evolutionary Biology of Aging_ by Michael Rose in order to get a background in the evolutionary causes of aging. Duane Hewitt duane@immortality.org From owner-ageing@net.bio.net Thu Jan 30 22:00:00 1997 Path: biosci!TENET.EDU!dashley From: dashley@TENET.EDU (Don Ashley) Newsgroups: bionet.molbio.ageing Subject: Sr Olympics/ H Chron 1/31/97 Date: 31 Jan 1997 07:07:50 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 35 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Please pass this notice along to anyone you know who is minimum age 50. Registration form for the Houston Senior Olympics (HSO) is in Friday 1/31/97 Houston Chronicle 50 Plus section 5. Dates for competition are March 13-23,'97. Entry fee is $22 and includes most events. Minimal add'l fees for golf, dance, bowling. $4 discount for early entry by Monday Feb 3, '97. HSO headquarters phone is 713-551-7250 for info or entry blanks. All participants who make it to the starting line are winners before the gun starts the timer. One primary benefit of entering is the motivation it provides for individuals to concentrate on physical fitness before the competition. Many other benefits follow. The $22 fee is one of the best bargains in fitness available anywhere. Check out the feature on BiRaKit in that section of the Chronicle. There is also a BiRaKit clinic and tournament at the University Club in the Galleria on at. Feb. 1, 1997 9 am. Events for individuals or teams include archery, Basketball, cycling, road race, throwing (football, softball), swimming, track & field (incl discus, javelin, etc), walk, badminton, BiRaKit, Handball, raquetball, horseshoes, table tennis, tennis. Top three placers (gold, silver, bronze) in each event qualify for Texas State Senior Olympics. Others who perform at the state minimum criteria may also compete in state, even if they didn't place. There is even a Senior Olympics competition in Bermuda each year. What else do you need for motivation? Remember, exercise, nutrition, and stress management are the closest things we have to the fountain of youth until they can 'cure the aging process' through technological advances. Don From owner-ageing@net.bio.net Thu Jan 30 22:00:00 1997 Path: biosci!york.ac.uk!cs132 From: cs132@york.ac.uk (christopher swainson) Newsgroups: bionet.molbio.ageing Subject: Re: They did not find the grail Date: 31 Jan 1997 09:36:55 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 42 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net On Fri, 31 Jan 1997 08:29:05 -0500 Duane Hewitt wrote: > From: Duane Hewitt > Date: Fri, 31 Jan 1997 08:29:05 -0500 > Subject: Re: They did not find the grail > To: cs132@york.ac.uk > Cc: ageing@net.bio.net > > > > > This argument is flawed because the conditions under which multicellular > organisms evolve favored those that reproduced quickly and in great > number. This may have been done at the expense of later life > (antagonistic pleitropy). The genes that cause aging were not > selected for that purpose but were caused by the decreasing force of > natural selection with age. > > I would suggest that you read _The Evolutionary Biology of Aging_ by > Michael Rose in order to get a background in the evolutionary causes of > aging. > > Duane Hewitt > duane@immortality.org Thank you very much for your reply Duane. I will track down the book you mentioned and see what I make of it. Chris