From owner-ageing@net.bio.net Sat Jun 01 23:00:00 1996 Path: biosci!bcm.tmc.edu!pendragon!news.msfc.nasa.gov!newsfeed.internetmci.com!news-feed.iguide.com!news.delphi.com!usenet From: Lou Pagnucco Newsgroups: bionet.molbio.ageing Subject: Re: 2nds ageing newsgroup help Date: Sat, 1 Jun 96 21:34:27 -0500 Organization: Delphi (info@delphi.com email, 800-695-4005 voice) Lines: 11 Message-ID: References: <4om72a$6qs@news2.h1.usa.pipeline.com> NNTP-Posting-Host: bos1e.delphi.com X-To: writes: > >hello, i'm an avid lurker in this newsgroup, and i remember once having >another anti-ageing related newsgroup once, but i forgot the name. >naturally having an unquenchable desire for all the anti-aging informatin i >can find, i'd like to know if anyone knows of this other newsgroup. if so >please let me know. thanx > The newsgroup is SCI.LIFE-EXTENSION. From owner-ageing@net.bio.net Sun Jun 02 23:00:00 1996 Newsgroups: bionet.molbio.ageing,bionet.molbio.bio-matrix,bionet.molbio.evolution,bionet.molbio.gene-linkage,bionet.molbio.gene-org,bionet.molbio.methds-reagnts Path: biosci!daresbury!yama.mcc.ac.uk!bofh.dot!thor.cf.ac.uk!news From: Nick Jacobsen Subject: Re: DNA ligation help Sender: news@cf.ac.uk (USENET News System) Message-ID: Date: Mon, 3 Jun 1996 09:19:49 GMT To: xcl@med.unc.edu X-Nntp-Posting-Host: d053.mg.cf.ac.uk Content-Transfer-Encoding: 7bit Content-Type: text/plain; charset=us-ascii References: <4opneu$nke@newz.oit.unc.edu> Mime-Version: 1.0 X-Mailer: Mozilla 1.22 (Windows; I; 16bit) Organization: Institute of Medical Genetics Cardiff Lines: 14 Xref: biosci bionet.molbio.ageing:2740 bionet.molbio.bio-matrix:728 bionet.molbio.evolution:4572 bionet.molbio.gene-linkage:1076 bionet.molbio.methds-reagnts:45232 Hi, I find that the majority of problems with DNA ligation inefficiency are due to ATP degradation in the reaction buffer. If in doubt order new buffer and freeze in small aliquots. You can also order Pharmacia ligase - you have to order separate 10mM ATP with it to add to the reaction as required. You have to be fairly accurate with the amount of ATP added as too much is as bad as too little. I hope this is of help to you cheers Nick Jacobsen. From owner-ageing@net.bio.net Sun Jun 02 23:00:00 1996 Path: biosci!internet!biosci!not-for-mail From: biohelp (BIOSCI Administrator) Newsgroups: bionet.molbio.ageing Subject: IMPORTANT - BIOSCI Fundraising Update! Date: 3 Jun 1996 02:00:47 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 154 Sender: daemon@net.bio.net Distribution: world Message-ID: <199606030900.CAA27651@net.bio.net> NNTP-Posting-Host: net.bio.net BIOSCI is about halfway to its funding goal!! I'm interrupting the usual monthly posting of the BIOSCI miniFAQ to bring you up to date on BIOSCI fundraising progress, a topic of concern to your future use of this resource. Thank you in advance for taking the time to read this message carefully. Last year we announced that BIOSCI was going to adopt the U.S. Public Broadcasting System model to fund its operations after our DOE/NSF grant runs out later this year. Unlike PBS, we are not soliciting contributions from users; we are only selling ads on our Web pages solely to cover our operating costs. Our goal is to seek sponsorships until we build up an operating reserve of about $100,000 and then cease further promotions until we need to build the reserve back up. (The accountants among our readership will be familiar with the problem of deferred revenue which we can not safely utilize until ads have been displayed for a period of time.) We are only about halfway to our funding goal and need to raise further funds to avoid having to curtail services at net.bio.net. Fundraising is time-consuming, however, and we need your help as explained further below. Our operating costs consist of our network connection, phone lines, hardware maintenance (we will be getting newer and faster hardware soon!), plus 0.7 FTE of salaries covering UNIX systems admin, technical support, quality assurance, i.e., testing, of our system, and administrative costs (such as the time it takes to actually find/write/call potential sponsors and raise money!). Although the BIOSCI staff does get compensated for a portion of the work that they do, this project has always received a lot of free after-hours and "vacation" time labor, so we hope that no one will begrudge the time that we do charge to the project to serve you. All of the three part-time staff members, Dave Mack, Julie Lawrence, and myself, have full time day jobs and families in addition to working hard to keep this service running for all of you. Julie and Dave Mack are subcontractors for BIOSCI; my time that is charged to the project defrays a portion of my regular salary instead of adding to my income. Besides having to relocate the project, we were very busy this last year building new infrastructure such as our WWW hypermail interface to the system. This was released last December along with scores of WAIS indices for the newsgroups. Virtually everything is complete, although we do continue to find and fix bugs (many through your helpful feedback!). We are still having some problems with our WAIS indexing. The archives continue to grow rapidly. We are running over 100 indexes now versus three previously and any systems crashes cause greater havoc with the indexing than before! We are still working to fix this as fast as our resources permit and appreciate your patience, but we have been able to automate a lot of the infrastructure to reduce labor as compared to past requirements. We have also implemented new software to make moderation of BIOSCI/bionet newsgroups much easier and combat the growing problem of Internet junk mail and USENET "spamming." About 20% of our groups are now moderated, many of them by the BIOSCI staff! This, for example, made a major difference last year in the quality of content in our EMPLOYMENT/bionet.jobs.offered newsgroup which many commercial concerns and recruiting firms are using **without charge** to recruit candidates for positions in the biological sciences. We are also now in a position to have sponsors for individual newsgroups as you will have noticed if you have visited http://www.bio.net/ and clicked on "Access the BIOSCI/bionet newsgroups" recently. So, how can you help?? ---------------------- As noted above it can take a lot of time to contact potential sponsors if I have to do it all myself. Our request is quite simple. You can do two important things which will take very little time for you individually. First, please use our WWW system at http://www.bio.net/ to access the archives. You can now post or reply to messages via your Web browser. 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. Our hope is to quickly raise several large corporate/institutional sponsors on our heavily-used WWW locations (some stats appended below), and then end this sponsorship campaign so that our resources can continue to be used for service provision, not fundraising. Many of our specialty newsgroup WWW archives are still used by small communities of scientists (and they haven't been heavily promoted yet). While these may be valuable niche markets to some advertisers, it will generate more labor and overhead having to find these sponsors, fairly price the locations, and deal with lots of smaller sponsorships than fewer mid-to large sponsors. We are striving to keep our operation as lean and efficient as possible since we are not trying to make careers out of running BIOSCI. We are trying if at all possible to avoid the administrative overhead entailed with processing lots of small payments to reach our fundraising goals. I'd like to thank all of you for your help in advance. In helping us, you are also helping yourselves, not only in keeping this resource available for all of the both large and small research communities that we serve, but also by alleviating the need for us to go back and compete with researchers for tight grant dollars! We promised NSF when we were awarded the BIOSCI grant that we would carry out this mission to make the service self-supporting. With your help, we will succeed in continuing BIOSCI's work into its second decade. Thank you very much! Sincerely, Dave Kristofferson BIOSCI/bionet Manager biosci-help@net.bio.net A list of our prime WWW sponsorship locations follow. Please contact us for further details. ---------------------------------------------------------------------- The overall BIOSCI WWW pages are currently visited by users from close to 5500 unique computer hosts per week. Web servers only log the Internet computer/host name and frequently more than one individual can connect to us from a particular host. Main home page, http://www.bio.net, visited recently by about 2100 unique hosts per week Main Newsgroups archives page, http://www.bio.net/archives.html, visited recently by about 1200 Unique hosts per week BIO-JOURNALS archive page, http://www.bio.net/BIO-JOURNALS.html, visited recently by about 1000 unique hosts per week. EMPLOYMENT archive pages: http://www.bio.net:80/hypermail/EMPLOYMENT/ and monthly header pages, visited recently by about 800 unique hosts per week. Address database search page, http://www.bio.net/addrsearch.html, visited recently by about 450 unique hosts per week. Methods newsgroup archive pages, http://www.bio.net:80/hypermail/METHDS- REAGNTS/ and monthly header pages, visited recently by about 350 unique hosts per week. Ads can also be displayed on various combinations of other BIOSCI/bionet newsgroups. Please contact us at biosci-help@net.bio.net for details. ---------------------------------------------------------------------- From owner-ageing@net.bio.net Sun Jun 02 23:00:00 1996 Path: biosci!bcm.tmc.edu!cs.utexas.edu!chi-news.cic.net!news.compuserve.com!news.production.compuserve.com!news From: Survey Administration <74750.1341@CompuServe.COM> Newsgroups: bionet.microbiology,bionet.molbio.ageing,bionet.molbio.evolution,bionet.molbio.gene-linkage,bionet.molbio.hiv Subject: WE NEED YOUR INPUT Date: 3 Jun 1996 03:18:43 GMT Organization: Kitty Knight Corporation Lines: 25 Message-ID: <4otlij$3ni$5@mhade.production.compuserve.com> Xref: biosci bionet.microbiology:6248 bionet.molbio.ageing:2738 bionet.molbio.evolution:4571 bionet.molbio.gene-linkage:1075 bionet.molbio.hiv:2349 Please excuse this brief intrusion, but we are trying to locate any and all holders of academic degrees conferred within the last ten (10) years. The Kitty Knight Corporation, Boston, MA, is currently searching for qualified individuals to participate in a ***PAID*** study focusing on post-secondary, graduate, and professional education in the United States. Holders of ALL types of degrees in ALL fields of study are needed. We would like to hear from you as long as your degree was earned at an accredited institution in the United States. After an initial screening, qualified participant will be asked to complete a questionaire of approx 150 questions. Everyone who completes the survey will receive a $100 stipend. Naturally, *ALL* information will be held in the strictest confidence. To express interest, please send your name, mailing address, and photocopies of **ALL** degrees you have earned to: The Kitty Knight Corporation, Attn: Study 96-3H, Back Bay Annex, P O Box 546, Boston, MA 02117. (If not obvious from the degree, please indicate the field of study.) Thank You Very Much! From owner-ageing@net.bio.net Sun Jun 02 23:00:00 1996 Newsgroups: bionet.molbio.ageing,bionet.molbio.bio-matrix,bionet.molbio.evolution,bionet.molbio.gene-linkage,bionet.molbio.gene-org,bionet.molbio.methds-reagnts Path: biosci!daresbury!yama.mcc.ac.uk!bofh.dot!thor.cf.ac.uk!news From: Nick Jacobsen Subject: Re: DNA ligation help Sender: news@cf.ac.uk (USENET News System) Message-ID: Date: Mon, 3 Jun 1996 09:20:12 GMT To: xcl@med.unc.edu X-Nntp-Posting-Host: d053.mg.cf.ac.uk Content-Transfer-Encoding: 7bit Content-Type: text/plain; charset=us-ascii References: <4opneu$nke@newz.oit.unc.edu> Mime-Version: 1.0 X-Mailer: Mozilla 1.22 (Windows; I; 16bit) Organization: Institute of Medical Genetics Cardiff Lines: 14 Xref: biosci bionet.molbio.ageing:2741 bionet.molbio.bio-matrix:729 bionet.molbio.evolution:4573 bionet.molbio.gene-linkage:1077 bionet.molbio.methds-reagnts:45233 Hi, I find that the majority of problems with DNA ligation inefficiency are due to ATP degradation in the reaction buffer. If in doubt order new buffer and freeze in small aliquots. You can also order Pharmacia ligase - you have to order separate 10mM ATP with it to add to the reaction as required. You have to be fairly accurate with the amount of ATP added as too much is as bad as too little. I hope this is of help to you cheers Nick Jacobsen. From owner-ageing@net.bio.net Sun Jun 02 23:00:00 1996 Newsgroups: bionet.molbio.ageing,bionet.molbio.bio-matrix,bionet.molbio.evolution,bionet.molbio.gene-linkage,bionet.molbio.gene-org,bionet.molbio.methds-reagnts Path: biosci!daresbury!yama.mcc.ac.uk!bofh.dot!thor.cf.ac.uk!news From: Nick Jacobsen Subject: Re: DNA ligation help Sender: news@cf.ac.uk (USENET News System) Message-ID: Date: Mon, 3 Jun 1996 09:21:04 GMT To: xcl@med.unc.edu X-Nntp-Posting-Host: d053.mg.cf.ac.uk Content-Transfer-Encoding: 7bit Content-Type: text/plain; charset=us-ascii References: <4opneu$nke@newz.oit.unc.edu> Mime-Version: 1.0 X-Mailer: Mozilla 1.22 (Windows; I; 16bit) Organization: Institute of Medical Genetics Cardiff Lines: 14 Xref: biosci bionet.molbio.ageing:2744 bionet.molbio.bio-matrix:732 bionet.molbio.evolution:4576 bionet.molbio.gene-linkage:1080 bionet.molbio.methds-reagnts:45236 Hi, I find that the majority of problems with DNA ligation inefficiency are due to ATP degradation in the reaction buffer. If in doubt order new buffer and freeze in small aliquots. You can also order Pharmacia ligase - you have to order separate 10mM ATP with it to add to the reaction as required. You have to be fairly accurate with the amount of ATP added as too much is as bad as too little. I hope this is of help to you cheers Nick Jacobsen. From owner-ageing@net.bio.net Sun Jun 02 23:00:00 1996 Newsgroups: bionet.molbio.ageing,bionet.molbio.bio-matrix,bionet.molbio.evolution,bionet.molbio.gene-linkage,bionet.molbio.gene-org,bionet.molbio.methds-reagnts Path: biosci!daresbury!yama.mcc.ac.uk!bofh.dot!thor.cf.ac.uk!news From: Nick Jacobsen Subject: Re: DNA ligation help Sender: news@cf.ac.uk (USENET News System) Message-ID: Date: Mon, 3 Jun 1996 09:20:58 GMT To: xcl@med.unc.edu X-Nntp-Posting-Host: d053.mg.cf.ac.uk Content-Transfer-Encoding: 7bit Content-Type: text/plain; charset=us-ascii References: <4opneu$nke@newz.oit.unc.edu> Mime-Version: 1.0 X-Mailer: Mozilla 1.22 (Windows; I; 16bit) Organization: Institute of Medical Genetics Cardiff Lines: 14 Xref: biosci bionet.molbio.ageing:2743 bionet.molbio.bio-matrix:731 bionet.molbio.evolution:4575 bionet.molbio.gene-linkage:1079 bionet.molbio.methds-reagnts:45235 Hi, I find that the majority of problems with DNA ligation inefficiency are due to ATP degradation in the reaction buffer. If in doubt order new buffer and freeze in small aliquots. You can also order Pharmacia ligase - you have to order separate 10mM ATP with it to add to the reaction as required. You have to be fairly accurate with the amount of ATP added as too much is as bad as too little. I hope this is of help to you cheers Nick Jacobsen. From owner-ageing@net.bio.net Sun Jun 02 23:00:00 1996 Newsgroups: bionet.molbio.ageing,bionet.molbio.bio-matrix,bionet.molbio.evolution,bionet.molbio.gene-linkage,bionet.molbio.gene-org,bionet.molbio.methds-reagnts Path: biosci!daresbury!yama.mcc.ac.uk!bofh.dot!thor.cf.ac.uk!news From: Nick Jacobsen Subject: Re: DNA ligation help Sender: news@cf.ac.uk (USENET News System) Message-ID: Date: Mon, 3 Jun 1996 09:20:40 GMT To: xcl@med.unc.edu X-Nntp-Posting-Host: d053.mg.cf.ac.uk Content-Transfer-Encoding: 7bit Content-Type: text/plain; charset=us-ascii References: <4opneu$nke@newz.oit.unc.edu> Mime-Version: 1.0 X-Mailer: Mozilla 1.22 (Windows; I; 16bit) Organization: Institute of Medical Genetics Cardiff Lines: 14 Xref: biosci bionet.molbio.ageing:2742 bionet.molbio.bio-matrix:730 bionet.molbio.evolution:4574 bionet.molbio.gene-linkage:1078 bionet.molbio.methds-reagnts:45234 Hi, I find that the majority of problems with DNA ligation inefficiency are due to ATP degradation in the reaction buffer. If in doubt order new buffer and freeze in small aliquots. You can also order Pharmacia ligase - you have to order separate 10mM ATP with it to add to the reaction as required. You have to be fairly accurate with the amount of ATP added as too much is as bad as too little. I hope this is of help to you cheers Nick Jacobsen. From owner-ageing@net.bio.net Sun Jun 02 23:00:00 1996 Path: biosci!bcm.tmc.edu!pendragon!news.msfc.nasa.gov!elroy.jpl.nasa.gov!lll-winken.llnl.gov!fnnews.fnal.gov!unixhub!news.Stanford.EDU!not-for-mail From: ladasky@leland.Stanford.EDU (John Ladasky) Newsgroups: bionet.molbio.ageing,bionet.molbio.bio-matrix,bionet.molbio.evolution,bionet.molbio.gene-linkage,bionet.molbio.gene-org,bionet.molbio.methds-reagnts Subject: Re: DNA ligation help Followup-To: bionet.molbio.methds-reagnts Date: 3 Jun 1996 10:47:29 -0700 Organization: Stanford University, CA 94305, USA Lines: 23 Message-ID: <4ov8fh$7gm@elaine35.Stanford.EDU> References: <4opneu$nke@newz.oit.unc.edu> NNTP-Posting-Host: elaine35.stanford.edu Xref: biosci bionet.molbio.ageing:2745 bionet.molbio.bio-matrix:733 bionet.molbio.evolution:4577 bionet.molbio.gene-linkage:1081 bionet.molbio.methds-reagnts:45260 Followups have been limited to bionet.molbio.methds-reagnts. In article <4opneu$nke@newz.oit.unc.edu>, chunlin xin wrote: >Hi, there, I have trouble in DNA ligation, the case below: > Insert Fragment: 16.3kb SalI Frag. > Vector: Bscrip-KS(-) SalI cut plasmid or other > salI cut expression vector > It looks like no ligation problem, but in fact, I cannot >success to ligate them and transfer them into DH5a no matter I use >chemical or electroparation method, Have anybody ever meet the same problem? >How can I solve them? Any suggestion is appreciated! Thanks for you attention! A 16.3 Kb insertion is quite large. DH5-alpha, and most other normal strains of E. coli, cannot reliably maintain plasmids larger than 10 Kb. (I'm not sure why this is so.) So your ligation and transformation may both be successful, but then you are not getting any ampicillin-resistant colonies. Can you subclone this fragment? -- Unique ID : Ladasky, John Joseph Jr. Title : BA Biochemistry, U.C. Berkeley, 1989 (Ph.D. perhaps 1998???) Location : Stanford University, Dept. of Structural Biology, Fairchild D-105 Keywords : immunology, music, running, Green From owner-ageing@net.bio.net Thu Jun 06 23:00:00 1996 Path: biosci!daresbury!not-for-mail From: jcoward@mail.islandnet.com (Jim Coward) Newsgroups: bionet.molbio.ageing Subject: ITCH'96 - APPROPRIATE SYSTEMS/APPROPRIATE DECISIONS Date: 7 Jun 1996 20:43:37 +0100 Lines: 16 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <4pa0p9$k5h@mserv1.dl.ac.uk> X-Sender: jcoward@mail.islandnet.com (Unverified) Original-To: JHCoward@bcsc02.gov.bc.ca ITCH'96 "APPROPRIATE SYSTEMS / APPROPRIATE DECISION" Victoria BC Canada - November 3-6 1996 ITCH'96 Is a high-quality, international conference that will provide an excellent forum for health professionals, physicians, and information and computer systems experts to present and exchange ideas and research results in the general areas of information technology for community health. Please visit the website at: http://www.hsd.uvic.ca/HIS/ITCH/ITCH.htm or send email for information to: ITCH@HSD.UVIC.CA James H. Coward, CHE, Management Consultant, Cordova Bay Consultants, inc. ITCH'96 Orgnanizing Committee - Sponsors, Exhibitors and Promotion 754 Doral Place, Victoria, BC Can V8Y 3C9 FAX (604) 658-6394 Tel: (604) 881-2537 JCoward@IslandNet.com Web: http://www.islandnet.com/`jcoward/homepage.htm From owner-ageing@net.bio.net Thu Jun 06 23:00:00 1996 Path: biosci!rutgers!uwm.edu!chi-news.cic.net!nntp.coast.net!howland.reston.ans.net!vixen.cso.uiuc.edu!newsfeed.internetmci.com!in2.uu.net!r2d2.fdn.org!med.univ-tours.fr!univ-angers.fr!jussieu.fr!unilim.fr!cict.fr!news From: melan@cict.fr (Jeff CAMPS) Newsgroups: bionet.microbiology,bionet.molbio.ageing,bionet.neuroscience,bionet.neuroscience.amyloid,bionet.toxicology Subject: Re: New Lab-Animal Res. Equip. Catalog Date: 7 Jun 1996 12:42:04 GMT Organization: Laboratoire de Neurobiologie du Comportement Lines: 31 Message-ID: <4p982s$afj@news.cict.fr> References: <4p86n8$mke$2@mhadf.production.compuserve.com> NNTP-Posting-Host: 130.120.104.81 Mime-Version: 1.0 Content-Type: Text/Plain; charset=ISO-8859-1 X-Newsreader: WinVN 0.99.5 Xref: biosci bionet.microbiology:6288 bionet.molbio.ageing:2747 bionet.neuroscience:14489 bionet.neuroscience.amyloid:471 bionet.toxicology:753 In article <4p86n8$mke$2@mhadf.production.compuserve.com>, 75144.2413@CompuServe.COM says... > >We at Columbus Instruments just published new 60-page Lab-Animal >Research Equipment Catalog. You will be able to find description >of over 60 scintific instruments for toxicology, pharmacology, >brain scinces, environmental scinces, physiology etc. >Cardiac Output Computers for mice and rats based on >thermodilution, animal activity meters based of TV camera and IR >beams, mazes, end tidal CO/N2O computers for rats and mice, >VO2/VCO2 metabolic computers ( indirect calorimeters) for rats, >dogs and horses, precission gas analyzers, bacteria respirometers >and many more equipment is described on the new catalog pages. >If you are intersted to receive a free copy and price list, >please e-mail your STREET ADDRESS to: >Jan Czekajewski >75144.2413@compuserve.com Please, could you send me one copy to Jean-François CAMPS laboratory of neurobiology and animal behavior U.F.R. S.V.T. , bat 4R3 university Paul SABATIER, TOULOUSE III 118 route de Narbonne, F-31062 TOULOUSE CEDEX FRANCE. best regards From owner-ageing@net.bio.net Thu Jun 06 23:00:00 1996 Path: biosci!rutgers!uwm.edu!chi-news.cic.net!news.compuserve.com!news.production.compuserve.com!news From: PG <75144.2413@CompuServe.COM> Newsgroups: bionet.microbiology,bionet.molbio.ageing,bionet.neuroscience,bionet.neuroscience.amyloid,bionet.toxicology Subject: New Lab-Animal Res. Equip. Catalog Date: 7 Jun 1996 03:12:40 GMT Organization: CI Lines: 14 Message-ID: <4p86n8$mke$2@mhadf.production.compuserve.com> Xref: biosci bionet.microbiology:6285 bionet.molbio.ageing:2746 bionet.neuroscience:14481 bionet.neuroscience.amyloid:470 bionet.toxicology:747 We at Columbus Instruments just published new 60-page Lab-Animal Research Equipment Catalog. You will be able to find description of over 60 scintific instruments for toxicology, pharmacology, brain scinces, environmental scinces, physiology etc. Cardiac Output Computers for mice and rats based on thermodilution, animal activity meters based of TV camera and IR beams, mazes, end tidal CO/N2O computers for rats and mice, VO2/VCO2 metabolic computers ( indirect calorimeters) for rats, dogs and horses, precission gas analyzers, bacteria respirometers and many more equipment is described on the new catalog pages. If you are intersted to receive a free copy and price list, please e-mail your STREET ADDRESS to: Jan Czekajewski 75144.2413@compuserve.com From owner-ageing@net.bio.net Fri Jun 07 23:00:00 1996 Path: biosci!bcm.tmc.edu!cs.utexas.edu!howland.reston.ans.net!newsfeed.internetmci.com!usenet.eel.ufl.edu!tank.news.pipex.net!pipex!oleane!jussieu.fr!univ-lyon1.fr!in2p3.fr!swidir.switch.ch!scsing.switch.ch!news.belwue.de!news.uni-stuttgart.de!uni-regensburg.de!lrz-muenchen.de!uni-erlangen.de!winx03!news From: Gerald Muench Newsgroups: bionet.molbio.ageing Subject: Ph.D. fellowship, Alzheimer's Date: 8 Jun 1996 08:20:50 GMT Organization: Theodor-Boveri-Institut fuer Biowissenschaften Lines: 64 Message-ID: <4pbd52$7i8@winx03.informatik.uni-wuerzburg.de> NNTP-Posting-Host: wbza25.biozentrum.uni-wuerzburg.de Mime-Version: 1.0 Content-Type: text/plain; charset=iso-8859-1 Content-Transfer-Encoding: 8bit X-Mailer: Mozilla 1.12(Macintosh; I; PPC) X-URL: news:bionet.molbio.ageing A Ph. D. fellowship for 2 years is available at the Department of Physiological Chemistry at the Biocenter of the University of Wuerzburg, Germany. In our esearch program, we investigate the role of Advanced Glycation Endproducts (AGEs) in Alzheimer's disease. The final target will be the development and testing of AGE-inhibitors as therapeutic drugs for the treatment of AD patients. Advanced Glycation Endproducts (AGEs) are formed by a complex cascade of dehydration, oxidation and cyclization reactions, subsequent to a non-enzymatic reaction of sugars with amino groups of proteins (²glycation²). Accumulation of AGE-crosslinked proteins throughout life is a general phenomenon of aging, it is accelerated in diabetes and renal failure. In Alzheimer¹s disease, cerebral AGEs levels in post mortem tissue of are significantly increased, with the highest immunoreactivity seen in neurofibrilary tangles and ß- amyloid plaques. In vitro, formation of insoluble, crosslinked ß-amyloid peptide and MAP-tau is accelerated by AGEs. The AGE-inhibitor tenilsetam (effective against AGE crosslinking in vitro and in animal models) significantly improved clinical and psychometric scores in two phase II clinical trials with Alzheimer¹s disease patients. Our project deals with three major questions: 1. Which factors increase the AGE level in brains of Alzheimer¹s patients ? 2. Which damaging effect do AGEs exert on (neuronal) cells ? 3. How do AGE-inhibitors interfere with AGE-mediated degenerative processes ? The site: Würzburg: www.wuerzburg.de/index.eng.html Capital of Lower Franconiam Inhabitants: 130.000. Located on both sides of the river Main, amid huge parks and vine covered hills. Nearly 50.000 students are living in Würzburg. The Julius-Maximilians-University, newly established in 1582, is he alma mater for more than 20.000 students. Six nobel prize winners have taught there (among them W. C. Röntgen, who discovered X-rays in 1895). The Biocenter: www.biozentrum.uni-wuerzburg.de The founders of the Biocenter deemed a close cooperation of the various disciplines vital in order to prevent a disintegration of Biology. The Biocenter is an interdisciplinary institute for scientific research and learning, comprising 6 biological, 1 chemical, and 3 medical departments. Individuals should have experience with biochemistry and cell culture techniques, preferably in the field of neurobiology. The fellowship is 18 000,- DM/ a (tax free) for 2 years. Although EU citizens are preferred due to immigration regulations, qualified researchers coming outside the EU are also encouraged to apply. Please send a description of research accomplishments, curriculum vitae and the names, addresses and telephone numbers of 2 references to: Dr. Gerald Muench Physiologische Chemie I Theodeor-Boveri-Institut fuer Biowissenschaften (Biozentrum) der Universitaet Am Hubland 97074 Wuerzburg Germany From owner-ageing@net.bio.net Sat Jun 08 23:00:00 1996 Path: biosci!BIOMED.MED.YALE.EDU!public From: public@BIOMED.MED.YALE.EDU (Public Workstation) Newsgroups: bionet.molbio.ageing Subject: "Reversing Human Aging" by M. Fossel Date: 9 Jun 1996 12:47:32 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 67 Sender: daemon@net.bio.net Distribution: world Message-ID: <31BAF175.2B8E@biomed.med.yale.edu> NNTP-Posting-Host: net.bio.net Michael Fossel, MD/PhD has authored a new book on aging "Reversing Human Aging" (William Morrow and Co., Inc, NY 1996). Although he book is written for primarily for laymen, it may be of interest to professionals as most of the arguments are also supported by references to scientific articles. Fossel believes that the evidence accumulated in past five years suggests that aging is due to telomere shortening occuring as a result of cell division. All other theories of aging are explaining secondary phenomena or effects, not the causes, of aging. According to Fossel, to prevent aging, it suffices to 'cap' the telomere with a protein that serves a primar for initiating replication (see the patent application PCT Publication No. 93/23572). To reverse aging, Fossel proposes three methods: (1) open delivery of telomerase or a telomerase-like compound to cells, (2) adding a sequence coding for telomerase to DNA by a vector, and (3) unrepressing the endogeneous telomerase sequence that is not expressed in somatic cells but is expressed in germ cells. Fossel thinks that 3) is most likely to be successful (see also the posting G.J. Griffits in March discussing these three methods). Finally, Fossel optimistically (?) forecasts that first trials on animals will be conducted by the end of the decade, firs clinical trials by 2005 and, by 2015, telomarase therapy should be available to most citizens in the wealthier part of the world (i.e., G-7 countries). Here are a few questions that the book inspired. 1. Should we take this book seriously? Are Fossel's predictions for the timetable of the aging research at all realistic? I hope that more knowledgeable readers of this newsgroup and researchers in the field, in particular, also respond to this question (if you haven't read the book, simply address the plausibility of the telomerase theory). 2. If cell division is used to replace worn-down cells with cells that are capable of maintaining homeostasis, fight free radicals etc., what about cells that don't divide, such as neurons and some muscle cells (if I remember correctly)? Shouldn't neurons wear down eventually and thus impose a limit to lifespan, even if we can sustain the immortality of other cells by a telomarase inducer? (I hope this is a sensible question, though I have a feeling that I'm missing a simple point somewhere). 3. Is it plausible that we will be able to engineer a narrow 'corridor' in which we can induce enough telomarase to stop, or even reverse, aging, but not enough to cause cancer in cell? What is the 'limiting condition' for such a corridor? The discussion between Jean-Pierra Issa of Johns Hopkins and Mike West of Geron has been very useful, but I would love to see some third opinions and/or a reiteration of the argument. 4. For a college student (or anybody for that matter) who hopes to go on and make a contribution in this fascinating field with massive social implications, what type of graduate education would you recommend and why? Obviously, this is related to the question which theory of aging is the correct one, but I would appreciate any mentorship or advice. Thank you. Jurgen Kaljuvee kaljuvee@fas.harvard.edu From owner-ageing@net.bio.net Sun Jun 09 23:00:00 1996 Path: biosci!AXESS.COM!tonit From: tonit@AXESS.COM (Toni Trepanier) Newsgroups: bionet.molbio.ageing Subject: New Book Date: 10 Jun 1996 08:41:20 -0700 Organization: Life Plus - World Plus Group Lines: 117 Sender: daemon@net.bio.net Distribution: world Message-ID: <31BC4045.2222@axess.com> NNTP-Posting-Host: net.bio.net ------------------------- Subj: NEW BOOK Date: 96-06-10 04:13:38 EDT From: SFSherrill NOTICE to all who are concerned about health and the roll that diet and nutrition have in our lives and the health care system in our country. A new book called "Reclaiming Our Health" by John Robbins will be released sometime in August. It will, no doubt be acclaimed as one of the most important books of our time and will most certainly become a number one best seller. Be sure to pick up a copy. Here are just a few mind-blowing facts you will read about: INFANT MORTALITY and LIFE EXPECTANCY Annual per capita income in Shanghai = $350. Annual per capita income in New York City = $20,500. Annual medical care expenditure in Shanghai = $38 person. Annual medical care expenditure in New York City = $3,000 per person. Annual infant deaths in first year of life in Shanghai = 10.9 per 1000. Annual infant deaths in first year of life in New York City = 13.3 per 1000. Life expectancy at birth in Shanghai = 75.5 years. Life expectancy at birth in New York City = 71.5 years. TOBACCO World's largest private cancer treatment and research center : Memorial Sloan-Kettering. Director, Memorial Sloan-Kettering's Board of Overseers and Managers: John S. Reed. John S. Reed's other job: Director, Philip Morris.(Tobacco Company) Health Insurance Companies heavily invested in tobacco stocks: Travelers, Prudential, Cigna, MetLife, Aetna. Prudential Insurance Company's 1995 investment in tobacco stocks: $248 million. HEART DISEASE: On average, what will the insurance companies pay for? Bypass surgery = $30,000 Balloon angioplasty = $7500 Nutrition and life style education for a heart patient = $150 Teaching a healthy person how to eat well and stay healthy = $0 MENOPAUSE Most widely prescribed drug in U.S.: Premarin (Estrogen Replacement Therapy). Percentage of women who obtained complete relief from hot flashes by taking 200 mg of vitamin C and 200 mg of bioflavonoids 6 times a day = 67%. Percentage of menopausal women who obtained relief from hot flashes by taking two capsules of licorice root, burdock root, wild yam root, dong quai root, and motherwort, 3 times a day in a double-blind placebo-controlled study = 100%! Percentage who obtained relief from placebo = 6%. Percentage of U.S. physicians who discuss natural approaches with their menopausal patients = 2%. Percentage of U.S. physicians who routinely prescribe estrogen = 84%. CANCER Percentage of cancer patients whose lives are saved by chemotherapy = 3%. Evidence for the vast majority of cancers that chemotherapy increases survival rate or quality of life = none. Percentage of oncologists (cancer specialists) who would refuse chemotherapy if they developed cancer = 75%. Percentage of cancer patients in the US who received chemotherapy = 75%. Company that manufactures and sells most of the worlds chemotherapy drugs = Bristol-Meyers Squibb. Chairman of the Board, Bristol-Meyers Squibb = Richard L. Gelb. Richard L. Gelb's other job = Vice-Chairman, Memorial Sloan-Kettering Cancer Center. Director, Bristol-Meyers Squibb = James D. Robinson III. James D. Robinson III's other job = Chairman of the Board, Memorial Sloan-Kettering Cancer Center. Folks, this is only a tiny fraction of what you will learn. This book is going to blow the lid off of health care in this country. Hang on to your hats. From owner-ageing@net.bio.net Sun Jun 09 23:00:00 1996 Path: biosci!bcm.tmc.edu!cs.utexas.edu!chi-news.cic.net!arclight.uoregon.edu!usenet.eel.ufl.edu!warwick!leicester!mac25.msb.le.ac.uk!user From: TJM@le.ac.uk (Tim Mitchell) Newsgroups: bionet.microbiology,bionet.molbio.ageing,bionet.neuroscience,bionet.neuroscience.amyloid,bionet.toxicology Subject: Re: New Lab-Animal Res. Equip. Catalog Date: Mon, 10 Jun 1996 13:31:14 +0100 Organization: University of Leicester Lines: 32 Message-ID: References: <4p86n8$mke$2@mhadf.production.compuserve.com> NNTP-Posting-Host: mac25.msb.le.ac.uk Xref: biosci bionet.microbiology:6306 bionet.molbio.ageing:2752 bionet.neuroscience:14522 bionet.neuroscience.amyloid:473 bionet.toxicology:761 In article <4p86n8$mke$2@mhadf.production.compuserve.com>, PG <75144.2413@CompuServe.COM> wrote: > We at Columbus Instruments just published new 60-page Lab-Animal > Research Equipment Catalog. You will be able to find description > of over 60 scintific instruments for toxicology, pharmacology, > brain scinces, environmental scinces, physiology etc. > Cardiac Output Computers for mice and rats based on > thermodilution, animal activity meters based of TV camera and IR > beams, mazes, end tidal CO/N2O computers for rats and mice, > VO2/VCO2 metabolic computers ( indirect calorimeters) for rats, > dogs and horses, precission gas analyzers, bacteria respirometers > and many more equipment is described on the new catalog pages. > If you are intersted to receive a free copy and price list, > please e-mail your STREET ADDRESS to: > Jan Czekajewski > 75144.2413@compuserve.com PLEASE COULD YOU SEND A COPY TO Dr Tim Mitchell Dept Microbiology and Immunology Medical Sciences Building University of Leicester Leicester LE1-9HN England Tel (44) (0)116 2522980 Fax (44) (0)116 2525675 E-mail TJM@leicester.ac.uk. From owner-ageing@net.bio.net Sun Jun 09 23:00:00 1996 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!swrinde!cs.utexas.edu!chi-news.cic.net!nntp.coast.net!fu-berlin.de!leucin.chemie.fu-berlin.DE!a_kowald From: a_kowald@chemie.fu-berlin.de (Axel Kowald) Newsgroups: bionet.molbio.ageing Subject: Re: "Reversing Human Aging" by M. Fossel Date: 10 Jun 1996 10:17:24 GMT Organization: Kristallographic Institute FU Berlin Lines: 62 Distribution: world Message-ID: <4pgsnk$8ef@fu-berlin.de> References: <31BAF175.2B8E@biomed.med.yale.edu> NNTP-Posting-Host: leucin.chemie.fu-berlin.de (160.45.24.34) NNTP-Posting-User: a_kowald X-Access: 16 17 19 Hi Reading the posting about Fossel's book I couldn't resist answering. I'm a biochemist and got my PhD about theoretical studies of the aging process (mathematical modelling). It is true that one of the most interesting results in aging research during the last years was the discovery that human telomeres are shortening with time. However, I believe one should be very (!!) cautious to believe that this is the true underlying cause of the aging process. This can be a very long discussion with pros and cons, so I just want to mention a few points to think about. Firstly, as with all other ideas about aging it is very difficult to decide if the telomere shortening is really the cause or only a consequence of the aging process. It could also be that telomere shortening has developed independently of aging as a evolutionary neutral event. What I mean is suppose that aging was there first and in the very early days all animals were happily expressing telomerase. Then there was a mutation which stopped the synthesis of telomerase in somatic cells. It could be that this was of no consequence whatsoever (it was neutral), because the animals die a long time before somatic telomere shortening causes any problems. Another point is that neurons don't divide and shouldn't have telomere shortening, but nevertheless they show age related changes. Why ? One could say that if the surrounding cells go down hill it could also affect the nerve cells. But a more drastic example in this respect are for instance insects. As soon as they are adult they are post-mitotic, which means that they have no dividing cells !! But of course you know that flies and also the flatworm Caenorhabditis elegans (which too is post mitotic) die after a few weeks. If you take their cells you will see that they show standard signs of aging like an increase in radical production, drop of protein synthesis or increase in oxidised proteins. And all that without telomere shortening !! I said when they are adult they are post-mitotic, but of course they have to divide from the point of the fertilised egg to the adult stage and during that time they have to maintain the lengths of their telomeres like all the other organisms. However, there are strains of Drosophila which are defective in maintaining their telomere lengths during that critical time. As expected their telomeres are shortening from generation to generation but the life-span is not affected !! The guess is that in the long term (after many generations) these strains will develop problems and may finally all die, but in the short term it doesn't seem to influence life-span. But having said all this I too think that it is very very important to express telomerase in somatic cells and see what happens. This will be the definitive experiment. And in this respect I agree with Fossel. I would guess the first transgenic animals which carry an active telomerase gene will be generated within the next 5-10 years. But unlike Fossel I wouldn't bet too much on telomere shortening as cause for the aging process. A telomerase inhibitor might however be useful as anti-cancer drug and as far as I know this is actually the main motivation of most people and companies with work on it. Axel Kowald From owner-ageing@net.bio.net Sun Jun 09 23:00:00 1996 Path: biosci!rutgers!csn!nntp-xfer-1.csn.net!imci3!newsfeed.internetmci.com!hunter.premier.net!uunet!in1.uu.net!newsfeed.pitt.edu!scramble.lm.com!pink.lm.com!not-for-mail From: vvt@telerama.lm.com Newsgroups: bionet.molbio.ageing Subject: Re: "Reversing Human Aging" by M. Fossel Date: 10 Jun 1996 15:09:19 -0400 Organization: Telerama Public Access Internet, Pittsburgh, PA Lines: 96 Distribution: world Message-ID: <4phrsv$4e4@pink.lm.com> References: <31BAF175.2B8E@biomed.med.yale.edu> <4pgsnk$8ef@fu-berlin.de> NNTP-Posting-Host: pink.lm.com X-Newsreader: TIN [version 1.2 PL2] Axel Kowald (a_kowald@chemie.fu-berlin.de) wrote: > Hi > Reading the posting about Fossel's book I couldn't resist answering. > I'm a biochemist and got my PhD about theoretical studies of the aging proce s > (mathematical modelling). It is true that one of the most interesting result in > aging research during the last years was the discovery that human telomeres re > shortening with time. However, I believe one should be very (!!) cautious to > believe that this is the true underlying cause of the aging process. This ca be > a very long discussion with pros and cons, so I just want to mention a few p ints > to think about. > Firstly, as with all other ideas about aging it is very difficult to decide f > the telomere shortening is really the cause or only a consequence of the agi g > process. It could also be that telomere shortening has developed independent y of > aging as a evolutionary neutral event. What I mean is suppose that aging was > there first and in the very early days all animals were happily expressing > telomerase. Then there was a mutation which stopped the synthesis of telomer se > in somatic cells. It could be that this was of no consequence whatsoever (it was > neutral), because the animals die a long time before somatic telomere shorte ing > causes any problems. > Another point is that neurons don't divide and shouldn't have telomere > shortening, but nevertheless they show age related changes. Why ? > One could say that if the surrounding cells go down hill it could also affec the > nerve cells. But a more drastic example in this respect are for instance ins cts. > As soon as they are adult they are post-mitotic, which means that they have o > dividing cells !! But of course you know that flies and also the flatworm > Caenorhabditis elegans (which too is post mitotic) die after a few weeks. > If you take their cells you will see that they show standard signs of aging ike > an increase in radical production, drop of protein synthesis or increase in > oxidised proteins. And all that without telomere shortening !! > I said when they are adult they are post-mitotic, but of course they have to > divide from the point of the fertilised egg to the adult stage and during th t > time they have to maintain the lengths of their telomeres like all the other > organisms. However, there are strains of Drosophila which are defective in > maintaining their telomere lengths during that critical time. As expected th ir > telomeres are shortening from generation to generation but the life-span is ot > affected !! The guess is that in the long term (after many generations) t ese > strains will develop problems and may finally all die, but in the short ter it > doesn't seem to influence life-span. > But having said all this I too think that it is very very important to expre s > telomerase in somatic cells and see what happens. This will be the definitiv > experiment. And in this respect I agree with Fossel. I would guess the first > transgenic animals which carry an active telomerase gene will be generated w thin > the next 5-10 years. But unlike Fossel I wouldn't bet too much on telomere > shortening as cause for the aging process. A telomerase inhibitor might howe er > be useful as anti-cancer drug and as far as I know this is actually the main > motivation of most people and companies with work on it. > Axel Kowald I read a report in LEF about Geron Corporation's work with telomeres. What I remember is that they were able to reverse aging inblood, brain, and skin cells. Also, that there were two genetic control mechanisms, M1 & M2, needed to keep the cells from turning cancerous. One of these mechanisms was decoded, but the other was still a work in progress. Recently, I read that Geron's primary (most funding) effort was in finding a method to force cancer cells to mature by destroying their ability to produce telomerase. From owner-ageing@net.bio.net Mon Jun 10 23:00:00 1996 Path: biosci!bcm.tmc.edu!pendragon!news.msfc.nasa.gov!newsfeed.internetmci.com!in1.uu.net!news.new-york.net!news.columbia.edu!konichiwa.cc.columbia.edu!tac2 From: tac2@konichiwa.cc.columbia.edu (Todd A Carter) Newsgroups: bionet.molbio.ageing Subject: Re: "Reversing Human Aging" by M. Fossel Date: 11 Jun 1996 02:27:53 GMT Organization: Columbia University Lines: 33 Message-ID: <4pilj9$mpj@apakabar.cc.columbia.edu> References: <31BAF175.2B8E@biomed.med.yale.edu> NNTP-Posting-Host: konichiwa.cc.columbia.edu In article <31BAF175.2B8E@biomed.med.yale.edu>, Public Workstation wrote: >Fossel believes that the evidence accumulated in past five years >suggests that aging is due to telomere shortening occuring as a result >of cell division. All other theories of aging are explaining secondary >phenomena or effects, not the causes, of aging. > >According to Fossel, to prevent aging, it suffices to 'cap' the >telomere with a protein that serves a primar for initiating >replication (see the patent application PCT Publication No. 93/23572). Regardless of the validity of the telomerase-aging theory, the methods described in "capping" the chromosomal ends and/or increasing telomerase activity in normal cells seem way too simplistic. As i understand it, the major hypothesis connecting telomerase with aging supposes that genes on the distal regions of the chromosomes get "chewed up" as telomere length reduces. Any aging reversals would need ot replace these genes activities. Regarding the theory itself, I believe that although telomerase activity has been correlated with the number of passes a cell culture can withstand, it has never been proven that this is directly related to organismal aging. Although the fact that cell cultures from elderly individuals can withstand fewer passes than those of infants is suggestive, as is the same phenomenon seen with Wener's Syndrome patients relative to normal controls without the disease. Even so, the isue is somewhat a controversial one. --Todd Carter --Dept. Genetics --Columbia University From owner-ageing@net.bio.net Mon Jun 10 23:00:00 1996 Path: biosci!HUSC.HARVARD.EDU!kaljuvee From: kaljuvee@HUSC.HARVARD.EDU (Jurgen Kaljuvee) Newsgroups: bionet.molbio.ageing Subject: LEF article Date: 10 Jun 1996 19:09:48 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 19 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net vvt@telerama.lm.com wrote: "I read a report in LEF about Geron Corporation's work with telomeres. What I remember is that they were able to reverse aging inblood, brain, and skin cells. Also, that there were two genetic control mechanisms, M1 & M2, needed to keep the cells from turning cancerous. One of these mechanisms was decoded, but the other was still a work in progress. Recently, I read that Geron's primary (most funding) effort was in finding a method to force cancer cells to mature by destroying their ability to produce telomerase". These results seem titillating, and I'm sure many of the readers of the newsgroup would love to see them, but what does the acronym LEF stand for (I apologize for my ignorance)? What issue did the article appear in? I hope you have chance to reply. Thanks. Jurgen Kaljuvee kaljuvee@fas.harvard.edu From owner-ageing@net.bio.net Mon Jun 10 23:00:00 1996 Path: biosci!bcm.tmc.edu!pendragon!news.msfc.nasa.gov!newsfeed.internetmci.com!chi-news.cic.net!news.compuserve.com!news.production.compuserve.com!news From: JAN CZEKAJEWSKI <75144.2413@CompuServe.COM> Newsgroups: bionet.general,bionet.molbio.ageing,bionet.neuroscience,bionet.toxicology Subject: TAIL-FLICK APPARATUS FOR ANIMALS Date: 10 Jun 1996 19:41:27 GMT Organization: Columbus Instruments Lines: 15 Message-ID: <4phtp7$efm$1@mhafn.production.compuserve.com> Xref: biosci bionet.general:22160 bionet.molbio.ageing:2755 bionet.neuroscience:14534 bionet.toxicology:762 Tail-flick apparatus is an analgesia meter and is helpful in determining pain sensitivity accurately and reproducibly in rats and mice. The instrument has a shutter controlled lamp as a heat source. Activation of an intense light beam to the tail through opening the shutter results in a discomfort at some point when the animal will flick its tail out of the beam. The photo detector detects the tail motion. The total time elapsed between shutter opening and animal's reaction is displayed on an easily read display. Data can be printed directly or may be collected via RS-232 port. If you need more information, please provide your street address. I will be happy to send you more information about Tail-flick apparatus. GHOSH Internet:75144.2413@compuserve.com. From owner-ageing@net.bio.net Mon Jun 10 23:00:00 1996 Path: biosci!rutgers!uwm.edu!newsfeed.internetmci.com!in1.uu.net!psinntp!psinntp!psinntp!psinntp!usenet From: yo_doc@usa.pipeline.com(Richard A. Lockshin) Newsgroups: bionet.neuroscience,bionet.immunology,bionet.molbio.ageing,bionet.drosophila,bionet.general,bionet.cellbiol Subject: NYC area cell death club meeting Date: 11 Jun 1996 04:13:23 GMT Organization: Pipeline USA Lines: 32 Message-ID: <4pirp3$i4k@news1.t1.usa.pipeline.com> NNTP-Posting-Host: 38.8.149.3 X-PipeUser: yo_doc X-PipeHub: usa.pipeline.com X-PipeGCOS: (Richard A. Lockshin) X-Newsreader: Pipeline v3.5.0 Xref: biosci bionet.neuroscience:14548 bionet.immunology:9075 bionet.molbio.ageing:2758 bionet.drosophila:2192 bionet.general:22184 bionet.cellbiol:4894 NYC Area Cell Death Club Next meeting: Wednesday, June 12, 1996 6:00-6:30 PM Pizza 6:30-8:00 PM Talks and discussion Rockefeller University, 1230 York Ave., Weiss Research Bldg Room 301 Free Parking after 5PM at 66th St. & York Ave (Please carpool as parking space is limited) Speakers: JUNE 12 1. Patrizia Casaccia-Bonnefil, Cornell University/N Y Hospital Cell death in primary oligodendrocytes 2. Richard Lockshin, St. John's University Apoptosis of the cytoplasm. To help plan for pizza call lab of Dr. Zahra Zakeri, 718: 997-3429 and let them know the number coming for pizza, talk, and if you need parking. Please RSVP by Tues, June 11, 1996. Otherwise email to me. Organizers: Zahra Zakeri, Fax 718: 997-3445 Phone 718: 997-3417 Raymond Birge: Fax 212 327-7943; Phone 212: 327-7412 Sponsored by: Oncor Appligene and the journal Cell Death and Differentiation We are planning eventually to drop this general world announcement. If you wish to continue receiving these messages, please send an email reply, including your phone & fax numbers and full address as well, along with your research interest. Richard A. Lockshin [also lockshin@sjumusic.stjohns.edu] From owner-ageing@net.bio.net Mon Jun 10 23:00:00 1996 Path: biosci!geron.com!mwest From: mwest@geron.com ("Mike West") Newsgroups: bionet.molbio.ageing Subject: FWD>RE>"Reversing Human Agi Date: 11 Jun 1996 12:09:55 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 23 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Mail*Link( SMTP FWD>RE>"Reversing Human Aging" by M. Fossel In reply to Todd Carter's comments "As i understand it, the major hypothesis connecting telomerase with aging supposes that genes on the distal regions of the chromosomes get "chewed up" as telomere length reduces" it is important to realize that this is not quite right. This is not the "major" theory. In fact, I don't know of anyone who is proposing that in the literature. The hypothesis is really that loss of telomeric repeats eventually leads to a chromosome end without repeats that "looks" like a double strand break leading to DNA damage checkpoint arrest, or alternatively, telomere shortening causes a shift of heterochromatin at the telomere altering expression of telomeric genes. In support of the former model, senescent cells have DNA damage-like alerations in cell cycle regulators like p21, indeed it was first cloned there and called "senescent derived inhibitor-1 (sdi-1)". Therefore, cells approaching senescence have not lost essential genes (as far anyone knows) and indeed recent results published in EMBO J suggest that extending the telomeric repeats in hybrids results in an extension of cell replicative lifespan. -MWest From owner-ageing@net.bio.net Tue Jun 11 23:00:00 1996 Path: biosci!HUSC.HARVARD.EDU!kaljuvee From: kaljuvee@HUSC.HARVARD.EDU (Jurgen Kaljuvee) Newsgroups: bionet.molbio.ageing Subject: RE: LEF article Date: 12 Jun 1996 14:27:44 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 28 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net ---------- Forwarded message ---------- Date: Mon, 10 Jun 1996 22:07:56 -0400 (EDT) From: Jurgen Kaljuvee To: vvt@telerama.lm.com Subject: LEF article vvt@telerama.lm.com wrote: "I read a report in LEF about Geron Corporation's work with telomeres. What I remember is that they were able to reverse aging inblood, brain, and skin cells. Also, that there were two genetic control mechanisms, M1 & M2, needed to keep the cells from turning cancerous. One of these mechanisms was decoded, but the other was still a work in progress. Recently, I read that Geron's primary (most funding) effort was in finding a method to force cancer cells to mature by destroying their ability to produce telomerase". These results seem titillating, and I'm sure many of the readers of the newsgroup would love to see them, but what does the acronym LEF stand for (I apologize for my ignorance)? What issue did the article appear in? I hope you have chance to reply. Thanks. Jurgen Kaljuvee kaljuvee@fas.harvard.edu From owner-ageing@net.bio.net Wed Jun 12 23:00:00 1996 Path: biosci!MALTANET.OMNES.NET!mtroisi From: mtroisi@MALTANET.OMNES.NET (mtroisi) Newsgroups: bionet.molbio.ageing Subject: WE NEED YOUR HELP Date: 13 Jun 1996 13:01:34 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 11 Sender: daemon@net.bio.net Distribution: world Message-ID: <31C0E5A2.A79@maltanet.omnes.net> NNTP-Posting-Host: net.bio.net In 1989 the University of Malta started an Institute of Gerontology and Geriatrics. The Institute runs a one year full time Postgraduate Diploma Course in Gerontology and Geriatrics. We also run a Master's degree based on research in thye field of ageing. Looking forward to know wich universities in the USA and the UK offer any courses in the fields of gerontology and geriatrics, at what level, and what duration. We are trying to set a data base of all these centres. Any kind of information will be more than welcome. I wish to thank you in advance for your attention and cooperation. Regards Dr.Joseph Troisi From owner-ageing@net.bio.net Wed Jun 12 23:00:00 1996 Path: biosci!LAFN.ORG!ba182 From: ba182@LAFN.ORG (John Guerin) Newsgroups: bionet.molbio.ageing Subject: Posting abstract on long-lived fishes Date: 13 Jun 1996 13:38:33 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 58 Sender: daemon@net.bio.net Distribution: world Message-ID: <199606132034.AA26017@lafn.org> Reply-To: ba182@lafn.org NNTP-Posting-Host: net.bio.net I would like to post my abstract if you have a forum for that; a discussion group would be especially useful. Attached is my abstract; please respond to me at ba182@lafn.org Sincerely, John C. Guerin Divergent Model of Aging? Negligible Senescence in Long-Lived Fishes (John C. Guerin, San Diego, CA). Like mammals, fish display patterns of rapid and gradual senescence, such as the Pacific salmon and Medaka, respectively. But unlike warm-blooded animals, some poikilotherms exhibit negligible senescence, which is chronological aging without an increase in mortality rate. Leonard Hayflick observed that "If they do age, it occurs at such a slow rate that their aging has not been demonstrated convincingly", and he felt this phenomenon was important to study (from his book "How and Why We Age", 1994, and personal communication Nov. 1995). Since fish with gradual senescence exhibit a decline in reproductive capacity, oxidative metabolism, protein utilisation and cell numbers (neurons), with an increase in mortality rate, cross-linking, lipofuscin, and lipid peroxidation, the lowered metabolism of cold-blooded animals alone can't be the answer. Perhaps then, the "information derived on the mechanism causing extended longevity in such species might be useful in finding clues for life extension strategies in humans" (quote and information in this paragraph from "Ageing in Cold-Blooded Vertebrates", guest editor B.K. Patnaik, International Journal of Experimental and Clinical Gerontology, V40, 1994). A sixty year old halibut was found still fertile and growing upon its capture, a rougheye rockfish was recorded at 140 years old, and sturgeon are documented at over 150 years old (compiled by Caleb Finch, "Longevity, Senescence and the Genome", 1990). In rockfish studied for fifteen years by Victoria O'Connell, Alaska Fish and Game, ages ranged up to 118 years old, with only three having been reproductively senescent during that time (personal communication Mar. 1996). In a recreational book on raising Koi in Japan, a record koi was reported to be 222 years old in 1973, determined by counting scale rings by electron microscope. Numerous koi are said to be 100-200 years in age, outliving their owners (Nishikigoi Fancy Koi, by Takehiko Tamaki 1974). Do these long-lived fishes offer a divergent model of senescence? Could we look at two closely related species of fish with very different patterns of senescence, and examine genetic, hormonal and environmental regulators? Would altering certain genetic alleles then alter the pattern of negligible senescence in long-lived fishes? If you are interested in working with this project, have ideas or would like additional information, contact John C. Guerin at e-mail address ba182@lafn.org, or call me at (619) 563-9473. -- John C. Guerin From owner-ageing@net.bio.net Wed Jun 12 23:00:00 1996 Path: biosci!LAFN.ORG!ba182 From: ba182@LAFN.ORG (John Guerin) Newsgroups: bionet.molbio.ageing Subject: Negligible senescence in long-lived fishes Date: 13 Jun 1996 14:34:46 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 53 Sender: daemon@net.bio.net Distribution: world Message-ID: <199606132130.AA11985@lafn.org> Reply-To: ba182@lafn.org NNTP-Posting-Host: net.bio.net Divergent Model of Aging? Negligible Senescence in Long-Lived Fishes (John C. Guerin, San Diego, CA). Like mammals, fish display patterns of rapid and gradual senescence, such as the Pacific salmon and Medaka, respectively. But unlike warm-blooded animals, some poikilotherms exhibit negligible senescence, which is chronological aging without an increase in mortality rate. Leonard Hayflick observed that "If they do age, it occurs at such a slow rate that their aging has not been demonstrated convincingly", and he felt this phenomenon was important to study (from his book "How and Why We Age", 1994, and personal communication Nov. 1995). Since fish with gradual senescence exhibit a decline in reproductive capacity, oxidative metabolism, protein utilisation and cell numbers (neurons), with an increase in mortality rate, cross-linking, lipofuscin, and lipid peroxidation, the lowered metabolism of cold-blooded animals alone can't be the answer. Perhaps then, the "information derived on the mechanism causing extended longevity in such species might be useful in finding clues for life extension strategies in humans" (quote and information in this paragraph from "Ageing in Cold-Blooded Vertebrates", guest editor B.K. Patnaik, International Journal of Experimental and Clinical Gerontology, V40, 1994). A sixty year old halibut was found still fertile and growing upon its capture, a rougheye rockfish was recorded at 140 years old, and sturgeon are documented at over 150 years old (compiled by Caleb Finch, "Longevity, Senescence and the Genome", 1990). In rockfish studied for fifteen years by Victoria O'Connell, Alaska Fish and Game, ages ranged up to 118 years old, with only three having been reproductively senescent during that time (personal communication Mar. 1996). In a recreational book on raising Koi in Japan, a record koi was reported to be 222 years old in 1973, determined by counting scale rings by electron microscope. Numerous koi are said to be 100-200 years in age, outliving their owners (Nishikigoi Fancy Koi, by Takehiko Tamaki 1974). Do these long-lived fishes offer a divergent model of senescence? Could we look at two closely related species of fish with very different patterns of senescence, and examine genetic, hormonal and environmental regulators? Would altering certain genetic alleles then alter the pattern of negligible senescence in long-lived fishes? If you are interested in working with this project, have ideas or would like additional information, contact John C. Guerin at e-mail address ba182@lafn.org, or call me at (619) 563-9473. -- John C. Guerin From owner-ageing@net.bio.net Thu Jun 13 23:00:00 1996 Path: biosci!ihnp4.ucsd.edu!news1.ucsd.edu!usenet From: Oliver Bogler Newsgroups: bionet.molbio.ageing Subject: Re: "Reversing Human Aging" by M. Fossel Date: Fri, 14 Jun 1996 14:49:52 -0700 Organization: The Avant-Garde of the Now, Ltd. Lines: 42 Message-ID: <31C1DE80.71B1@ucsd.edu> References: <31BAF175.2B8E@biomed.med.yale.edu> NNTP-Posting-Host: licr-user003.ucsd.edu Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 2.01 (Macintosh; I; 68K) I wanted to add some more to the interesting questions that you raise in response to the book by Fossel. The link between telomere shortening and organismal ageing, which forms the basis of the book, and the proposed anti-ageing therapies is unfortunately fragile at present. As such the book represents an extremely premature popularisation of frontier science. In my opinion such books, and the associated news coverage, are detrimental to medical research as they foster unrealistic expectations among the general public, expectations whose repeated dashing feeds back negatively on science, and science funding. In my opinion this is an irresponsible act. First, let's take the underlying theory. As pointed out by another respondent, telomere shortening has been shown to *correlate* with *cellular* ageing. That means that it has not been shown to be causative in the process of cellular senescence. It is clear that cells need to maintain their chromosomes to be immortal. However, it remains distinctly possible that other events make them immortal, and that they switch on telomerase as a consequence of these other events. Of course, the link between cellular senescence and organismal ageing is itself far from clear. As you pointed out, some cells, such as neurons, are non-dividing from early childhood until death, yet can function adequately without telomerase. Second, the therapies suggested are even more facile. If, as the book demands, telomerase is really the master controller of cellular ageing, and by inference critical in cellular transformation, then simply making more of it all the cells of the human body is likely to have negative consequences! Of course, of telomerase is irrelevant, then so are the therapies. My personal opinion is that this hypothesis is an illustration of the old axiom that a little knowledge is a dangerous thing. It reminds me of the anecdote popular in my field, of a now-Nobel laureate, who upon the discovery of viral oncogenes (20 years ago), remarked to a colleague something like: "now that we have the genes we'll have cancer wrapped up in no time." As the therapist of the anti-ageing clinic of the future might ask: "Perhaps you'd like a little melatonin with your telomere therapy, sir? And while you wait for it to take effect, perhaps you'd care to browse through this catalogue of famous bridges we have on special offer this week?" From owner-ageing@net.bio.net Fri Jun 14 23:00:00 1996 Path: biosci!rutgers!sgigate.sgi.com!esiee.fr!jussieu.fr!oleane!in2p3.fr!swidir.switch.ch!scsing.switch.ch!news.belwue.de!fu-berlin.de!cs.tu-berlin.de!uni-erlangen.de!winx03!news From: Gerald Muench Newsgroups: bionet.molbio.ageing Subject: Re: Negligible senescence in long-lived fishes Date: 15 Jun 1996 07:41:26 GMT Organization: Theodor-Boveri-Institut fuer Biowissenschaften Lines: 13 Message-ID: <4ptpf6$ks6@winx03.informatik.uni-wuerzburg.de> References: <199606132130.AA11985@lafn.org> NNTP-Posting-Host: wbza25.biozentrum.uni-wuerzburg.de Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 1.12(Macintosh; I; PPC) To: ba182@lafn.org X-URL: news:199606132130.AA11985@lafn.org - Dear Dr. Guerin, what do you think about measuring Advanced glycation endproducts (as a tissue marker for protein turnover and oxidative stress) in long-lived fish ? Yours sincerely Gerald Munch From owner-ageing@net.bio.net Sat Jun 15 23:00:00 1996 Path: biosci!bcm.tmc.edu!cs.utexas.edu!howland.reston.ans.net!psinntp!psinntp!psinntp!usenet From: yo_doc@usa.pipeline.com(Richard A. Lockshin) Newsgroups: bionet.molbio.ageing Subject: Re: WE NEED YOUR HELP Date: 15 Jun 1996 21:06:24 GMT Organization: Pipeline USA Lines: 36 Message-ID: <4pv8kg$qjq@news1.t1.usa.pipeline.com> References: <31C0E5A2.A79@maltanet.omnes.net> NNTP-Posting-Host: 38.8.150.3 X-PipeUser: yo_doc X-PipeHub: usa.pipeline.com X-PipeGCOS: (Richard A. Lockshin) X-Newsreader: Pipeline v3.5.0 On Jun 13, 1996 13:01:34 in article , 'mtroisi@MALTANET.OMNES.NET (mtroisi)' wrote: Contact Gerontol. Soc. of America 1275 K St. NW, Suite 350 Washington DC 20005-4006 206: 842-1275 >Path: >psinntp!psinntp!howland.reston.ans.net!nntp.coast.net!sgigate.sgi.com!olivea!bio >sci!MALTANET.OMNES.NET!mtroisi >From: mtroisi@MALTANET.OMNES.NET (mtroisi) >Newsgroups: bionet.molbio.ageing >Subject: WE NEED YOUR HELP >Date: 13 Jun 1996 13:01:34 -0700 >Organization: BIOSCI International Newsgroups for Molecular Biology >Lines: 11 >Sender: daemon@net.bio.net >Distribution: world >Message-ID: <31C0E5A2.A79@maltanet.omnes.net> >NNTP-Posting-Host: net.bio.net > >In 1989 the University of Malta started an Institute of Gerontology and >Geriatrics. The Institute runs a one year full time Postgraduate Diploma >Course in Gerontology and Geriatrics. We also run a Master's degree based >on research in thye field of ageing. >Looking forward to know wich universities in the USA and the UK offer >any courses in the fields of gerontology and geriatrics, at what level, >and what duration. We are trying to set a data base of all these centres. >Any kind of information will be more than welcome. >I wish to thank you in advance for your attention and cooperation. >Regards >Dr.Joseph Troisi -- Richard A. Lockshin From owner-ageing@net.bio.net Tue Jun 18 23:00:00 1996 Path: biosci!IMB.IMB.AC.RU!koudin From: koudin@IMB.IMB.AC.RU ("Alexei R. Koudinov") Newsgroups: bionet.molbio.ageing Subject: POSITION REQUEST Date: 19 Jun 1996 14:56:16 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 306 Sender: daemon@net.bio.net Distribution: world Message-ID: <199606192150.BAA03306@imb.imb.ac.ru> NNTP-Posting-Host: net.bio.net Dear Amyloid/Ageing subscribers: I began to study Alzheimer's amyloid beta (Ab) protein in 1992, at the time when it was becoming clear that this protein exists normally in a soluble form (soluble Ab) and that it is not just a pathological protein. My research activities yielded an on-going project, devoted to understanding in more detail the normal biology of amyloid beta. Understanding the normal biology of Ab would answer the questions of why soluble Ab does not undergo fibrillogenesis in biological fluids but does polymerize into amyloid fibrils in the disease, and what the biological consequences of Ab deposition within the brain tissue are. This, in turn, would be crucial for understanding the pathophysiology of Alzheimer's disease and for delineating pathologically grounded new approaches to therapy. My current postdoctoral position at NYU Medical Center just expired. Thus, to continue my research I have to find another position. I would be happy to continue my research as a part of your Department/ University/ Center, if you might wish to consider such a possibility. Sincerely Yours, Alexei R. Koudinov, M.D., Ph.D. P.S. Enclosed please find CV and ABSTRACTS of my recent papers ______________________________________________________________________________ NAME: ALEXEI R. KOUDINOV E.MAIL: koudin@imb.imb.ac.ru EDUCATION: University Years Degree Major Moscow Medical University 1984- `MD Biochemistry, 1992 Cell/Molecular Biology, Medicine Engelhardt Institute of 1992- PhD Biochemistry Molecular Biology, Russian 1995 Academy of Sciences, Moscow. ( The Ph.D. research project was performed in the Department of Pathology, New York University Medical Center. Ph.D. thesis: "Soluble amyloid beta is complexed to high density lipoprotein 3 and very high density lipoproteins", Sponsor/advisor: Professor B. Frangione, M.D., Ph.D.). WORK EXPERIENCE: 1983-1984 Laboratory Assistant, Chemical Analysis Laboratory, Chelyabinsk Tractor Plant. 1989 Laboratory Assistant, Genetics Department, Moscow Medical University. 1990 Research Assistant, Enzymology Braunstein Memorial Laboratory, Engelhardt Institute of Molecular Biology. 1991-1992 Medical Assistant, Second Department of Neurology, Moscow Medical University. 1992-present Assistant Research Scientist, Department of Pathology, New York University Medical Center RESEARCH EXPERIENCE: 1. Studies of structure-function relationship of two subforms of eukaryotic Topoisomerase I (Masters' thesis research project, 1990-1992). Enzymology Braunstein Memorial Laboratory, Engelhardt Institute of Molecular Biology, Moscow, Russia. Sponsor: Dr. A. Gabibov, Ph.D. Major techniques used: affinity, ion-exchange and hydrophobic interaction chromatography, routinely and HPLC modification; protein quantification; protein and DNA electrophoresis; isoelectrofocusing; enzymatic kinetic studies; partial proteolysis; immunoblot analysis and enzyme-linked immunosorbent analysis. 2. Studies of DNA-hydrolysing catalytic antibodies from autoimmune sera (1991-1992) Enzymology Braunstein Memorial Laboratory, Engelhardt Institute of Molecular Biology, Moscow, Russia. Advisors: Dr. A. Gabibov, Ph.D. Major techniques used: IgG preparation from autoimmune sera by chromatography, routine and HPLC modification; DNA isolation; DNA hydrolysing activity assay. 3. Studies of autoimmune reaction in psoriatic skin (collaborative project with Dr. A. Tkachenko, M.D., Ph.D., 1991-1992) Laboratory of cancerogenesis, Engelhardt Institute of Molecular Biology, Moscow, Russia. Major techiques used: skin biopsy preparations; IgG preparation from human plasma ( routine chromatography and HPLC on ProteinG Sepharose ); gel electrophoresis and immunoblot analysis; 2D-gel electrophoresis. 4. Studies of connectivity of visual cortex in rats and human cortical brain slices in vitro (Summer studentship program, Summer, 1992) Department of Neurobiology, Brain Research Center, Weizmann Institute of Science, Rehovot, Israel. Advisor: Dr. G. Kenan-Vaknin, Ph.D. Major techniques used: preparation and maintaing in vitro mice, rat and human cortical brain slices; probing of cortical connectivity in live brain slices with tracer biocytin (a derivative of biotin); potential recording; immunohistochemistry. 5. Studies of killing of Trypanosoma brucei by human serum (collaborative project with Dr. S. Tomlinson, Ph.D., 1994-1995) Michael Heidelberger Division of Immunology, Department of Pathology, New York University Medical center, New York. Advisor: Dr. V. Nussenzweig, M.D., Ph.D. Major techniques used: gradient ultracentrifugation; size exclusion chromatography, FPLC modification; Trypanosoma brucei killing assay; gel electrophoresis and immunoblot analysis. 6. Studies of normal biochemistry of soluble amyloid beta protein (Ph.D. thesis research project, 1992-1996) Department of Pathology, New York University Medical center, New York. Sponsor: Dr. B. Frangione, M.D., Ph.D. Major techniques used: sequential flotation ultracentrifugation; immunoaffinity chromatography; size exclusion and reverse phase HPLC; thin-layer chromatography; gel electrophoresis and immunoblot analysis; enzyme-linked immunosorbent analysis; chemiluminescence; optical and chemiluminescent densitometry; amino acid sequence analysis; electron and immunoelectron microscopy; immunocytochemistry; biotin technology for tracing proteins in biological fluids; animal cell culture; metabolic labelling of cell protein and lipid; lipid extraction; lyposome preparation; enzymatic quantification of triglycerides, phospholipids, nonesterified and total cholesterol; statistical analysis. PUBLICATIONS: KUDINOV, Alexei R., Bronstein, Igor B., Gabibov, Alexander G. and Gololobov, Gennady V. (1992) Two subforms of eukaryotic topoisomerase I: Purification and structure-function relationship. FEBS Lett 314: 267-270. Tkachenko, Andrei V., Starkov, Ivan V., Shuster, Alexander M., KOUDINOV, Alexei R., Zakharov, Sergei F., Shishkin, Sergei S., Mordovtsev, Vladimir N., and Kisselev, Lev, L. (1992) Autoimmune reaction in psoriatic skin. In Proceedings of the conference "Modern Enzymology: problems and trends". St.Petersburg. Ghiso, Jorge, Matsubara, Etsuro, KOUDINOV, Alexei, ChoiMiura, Nam Ho, Tomita, Motono, Wisniewski, Thomas, Frangione, Blas. (1993). The cerebrospinal fluid soluble form of Alzheimer's amyloid beta is complexed to SP-40,40 (apolipoprotein J), an inhibitor of the complement membrane-attack complex. Biochem J 293: 2730. KOUDINOV, Alexei, Matsubara, Etsuro, Frangione, Blas, Ghiso, Jorge. (1994). The Soluble Form of Alzheimer's Amyloid Beta Protein is Complexed to High Density Lipoprotein 3 and Very High Density Lipoprotein in Normal Human Plasma Biochem Biophys Res Commun 205: 1164-1171. Tomlinson, Stephen, Jansen, Ana-Maria, KOUDINOV, Alexei, Ghiso, Jorge, Choi-Miura, Nam-ho, Rifkin, Mary, Ohtaki, Sachiya, and Nussenzweig, Victor. (1995) High-density-lipoprotein-independent killing of Trypanosoma brucei by human serum. Molecular and Biochemical Parasitology 70: 131-138. KOUDINOV, Alexei, R., Koudinova, Natalia, V., and Berezov, Temirbolat, T. (1996). Alzheimer's peptides Ab1-40 and Ab1-28 inhibit the plasma cholesterol esterification rate. Biochem Mol Biol Internat. 38(4): 747-752. KOUDINOV, Alexei, R., Berezov, Temirbolat, T., and Koudinova, Natalia, V. Multiple inhibitory effects of Alzheimer's peptide Ab1-40 on lipid byosynthesis in cultured human HepG2 cells. In press. (SEE ABSTRACT BELOW) KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok, Beavis, Ronald, and Ghiso, Jorge. (1996) Biochemical Biophysical Research Communication. Biochemical characterization of Alzheimer's soluble amyloid beta protein in human cerebrospinal fluid: association with high density lipoproteins. Biochem Biophys Res Commun. In Press. (SEE ABSTRACT BELOW) MEETING PRESENTATIONS: KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok. Is amyloid beta an apolipoprotein? New York University Medical Center Neuroscience Meeting. New York. December 1995. KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok, Beavis, Ronald, and Ghiso, Jorge. Alzheimer's soluble amyloid beta protein is associated with high density lipoproteins in normal human cerebrospinal fluid and is secreted by HepG2 cells as a part of lipoprotein complexes. Society for Neuroscience Annual Meeting. Washington, DC, 1996. Submitted. (SEE ABSTRACT BELOW). AWARDS: 1989-1992 All Russian Government Scholarship for outstanding success in studies. 1992 Honorary Diploma of Medical Doctor. Moscow Medical University. 1992 Summer student fellowship. Weizmann Institute of Science. Rehovot. Israel 1994-1995 Pilot Research Grant from The Aging and Dementia Research Center at NYU Medical Center. Project title: "HepG2 as a model for studies of sAb secretion by human cells" (NIH Grant AG08051, Dr. S.Ferris, P.I.). REFERENCES available upon request 10 June 1996 _______________________________________________________________________ MULTIPLE INHIBITORY EFFECTS OF ALZHEIMER'S PEPTIDE Ab1-40 ON LIPID BIOSYNTHESIS IN CULTURED HUMAN HEPG2 CELLS. Alexei R KOUDINOV(1), Temirbolat T BEREZOV(2) and Natalia V KOUDINOVA2,3* Department of Pathology(1) and Medicine(3), New York University Medical Center, 560 First Avenue, TH427, New York, NY 10016, USA and Department of Biochemistry(2), Russian Peoples' Friendship University School of Medicine, Miklucho-Maklay St., 8, Moscow 117198, Russia ____________________________________________________________________________ BIOCHEMICAL CHARACTERIZATION OF ALZHEIMER'S SOLUBLE AMYLOID BETA PROTEIN IN HUMAN CEREBROSPINAL FLUID: ASSOCIATION WITH HIGH DENSITY LIPOPROTEINS. Alexei R. Koudinov, Natalia V. Koudinova(1), Asok Kumar, Ronald C. Beavis(2) and Jorge Ghiso Departments of Pathology, Medicine(1) and Pharmacology(2), New York University Medical Center, 560 First Avenue, New York, NY 10016 ABSTRACT The soluble form of Alzheimer's amyloid b protein (sAb) is associated with high density lipoprotein (HDL) in normal human plasma (BBRC (1994) 205, 1164-71). Since sAb is also present in cerebrospinal fluid (CSF) and the lipoprotein pattern of CSF is different from that of plasma, it was of interest to ascertain whether the interaction of sAb with HDL also occurs in CSF. Normal human CSF lipoproteins were obtained by sequential flotation ultracentrifugation and analysed for the presence of sAb via immunoblot, size-exclusion chromatography, immunoelectron microscopy, N-terminal sequence and mass-spectrometry analyses. Soluble Ab was associated with CSF-HDL particles of 16.8 +/- 3.2 nm in diameter and approximately 200 kDa of relative molecular mass. A ~4.3 kDa component purified by HPLC was immunoreactive with anti-Ab antibodies, exhibited an N-terminal sequence identical to the Ab peptide and a mass of 4325.1 Da, indicating that the main sAb specie associated with CSF-HDL is sAb1-40. _________________________________________________________________________ ALZHEIMER'S SOLUBLE AMYLOID BETA PROTEIN IS ASSOCIATED WITH HIGH DENSITY LIPOPROTEINS IN NORMAL HUMAN CEREBROSPINAL FLUID AND IS SECRETED BY HEPG2 CELLS AS A PART OF LIPOPROTEIN COMPLEXES A. R. Koudinov*, N. V. Koudinova, A. Kumar, R. C. Beavis and J. Ghiso, New York University Medical Center, TH 427, 560 First Avenue, New York, NY 10016. ABSTRACT The soluble form of amyloid b protein (sAb) is associated with high density lipoprotein (HDL) in normal human plasma (Biochem Biophys Res Commun (1994) 205, 1164-71). This suggests that sAb to HDL association is rather a more general phenomenon taking place in other biological fluids and tissues. To ascertain this hypothesis the colocalization of sAb with lipoproteins (LP) was investigated in cerebrospinal fluid (CSF) and in cell culture supernatant. Normal human CSF LPs were obtained by sequential flotation ultracentrifugation and analyzed for the presence of sAb via immunoblot, size-exclusion HPLC, immunoelectron microscopy, N-terminal sequence and mass-spectrometry analyses. Soluble Ab was associated with ~200 kDa CSF- HDL particles of 16.8 +/- 3.2 nm in diameter. A ~4.3 kDa component purified by reverse phase HPLC was immunoreactive with anti-Ab antibodies, exhibited an N-terminal sequence identical to the Ab peptide and a mass of 4325.1 Da, and therefore indicates that the main sAb specie associated with CSF-HDL is sAb1-40. The sAb secretion by cells in association with LPs was tested in human hepatoma HepG2 cell line. Soluble Ab in the cell culture supernatant was detected in ~200 kDa molecular mass LP complexes in association with apoJ, apoA-I, phospholipids, triglycerides and free and esterified cholesterol. Our results suggest that the association of sAb with LP represents a common mechanism for the peptide transport in biological fluids. _____________________________________________________________________________ Alexei Rudolphovich Koudinov Institute of Molecular Biology, Russian Academy of Sciences koudin@imb.imb.ac.ru From owner-ageing@net.bio.net Fri Jun 21 23:00:00 1996 Path: biosci!ilr.rc.ac.ru!ageing From: ageing@ilr.rc.ac.ru ("Leonid A.Gavrilov") Newsgroups: bionet.molbio.ageing Subject: Predictors of human longevity Date: 22 Jun 1996 03:23:31 -0700 Organization: A.N.Belozersky Institute Lines: 37 Sender: daemon@net.bio.net Distribution: world Message-ID: NNTP-Posting-Host: net.bio.net Dear Colleagues, Recently we have found new strong predictors of human longevity at personal level. These new results were published partially in the following papers: Gavrilov, L.A., N.S.Gavrilova, G.N.Evdokushkina G.N., Y.E.Kushnareva, V.G.Semyonova, A.L.Gavrilova, E.V.Lapshin, N.N.Evdokushkina (1996) Determinants of human longevity: parental age at reproduction and offspring longevity, Longevity Report (ISSN 0964-5659), 10, 54, 7-15. Gavrilov, L.A., N.S.Gavrilova, G.N.Evdokushkina G.N., Y.E.Kushnareva, V.G.Semyonova, A.L.Gavrilova, E.V.Lapshin, N.N.Evdokushkina (1996) The revival of longevity genetics, Longevity Report (ISSN 0964-5659), 10, 55, 3-4. Another part of our results is kept strictly confidential because of their commercial value for life insurance market. We would greatly appreciate any collaboration in this area including practical applications to life insurance business. Sincerely yours, Dr.Leonid A.Gavrilov, Ph.D. Director, Center for Longevity Research A.N.Belozersky Institute Moscow State University 119899 Moscow, Russia FAX: 7-095-939-0338 7-095-939-3181 Email: gavrilov@ilr.rc.ac.ru From owner-ageing@net.bio.net Sat Jun 22 23:00:00 1996 Path: biosci!IMB.IMB.AC.RU!koudin From: koudin@IMB.IMB.AC.RU ("Alexei R. Koudinov") Newsgroups: bionet.molbio.ageing Subject: POSITION REQUEST Date: 23 Jun 1996 13:24:10 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 89 Sender: daemon@net.bio.net Distribution: world Message-ID: <9606232021.AA11041@mchip00.med.nyu.edu> NNTP-Posting-Host: net.bio.net Dear Amyloid/Ageing subscribers: I began to study Alzheimer's amyloid beta (Ab) protein in 1992, at the time when it was becoming clear that this protein exists normally in a soluble form (soluble Ab) and that it is not just a pathological protein. My research activities yielded an on-going project, devoted to understanding in more detail the normal biology of amyloid beta. Understanding the normal biology of Ab would answer the questions of why soluble Ab does not undergo fibrillogenesis in biological fluids but does polymerize into amyloid fibrils in the disease, and what the biological consequences of Ab deposition within the brain tissue are. This, in turn, would be crucial for understanding the pathophysiology of Alzheimer's disease and for delineating pathologically grounded new approaches to therapy. My current postdoctoral position at NYU Medical Center just expired. Thus, to continue my research I have to find another position. I would be happy to continue my research as a part of your Department/ University/ Center, if you might wish to consider such a possibility. Sincerely Yours, Alexei R. Koudinov, M.D., Ph.D. P.S. My CV is available in David Small (special thanks to him for this possibility) WEB site under JOB CORNER. _________________________________________________________________ Alexei Koudinov PUBLICATIONS: KUDINOV, Alexei R., Bronstein, Igor B., Gabibov, Alexander G. and Gololobov, Gennady V. (1992) Two subforms of eukaryotic topoisomerase I: Purification and structure-function relationship. FEBS Lett 314: 267-270. Tkachenko, Andrei V., Starkov, Ivan V., Shuster, Alexander M., KOUDINOV, Alexei R., Zakharov, Sergei F., Shishkin, Sergei S., Mordovtsev, Vladimir N., and Kisselev, Lev, L. (1992) Autoimmune reaction in psoriatic skin. In Proceedings of the conference "Modern Enzymology: problems and trends". St.Petersburg. Ghiso, Jorge, Matsubara, Etsuro, KOUDINOV, Alexei, ChoiMiura, Nam Ho, Tomita, Motono, Wisniewski, Thomas, Frangione, Blas. (1993). The cerebrospinal fluid soluble form of Alzheimer's amyloid beta is complexed to SP-40,40 (apolipoprotein J), an inhibitor of the complement membrane-attack complex. Biochem J 293: 2730. KOUDINOV, Alexei, Matsubara, Etsuro, Frangione, Blas, Ghiso, Jorge. (1994). The Soluble Form of Alzheimer's Amyloid Beta Protein is Complexed to High Density Lipoprotein 3 and Very High Density Lipoprotein in Normal Human Plasma Biochem Biophys Res Commun 205: 1164-1171. Tomlinson, Stephen, Jansen, Ana-Maria, KOUDINOV, Alexei, Ghiso, Jorge, Choi-Miura, Nam-ho, Rifkin, Mary, Ohtaki, Sachiya, and Nussenzweig, Victor. (1995) High-density-lipoprotein-independent killing of Trypanosoma brucei by human serum. Molecular and Biochemical Parasitology 70: 131-138. KOUDINOV, Alexei, R., Koudinova, Natalia, V., and Berezov, Temirbolat, T. (1996). Alzheimer's peptides Ab1-40 and Ab1-28 inhibit the plasma cholesterol esterification rate. Biochem Mol Biol Internat. 38(4): 747-752. KOUDINOV, Alexei, R., Berezov, Temirbolat, T., and Koudinova, Natalia, V. Multiple inhibitory effects of Alzheimer's peptide Ab1-40 on lipid byosynthesis in cultured human HepG2 cells. In press. (SEE ABSTRACT BELOW) KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok, Beavis, Ronald, and Ghiso, Jorge. (1996) Biochemical Biophysical Research Communication. Biochemical characterization of Alzheimer's soluble amyloid beta protein in human cerebrospinal fluid: association with high density lipoproteins. Biochem Biophys Res Commun. In Press. (SEE ABSTRACT BELOW) MEETING PRESENTATIONS: KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok. Is amyloid beta an apolipoprotein? New York University Medical Center Neuroscience Meeting. New York. December 1995. KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok, Beavis, Ronald, and Ghiso, Jorge. Alzheimer's soluble amyloid beta protein is associated with high density lipoproteins in normal human cerebrospinal fluid and is secreted by HepG2 cells as a part of lipoprotein complexes. Society for Neuroscience Annual Meeting. Washington, DC, 1996. Submitted. (SEE ABSTRACT BELOW). _______________________________________________________________________ From owner-ageing@net.bio.net Sat Jun 22 23:00:00 1996 Path: biosci!IMB.IMB.AC.RU!koudin From: koudin@IMB.IMB.AC.RU ("Alexei R. Koudinov") Newsgroups: bionet.molbio.ageing Subject: POSITION REQUEST Date: 23 Jun 1996 12:52:52 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 308 Sender: daemon@net.bio.net Distribution: world Message-ID: <9606231950.AA10679@mchip00.med.nyu.edu> NNTP-Posting-Host: net.bio.net Dear Amyloid/Ageing subscribers: I began to study Alzheimer's amyloid beta (Ab) protein in 1992, at the time when it was becoming clear that this protein exists normally in a soluble form (soluble Ab) and that it is not just a pathological protein. My research activities yielded an on-going project, devoted to understanding in more detail the normal biology of amyloid beta. Understanding the normal biology of Ab would answer the questions of why soluble Ab does not undergo fibrillogenesis in biological fluids but does polymerize into amyloid fibrils in the disease, and what the biological consequences of Ab deposition within the brain tissue are. This, in turn, would be crucial for understanding the pathophysiology of Alzheimer's disease and for delineating pathologically grounded new approaches to therapy. My current postdoctoral position at NYU Medical Center just expired. Thus, to continue my research I have to find another position. I would be happy to continue my research as a part of your Department/ University/ Center, if you might wish to consider such a possibility. Sincerely Yours, Alexei R. Koudinov, M.D., Ph.D. P.S. Enclosed please find CV and ABSTRACTS of my recent papers ______________________________________________________________________________ NAME: ALEXEI R. KOUDINOV E.MAIL: koudin@imb.imb.ac.ru EDUCATION: University Years Degree Major Moscow Medical University 1984- `MD Biochemistry, 1992 Cell/Molecular Biology, Medicine Engelhardt Institute of 1992- PhD Biochemistry Molecular Biology, Russian 1995 Academy of Sciences, Moscow. ( The Ph.D. research project was performed in the Department of Pathology, New York University Medical Center. Ph.D. thesis: "Soluble amyloid beta is complexed to high density lipoprotein 3 and very high density lipoproteins", Sponsor/advisor: Professor B. Frangione, M.D., Ph.D.). WORK EXPERIENCE: 1989 Laboratory Assistant, Genetics Department, Moscow Medical University. 1990 Research Assistant, Enzymology Braunstein Memorial Laboratory, Engelhardt Institute of Molecular Biology. 1991-1992 Medical Assistant, Second Department of Neurology, Moscow Medical University. 1992-present Assistant Research Scientist, Department of Pathology, New York University Medical Center RESEARCH EXPERIENCE: 1. Studies of structure-function relationship of two subforms of eukaryotic Topoisomerase I (Masters' thesis research project, 1990-1992). Enzymology Braunstein Memorial Laboratory, Engelhardt Institute of Molecular Biology, Moscow, Russia. Sponsor: Dr. A. Gabibov, Ph.D. Major techniques used: affinity, ion-exchange and hydrophobic interaction chromatography, routinely and HPLC modification; protein quantification; protein and DNA electrophoresis; isoelectrofocusing; enzymatic kinetic studies; partial proteolysis; immunoblot analysis and enzyme-linked immunosorbent analysis. 2. Studies of DNA-hydrolysing catalytic antibodies from autoimmune sera (1991-1992) Enzymology Braunstein Memorial Laboratory, Engelhardt Institute of Molecular Biology, Moscow, Russia. Advisors: Dr. A. Gabibov, Ph.D. Major techniques used: IgG preparation from autoimmune sera by chromatography, routine and HPLC modification; DNA isolation; DNA hydrolysing activity assay. 3. Studies of autoimmune reaction in psoriatic skin (collaborative project with Dr. A. Tkachenko, M.D., Ph.D., 1991-1992) Laboratory of cancerogenesis, Engelhardt Institute of Moleculr Biology, Moscow, Russia. Major techiques used: skin biopsy preparations; IgG preparation from human plasma ( routine chromatography and HPLC on ProteinG Sepharose ); gel electrophoresis and immunoblot analysis; 2D-gel electrophoresis. 4. Studies of connectivity of visual cortex in rats and human cortical brain slices in vitro (Summer studentship program, Summer, 1992) Department of Neurobiology, Brain Research Center, Weizmann Institute of Science, Rehovot, Israel. Advisor: Dr. G. Kenan-Vaknin, Ph.D. Major techniques used: preparation and maintaing in vitro mice, rat and human cortical brain slices; probing of cortical connectivity in live brain slices with tracer biocytin (a derivative of biotin); potential recording; immunohistochemistry. 5. Studies of killing of Trypanosoma brucei by human serum (collaborative project with Dr. S. Tomlinson, Ph.D., 1994-1995) Michael Heidelberger Division of Immunology, Department of Pathology, New York University Medical center, New York. Advisor: Dr. V. Nussenzweig, M.D., Ph.D. Major techniques used: gradient ultracentrifugation; size exclusion chromatography, FPLC modification; Trypanosoma brucei killing assay; gel electrophoresis and immunoblot analysis. 6. Studies of normal biochemistry of soluble amyloid beta protein (Ph.D. thesis research project, 1992-1996) Department of Pathology, New York University Medical center, New York. Sponsor: Dr. B. Frangione, M.D., Ph.D. Major techniques used: sequential flotation ultracentrifugation; immunoaffinity chromatography; size exclusion and reverse phase HPLC; thin-layer chromatography; gel electrophoresis and immunoblot analysis; enzyme-linked immunosorbent analysis; chemiluminescence; optical and chemiluminescent densitometry; amino acid sequence analysis; electron and immunoelectron microscopy; immunocytochemistry; biotin technology for tracing proteins in biological fluids; animal cell culture; metabolic labelling of cell protein and lipid; lipid extraction; lyposome preparation; enzymatic quantification of triglycerides, phospholipids, nonesterified and total cholesterol; statistical analysis. PUBLICATIONS: KUDINOV, Alexei R., Bronstein, Igor B., Gabibov, Alexander G. and Gololobov, Gennady V. (1992) Two subforms of eukaryotic topoisomerase I: Purification and structure-function relationship. FEBS Lett 314: 267-270. Tkachenko, Andrei V., Starkov, Ivan V., Shuster, Alexander M., KOUDINOV, Alexei R., Zakharov, Sergei F., Shishkin, Sergei S., Mordovtsev, Vladimir N., and Kisselev, Lev, L. (1992) Autoimmune reaction in psoriatic skin. In Proceedings of the conference "Modern Enzymology: problems and trends". St.Petersburg. Ghiso, Jorge, Matsubara, Etsuro, KOUDINOV, Alexei, ChoiMiura, Nam Ho, Tomita, Motono, Wisniewski, Thomas, Frangione, Blas. (1993). The cerebrospinal fluid soluble form of Alzheimer's amyloid beta is complexed to SP-40,40 (apolipoprotein J), an inhibitor of the complement membrane-attack complex. Biochem J 293: 2730. KOUDINOV, Alexei, Matsubara, Etsuro, Frangione, Blas, Ghiso, Jorge. (1994). The Soluble Form of Alzheimer's Amyloid Beta Protein is Complexed to High Density Lipoprotein 3 and Very High Density Lipoprotein in Normal Human Plasma Biochem Biophys Res Commun 205: 1164-1171. Tomlinson, Stephen, Jansen, Ana-Maria, KOUDINOV, Alexei, Ghiso, Jorge, Choi-Miura, Nam-ho, Rifkin, Mary, Ohtaki, Sachiya, and Nussenzweig, Victor. (1995) High-density-lipoprotein-independent killing of Trypanosoma brucei by human serum. Molecular and Biochemical Parasitology 70: 131-138. KOUDINOV, Alexei, R., Koudinova, Natalia, V., and Berezov, Temirbolat, T. (1996). Alzheimer's peptides Ab1-40 and Ab1-28 inhibit the plasma cholesterol esterification rate. Biochem Mol Biol Internat. 38(4): 747-752. KOUDINOV, Alexei, R., Berezov, Temirbolat, T., and Koudinova, Natalia, V. Multiple inhibitory effects of Alzheimer's peptide Ab1-40 on lipid byosynthesis in cultured human HepG2 cells. In press. (SEE ABSTRACT BELOW) KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok, Beavis, Ronald, and Ghiso, Jorge. (1996) Biochemical Biophysical Research Communication. Biochemical characterization of Alzheimer's soluble amyloid beta protein in human cerebrospinal fluid: association with high density lipoproteins. Biochem Biophys Res Commun. In Press. (SEE ABSTRACT BELOW) MEETING PRESENTATIONS: KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok. Is amyloid beta an apolipoprotein? New York University Medical Center Neuroscience Meeting. New York. December 1995. KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok, Beavis, Ronald, and Ghiso, Jorge. Alzheimer's soluble amyloid beta protein is associated with high density lipoproteins in normal human cerebrospinal fluid and is secreted by HepG2 cells as a part of lipoprotein complexes. Society for Neuroscience Annual Meeting. Washington, DC, 1996. Submitted. (SEE ABSTRACT BELOW). AWARDS: 1989-1992 All Russian Government Scholarship for outstanding success in studies. 1992 Honorary Diploma of Medical Doctor. Moscow Medical University. 1992 Summer student fellowship. Weizmann Institute of Science. Rehovot. Israel 1994-1995 Pilot Research Grant from The Aging and Dementia Research Center at NYU Medical Center. Project title: "HepG2 as a model for studies of sAb secretion by human cells" (NIH Grant AG08051, Dr. S.Ferris, P.I.). REFERENCES available upon request 10 June 1996 _______________________________________________________________________ MULTIPLE INHIBITORY EFFECTS OF ALZHEIMER'S PEPTIDE Ab1-40 ON LIPID BIOSYNTHESIS IN CULTURED HUMAN HEPG2 CELLS. Alexei R KOUDINOV(1), Temirbolat T BEREZOV(2) and Natalia V KOUDINOVA2,3* Department of Pathology(1) and Medicine(3), New York University Medical Center, 560 First Avenue, TH427, New York, NY 10016, USA and Department of Biochemistry(2), Russian Peoples' Friendship University School of Medicine, Miklucho-Maklay St., 8, Moscow 117198, Russia ____________________________________________________________________________ BIOCHEMICAL CHARACTERIZATION OF ALZHEIMER'S SOLUBLE AMYLOID BETA PROTEIN IN HUMAN CEREBROSPINAL FLUID: ASSOCIATION WITH HIGH DENSITY LIPOPROTEINS. Alexei R. Koudinov, Natalia V. Koudinova(1), Asok Kumar, Ronald C. Beavis(2) and Jorge Ghiso Departments of Pathology, Medicine(1) and Pharmacology(2), New York University Medical Center, 560 First Avenue, New York, NY 10016 ABSTRACT The soluble form of Alzheimer's amyloid b protein (sAb) is associated with high density lipoprotein (HDL) in normal human plasma (BBRC (1994) 205, 1164-71). Since sAb is also present in cerebrospinal fluid (CSF) and the lipoprotein pattern of CSF is different from that of plasma, it was of interest to ascertain whether the interaction of sAb with HDL also occurs in CSF. Normal human CSF lipoproteins were obtained by sequential flotation ultracentrifugation and analysed for the presence of sAb via immunoblot, size-exclusion chromatography, immunoelectron microscopy, N-terminal sequence and mass-spectrometry analyses. Soluble Ab was associated with CSF-HDL particles of 16.8 +/- 3.2 nm in diameter and approximately 200 kDa of relative molecular mass. A ~4.3 kDa component purified by HPLC was immunoreactive with anti-Ab antibodies, exhibited an N-terminal sequence identical to the Ab peptide and a mass of 4325.1 Da, indicating that the main sAb specie associated with CSF-HDL is sAb1-40. _________________________________________________________________________ ALZHEIMER'S SOLUBLE AMYLOID BETA PROTEIN IS ASSOCIATED WITH HIGH DENSITY LIPOPROTEINS IN NORMAL HUMAN CEREBROSPINAL FLUID AND IS SECRETED BY HEPG2 CELLS AS A PART OF LIPOPROTEIN COMPLEXES A. R. Koudinov*, N. V. Koudinova, A. Kumar, R. C. Beavis and J. Ghiso, New York University Medical Center, TH 427, 560 First Avenue, New York, NY 10016. ABSTRACT The soluble form of amyloid b protein (sAb) is associated with high density lipoprotein (HDL) in normal human plasma (Biochem Biophys Res Commun (1994) 205, 1164-71). This suggests that sAb to HDL association is rather a more general phenomenon taking place in other biological fluids and tissues. To ascertain this hypothesis the colocalization of sAb with lipoproteins (LP) was investigated in cerebrospinal fluid (CSF) and in cell culture supernatant. Normal human CSF LPs were obtained by sequential flotation ultracentrifugation and analyzed for the presence of sAb via immunoblot, size-exclusion HPLC, immunoelectron microscopy, N-terminal sequence and mass-spectrometry analyses. Soluble Ab was associated with ~200 kDa CSF- HDL particles of 16.8 +/- 3.2 nm in diameter. A ~4.3 kDa component purified by reverse phase HPLC was immunoreactive with anti-Ab antibodies, exhibited an N-terminal sequence identical to the Ab peptide and a mass of 4325.1 Da, and therefore indicates that the main sAb specie associated with CSF-HDL is sAb1-40. The sAb secretion by cells in association with LPs was tested in human hepatoma HepG2 cell line. Soluble Ab in the cell culture supernatant was detected in ~200 kDa molecular mass LP complexes in association with apoJ, apoA-I, phospholipids, triglycerides and free and esterified cholesterol. Our results suggest that the association of sAb with LP represents a common mechanism for the peptide transport in biological fluids. _____________________________________________________________________________ Alexei Rudolphovich Koudinov Institute of Molecular Biology, Russian Academy of Sciences koudin@imb.imb.ac.ru From owner-ageing@net.bio.net Sat Jun 22 23:00:00 1996 Path: biosci!IMB.IMB.AC.RU!koudin From: koudin@IMB.IMB.AC.RU ("Alexei R. Koudinov") Newsgroups: bionet.molbio.ageing Subject: POSITION REQUEST Date: 23 Jun 1996 12:49:02 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 309 Sender: daemon@net.bio.net Distribution: world Message-ID: <9606231946.AA10658@mchip00.med.nyu.edu> NNTP-Posting-Host: net.bio.net Dear Amyloid/Ageing subscribers: I began to study Alzheimer's amyloid beta (Ab) protein in 1992, at the time when it was becoming clear that this protein exists normally in a soluble form (soluble Ab) and that it is not just a pathological protein. My research activities yielded an on-going project, devoted to understanding in more detail the normal biology of amyloid beta. Understanding the normal biology of Ab would answer the questions of why soluble Ab does not undergo fibrillogenesis in biological fluids but does polymerize into amyloid fibrils in the disease, and what the biological consequences of Ab deposition within the brain tissue are. This, in turn, would be crucial for understanding the pathophysiology of Alzheimer's disease and for delineating pathologically grounded new approaches to therapy. My current postdoctoral position at NYU Medical Center just expired. Thus, to continue my research I have to find another position. I would be happy to continue my research as a part of your Department/ University/ Center, if you might wish to consider such a possibility. Sincerely Yours, Alexei R. Koudinov, M.D., Ph.D. P.S. Enclosed please find CV and ABSTRACTS of my recent papers ______________________________________________________________________________ NAME: ALEXEI R. KOUDINOV E.MAIL: koudin@imb.imb.ac.ru EDUCATION: University Years Degree Major Moscow Medical University 1984- `MD Biochemistry, 1992 Cell/Molecular Biology, Medicine Engelhardt Institute of 1992- PhD Biochemistry Molecular Biology, Russian 1995 Academy of Sciences, Moscow. ( The Ph.D. research project was performed in the Department of Pathology, New York University Medical Center. Ph.D. thesis: "Soluble amyloid beta is complexed to high density lipoprotein 3 and very high density lipoproteins", Sponsor/advisor: Professor B. Frangione, M.D., Ph.D.). WORK EXPERIENCE: 1983-1984 Laboratory Assistant, Chemical Analysis Laboratory, Chelyabinsk Tractor Plant. 1989 Laboratory Assistant, Genetics Department, Moscow Medical University. 1990 Research Assistant, Enzymology Braunstein Memorial Laboratory, Engelhardt Institute of Molecular Biology. 1991-1992 Medical Assistant, Second Department of Neurology, Moscow Medical University. 1992-present Assistant Research Scientist, Department of Pathology, New York University Medical Center RESEARCH EXPERIENCE: 1. Studies of structure-function relationship of two subforms of eukaryotic Topoisomerase I (Masters' thesis research project, 1990-1992). Enzymology Braunstein Memorial Laboratory, Engelhardt Institute of Molecular Biology, Moscow, Russia. Sponsor: Dr. A. Gabibov, Ph.D. Major techniques used: affinity, ion-exchange and hydrophobic interaction chromatography, routinely and HPLC modification; protein quantification; protein and DNA electrophoresis; isoelectrofocusing; enzymatic kinetic studies; partial proteolysis; immunoblot analysis and enzyme-linked immunosorbent analysis. 2. Studies of DNA-hydrolysing catalytic antibodies from autoimmune sera (1991-1992) Enzymology Braunstein Memorial Laboratory, Engelhardt Institute of Molecular Biology, Moscow, Russia. Advisors: Dr. A. Gabibov, Ph.D. Major techniques used: IgG preparation from autoimmune sera by chromatography, routine and HPLC modification; DNA isolation; DNA hydrolysing activity assay. 3. Studies of autoimmune reaction in psoriatic skin (collaborative project with Dr. A. Tkachenko, M.D., Ph.D., 1991-1992) Laboratory of cancerogenesis, Engelhardt Institute of Molecular Biology, Moscow, Russia. Maor techiques used: skin biopsy preparations; IgG preparation from human plasma ( routine chromatography and HPLC on ProteinG Sepharose ); gel electrophoresis and immunoblot analysis; 2D-gel electrophoresis. 4. Studies of connectivity of visual cortex in rats and human cortical brain slices in vitro (Summer studentship program, Summer, 1992) Department of Neurobiology, Brain Research Center, Weizmann Institute of Science, Rehovot, Israel. Advisor: Dr. G. Kenan-Vaknin, Ph.D. Major techniques used: preparation and maintaing in vitro mice, rat and human cortical brain slices; probing of cortical connectivity in live brain slices with tracer biocytin (a derivative of biotin); potential recording; immunohistochemistry. 5. Studies of killing of Trypanosoma brucei by human serum (collaborative project with Dr. S. Tomlinson, Ph.D., 1994-1995) Michael Heidelberger Division of Immunology, Department of Pathology, New York University Medical center, New York. Advisor: Dr. V. Nussenzweig, M.D., Ph.D. Major techniques used: gradient ultracentrifugation; size exclusion chromatography, FPLC modification; Trypanosoma brucei killing assay; gel electrophoresis and immunoblot analysis. 6. Studies of normal biochemistry of soluble amyloid beta protein (Ph.D. thesis research project, 1992-1996) Department of Pathology, New York University Medical center, New York. Sponsor: Dr. B. Frangione, M.D., Ph.D. Major techniques used: sequential flotation ultracentrifugation; immunoaffinity chromatography; size exclusion and reverse phase HPLC; thin-layer chromatography; gel electrophoresis and immunoblot analysis; enzyme-linked immunosorbent analysis; chemiluminescence; optical and chemiluminescent densitometry; amino acid sequence analysis; electron and immunoelectron microscopy; immunocytochemistry; biotin technology for tracing proteins in biological fluids; animal cell culture; metabolic labelling of cell protein and lipid; lipid extraction; lyposome preparation; enzymatic quantification of triglycerides, phospholipids, nonesterified and total cholesterol; statistical analysis. PUBLICATIONS: KUDINOV, Alexei R., Bronstein, Igor B., Gabibov, Alexander G. and Gololobov, Gennady V. (1992) Two subforms of eukaryotic topoisomerase I: Purification and structure-function relationship. FEBS Lett 314: 267-270. Tkachenko, Andrei V., Starkov, Ivan V., Shuster, Alexander M., KOUDINOV, Alexei R., Zakharov, Sergei F., Shishkin, Sergei S., Mordovtsev, Vladimir N., and Kisselev, Lev, L. (1992) Autoimmune reaction in psoriatic skin. In Proceedings of the conference "Modern Enzymology: problems and trends". St.Petersburg. Ghiso, Jorge, Matsubara, Etsuro, KOUDINOV, Alexei, ChoiMiura, Nam Ho, Tomita, Motono, Wisniewski, Thomas, Frangione, Blas. (1993). The cerebrospinal fluid soluble form of Alzheimer's amyloid beta is complexed to SP-40,40 (apolipoprotein J), an inhibitor of the complement membrane-attack complex. Biochem J 293: 2730. KOUDINOV, Alexei, Matsubara, Etsuro, Frangione, Blas, Ghiso, Jorge. (1994). The Soluble Form of Alzheimer's Amyloid Beta Protein is Complexed to High Density Lipoprotein 3 and Very High Density Lipoprotein in Normal Human Plasma Biochem Biophys Res Commun 205: 1164-1171. Tomlinson, Stephen, Jansen, Ana-Maria, KOUDINOV, Alexei, Ghiso, Jorge, Choi-Miura, Nam-ho, Rifkin, Mary, Ohtaki, Sachiya, and Nussenzweig, Victor. (1995) High-density-lipoprotein-independent killing of Trypanosoma brucei by human serum. Molecular and Biochemical Parasitology 70: 131-138. KOUDINOV, Alexei, R., Koudinova, Natalia, V., and Berezov, Temirbolat, T. (1996). Alzheimer's peptides Ab1-40 and Ab1-28 inhibit the plasma cholesterol esterification rate. Biochem Mol Biol Internat. 38(4): 747-752. KOUDINOV, Alexei, R., Berezov, Temirbolat, T., and Koudinova, Natalia, V. Multiple inhibitory effects of Alzheimer's peptide Ab1-40 on lipid byosynthesis in cultured human HepG2 cells. In press. (SEE ABSTRACT BELOW) KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok, Beavis, Ronald, and Ghiso, Jorge. (1996) Biochemical Biophysical Research Communication. Biochemical characterization of Alzheimer's soluble amyloid beta protein in human cerebrospinal fluid: association with high density lipoproteins. Biochem Biophys Res Commun. In Press. (SEE ABSTRACT BELOW) MEETING PRESENTATIONS: KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok. Is amyloid beta an apolipoprotein? New York University Medical Center Neuroscience Meeting. New York. December 1995. KOUDINOV, Alexei, R., Koudinova, Natalia, V., Kumar, Asok, Beavis, Ronald, and Ghiso, Jorge. Alzheimer's soluble amyloid beta protein is associated with high density lipoproteins in normal human cerebrospinal fluid and is secreted by HepG2 cells as a part of lipoprotein complexes. Society for Neuroscience Annual Meeting. Washington, DC, 1996. Submitted. (SEE ABSTRACT BELOW). AWARDS: 1989-1992 All Russian Government Scholarship for outstanding success in studies. 1992 Honorary Diploma of Medical Doctor. Moscow Medical University. 1992 Summer student fellowship. Weizmann Institute of Science. Rehovot. Israel 1994-1995 Pilot Research Grant from The Aging and Dementia Research Center at NYU Medical Center. Project title: "HepG2 as a model for studies of sAb secretion by human cells" (NIH Grant AG08051, Dr. S.Ferris, P.I.). REFERENCES available upon request 10 June 1996 _______________________________________________________________________ MULTIPLE INHIBITORY EFFECTS OF ALZHEIMER'S PEPTIDE Ab1-40 ON LIPID BIOSYNTHESIS IN CULTURED HUMAN HEPG2 CELLS. Alexei R KOUDINOV(1), Temirbolat T BEREZOV(2) and Natalia V KOUDINOVA2,3* Department of Pathology(1) and Medicine(3), New York University Medical Center, 560 First Avenue, TH427, New York, NY 10016, USA and Department of Biochemistry(2), Russian Peoples' Friendship University School of Medicine, Miklucho-Maklay St., 8, Moscow 117198, Russia ____________________________________________________________________________ BIOCHEMICAL CHARACTERIZATION OF ALZHEIMER'S SOLUBLE AMYLOID BETA PROTEIN IN HUMAN CEREBROSPINAL FLUID: ASSOCIATION WITH HIGH DENSITY LIPOPROTEINS. Alexei R. Koudinov, Natalia V. Koudinova(1), Asok Kumar, Ronald C. Beavis(2) and Jorge Ghiso Departments of Pathology, Medicine(1) and Pharmacology(2), New York University Medical Center, 560 First Avenue, New York, NY 10016 ABSTRACT The soluble form of Alzheimer's amyloid b protein (sAb) is associated with high density lipoprotein (HDL) in normal human plasma (BBRC (1994) 205, 1164-71). Since sAb is also present in cerebrospinal fluid (CSF) and the lipoprotein pattern of CSF is different from that of plasma, it was of interest to ascertain whether the interaction of sAb with HDL also occurs in CSF. Normal human CSF lipoproteins were obtained by sequential flotation ultracentrifugation and analysed for the presence of sAb via immunoblot, size-exclusion chromatography, immunoelectron microscopy, N-terminal sequence and mass-spectrometry analyses. Soluble Ab was associated with CSF-HDL particles of 16.8 +/- 3.2 nm in diameter and approximately 200 kDa of relative molecular mass. A ~4.3 kDa component purified by HPLC was immunoreactive with anti-Ab antibodies, exhibited an N-terminal sequence identical to the Ab peptide and a mass of 4325.1 Da, indicating that the main sAb specie associated with CSF-HDL is sAb1-40. _________________________________________________________________________ ALZHEIMER'S SOLUBLE AMYLOID BETA PROTEIN IS ASSOCIATED WITH HIGH DENSITY LIPOPROTEINS IN NORMAL HUMAN CEREBROSPINAL FLUID AND IS SECRETED BY HEPG2 CELLS AS A PART OF LIPOPROTEIN COMPLEXES A. R. Koudinov*, N. V. Koudinova, A. Kumar, R. C. Beavis and J. Ghiso, New York University Medical Center, TH 427, 560 First Avenue, New York, NY 10016. ABSTRACT The soluble form of amyloid b protein (sAb) is associated with high density lipoprotein (HDL) in normal human plasma (Biochem Biophys Res Commun (1994) 205, 1164-71). This suggests that sAb to HDL association is rather a more general phenomenon taking place in other biological fluids and tissues. To ascertain this hypothesis the colocalization of sAb with lipoproteins (LP) was investigated in cerebrospinal fluid (CSF) and in cell culture supernatant. Normal human CSF LPs were obtained by sequential flotation ultracentrifugation and analyzed for the presence of sAb via immunoblot, size-exclusion HPLC, immunoelectron microscopy, N-terminal sequence and mass-spectrometry analyses. Soluble Ab was associated with ~200 kDa CSF- HDL particles of 16.8 +/- 3.2 nm in diameter. A ~4.3 kDa component purified by reverse phase HPLC was immunoreactive with anti-Ab antibodies, exhibited an N-terminal sequence identical to the Ab peptide and a mass of 4325.1 Da, and therefore indicates that the main sAb specie associated with CSF-HDL is sAb1-40. The sAb secretion by cells in association with LPs was tested in human hepatoma HepG2 cell line. Soluble Ab in the cell culture supernatant was detected in ~200 kDa molecular mass LP complexes in association with apoJ, apoA-I, phospholipids, triglycerides and free and esterified cholesterol. Our results suggest that the association of sAb with LP represents a common mechanism for the peptide transport in biological fluids. _____________________________________________________________________________ Alexei Rudolphovich Koudinov Institute of Molecular Biology, Russian Academy of Sciences koudin@imb.imb.ac.ru From owner-ageing@net.bio.net Sun Jun 23 23:00:00 1996 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!munnari.OZ.AU!news.mel.connect.com.au!news.uwa.edu.au!newsman.murdoch.edu.au!vetmac3.murdoch.edu.au!user From: cummins@central.murdoch.edu.au (Jim Cummins) Newsgroups: bionet.molbio.ageing Subject: Re: Predictors of human longevity Date: Mon, 24 Jun 1996 13:00:17 +0800 Organization: Murdoch University Lines: 17 Distribution: world Message-ID: References: NNTP-Posting-Host: vetmac3.murdoch.edu.au In article , ageing@ilr.rc.ac.ru ("Leonid A.Gavrilov") wrote: > Dear Colleagues, > > Recently we have found new strong predictors of human longevity > at personal level. > > These new results were published partially in the following papers: > I'd appreciate a summary of your findings. We are interested in the topic of maternal age and possible infertility in male offspring. -- URL http://numbat.murdoch.edu.au/spermatology/spermhp.html From owner-ageing@net.bio.net Mon Jun 24 23:00:00 1996 Path: biosci!daresbury!not-for-mail From: samuelc@max.roehampton.ac.uk (Samuel Cronin) Newsgroups: bionet.molbio.ageing Subject: Re: WE NEED YOUR HELP Date: 25 Jun 1996 14:48:26 +0100 Lines: 68 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <4qoqna$t56@mserv1.dl.ac.uk> Fcc: outgoing Security: None Original-To: ageing@dl.ac.uk Type: External Classification: Certified Dr Troisi, Such a database of institutes involved in research into ageing would be very valuable - in the least it would offer students of gerontology such as myself a great resource when looking for opportunities abroad. I have been slowly building such a dbase over the last half year but its far from complete, however, when its finished I intend to puplish it on the WWW. I would be interested in knowing if you have any intentions to make the list available to the public. If you havn't started yet a way to dive into the deep end would be to perform a web search for AGEING and RESEARCH which will give you hundereds of institution performing research in gerontology. Particularly relevant would be... Ageing Research Centre (ARC) http://www.hookup.net/mall/aging/agesit59.html WSU Institute of Gerontology http://www.iog.wayne.edu/ USC (Caleb Finch) http://www.usc.edu/dept/nbio/nibs/brochure.html#aging Also good link sites... Internet Resources on Aging http://www.aoa.dhhs.gov/aoa/post/jpostlst.txt Human Ageing WWW Resources http://www.drake.edu/bgil/www/disc/age/age.html Life Extension Foundation http://aeiveos.wa.com/lef/index.html Two important sites in the UK (although I dont think they have WWW pages yet) are the gerontology MSc in Kings College London, and in particular the Biological Gerontology department in Manchester University headed by Prof. Tom Kirkwood. The latter will soon be expanding into Newcastle University at which point it will have the largest facilities for research into ageing in Europe. Again, please let me know if you intend to make this freely available as I would be particularly interested in seeing it. Regards Sam On 13 Jun 1996 mtroisi@MALTANET.OMNES.NET wrote: > In 1989 the University of Malta started an Institute of Gerontology and > Geriatrics. The Institute runs a one year full time Postgraduate Diploma > Course in Gerontology and Geriatrics. We also run a Master's degree based > on research in thye field of ageing. > Looking forward to know wich universities in the USA and the UK offer > any courses in the fields of gerontology and geriatrics, at what level, > and what duration. We are trying to set a data base of all these centres. > Any kind of information will be more than welcome. > I wish to thank you in advance for your attention and cooperation. > Regards > Dr.Joseph Troisi > > > > ~ From owner-ageing@net.bio.net Wed Jun 26 23:00:00 1996 Path: biosci!rutgers!uwm.edu!lll-winken.llnl.gov!nntp.coast.net!netnews.worldnet.att.net!ix.netcom.com!news From: belsare@ix.netcom.com(Girish V Belsare) Newsgroups: bionet.molbio.ageing Subject: HELP : POSTDOC info required Date: 27 Jun 1996 03:51:42 GMT Organization: Netcom Lines: 23 Message-ID: <4qt0ge$i3n@dfw-ixnews2.ix.netcom.com> NNTP-Posting-Host: dgr-il2-03.ix.netcom.com X-NETCOM-Date: Wed Jun 26 10:51:42 PM CDT 1996 Hello. I am trying to gather information regarding postdocterate positions available nearby Chicago ( IL , USA ) area. This information is requested by a friend of mine who is doing a Ph.D. in cancer research in India. Her thesis is regarding studies on the expression of myeloid antigens on human granulocytes. I do not have enough background in this area and so , I am finding it difficult to proceed. After checking through the available newsgroups , I found this one to be closest in terms of terminology ( pardon my ignorance please ! ) Hence , the request. Any help/direction you can give me in this regard is welcome. My e-mail address is : belsare@ix.netcom.com Thanx Belsare From owner-ageing@net.bio.net Wed Jun 26 23:00:00 1996 Path: biosci!LAFN.ORG!ba182 From: ba182@LAFN.ORG (John Guerin) Newsgroups: bionet.molbio.ageing Subject: Update on Negligible Senescence in Long-Lived Fishes Date: 27 Jun 1996 16:49:22 -0700 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 60 Sender: daemon@net.bio.net Distribution: world Message-ID: <199606272345.AA27564@lafn.org> Reply-To: ba182@lafn.org NNTP-Posting-Host: net.bio.net My abstract "Divergent Model of Aging? Negligible Senescence in Long-Lived Fishes" summarized a literature search and personal communications over many months. This update is as of June 27th, 1996. Of the long-lived fishes listed in the abstract, most are not good candidates for study: they potentially have other explanations for their longevity, they are difficult to acquire, or not much information is known about them. For example, many rockfish and flatfish live at deep levels with very little oxygen, so it's possible they are just "stretching out" their lifespan (further than from already being cold-blooded). Also, some fish, such as the tautog, go into torpor in the winter, so this complicates the issue of just how biologically old they are. My most promising candidate currently is the "fancy" koi, that live at the surface in ponds are are reputed to have lived 100-200 years. I am searching for scientific verification of this. If it turns out to be true, then the next step is formulating a method for isolating the pattern of aging of a koi from that of a fish that does senesce, such as the guppy or platyfish. It makes sense the difference is in the genetic code, and probably juvenile maturation is the time aging is first expressed for those animals that do age (the "usual" pattern of aging is called gradual senescence, as opposed to animals with negligible senescence, which have not been proven to biologically age). There is a lot of activity in DNA identification in fish, but none I'm aware of looking for genetic markers of senescence. Could it be that senescence as an evolutionary force evolved after life was already established? George C. Williams, whose 1957 paper laid a theoretical basis for the evolution of senescence, noted in that paper "It is indeed remarkable that after a seemingly miraculous feat of morphogenesis a complex metazoan should be unable to perform the much simpler task of merely maintaining what is already formed" (Pleiotropy, Natural Selection, and the Evolution of Senescence, George C. Williams, Evolution 11: 398-411 December, 1957). Do these fishes (as well as some reptiles and amphibians) have a non-senescing biological functioning, that remains optimal until such time as disease, accident or predation does them in? If so, we currently lack the knowledge and resources to examine these animals and isolate what allows them to live indefinitely. With competing research priorities, proof of an "ideal" candidate exhibiting negligible senescence is necessary to attract funding. In conclusion, this project needs scientifically verified research on longevity in koi or another "ideal" candidate, contacts with scientists studying fish DNA, especially those interested in senescence, and funding sources to make it happen once the above is in place. If you are interested in participating, have information or questions, or know of researchers in this field, please contact John C. Guerin at e-mail ba182@lafn.org, or via telephone at (619) 563-9473. -- John C. Guerin From owner-ageing@net.bio.net Thu Jun 27 23:00:00 1996 Path: biosci!rutgers!uwm.edu!cs.utexas.edu!howland.reston.ans.net!newsfeed.internetmci.com!in1.uu.net!EU.net!usenet2.news.uk.psi.net!uknet!usenet1.news.uk.psi.net!uknet!dispatch.news.demon.net!demon!mail2news.demon.co.uk!longevb.demon.co.uk From: John de Rivaz Newsgroups: bionet.molbio.ageing Subject: Re: Update on Negligible Senescence in Long-Lived Fishes Date: Fri, 28 Jun 1996 11:27:57 +0100 Organization: Myorganisation Lines: 27 Message-ID: <5607588wnr@longevb.demon.co.uk> References: <199606272345.AA27564@lafn.org> Reply-To: John@longevb.demon.co.uk X-NNTP-Posting-Host: longevb.demon.co.uk X-Newsreader: Newswin Alpha 0.9.1 X-Mail2News-Path: relay-4.mail.demon.net!post.demon.co.uk!longevb.demon.co.uk > Could it be that senescence as an evolutionary force evolved after > life was already established? If so, then it must have evolved in species against species competition against something. What? I wonder whether life is a complex system of many variable, each one of which has an undesireable side effect. These can keep the "pin on its point" only for so long before it falls over. If you can find an immortal fish, then this theory must be disproved, at least as far as fishes go. Then maybe we could see why the fish is immortal and what genetic modifications we can make to existing people to give their systems the same properties. -- Sincerely, **************************************** * Publisher of Longevity Report * John de Rivaz * Fractal Report * * details on request * **************************************** In the information age, sharing can increase world wealth enormously, because giving information does not decrease your information. http://ourworld.compuserve.com/homepages/JohndeR Fast loading, very few slow pictures From owner-ageing@net.bio.net Sat Jun 29 23:00:00 1996 Path: biosci!daresbury!yama.mcc.ac.uk!zippy.dct.ac.uk!uknet!usenet2.news.uk.psi.net!uknet!usenet1.news.uk.psi.net!uknet!EU.net!sun4nl!surfnet.nl!news.rotterdam.luna.net!news Newsgroups: bionet.molbio.ageing Subject: Immortality research Message-ID: <4r5llv$aca@aladdin.rotterdam.luna.net> From: peck@luna.nl (Mischa Coster) Date: Sun, 30 Jun 1996 10:30:11 GMT Organization: Luna Internet Services NNTP-Posting-Host: 17-pstn.rotterdam.luna.net X-Newsreader: Forte Free Agent 1.0.82 Lines: 6 I have a question. Has anyone ever heard about telosomes? I read an newspaper-article about half a year ago about some guy doin a lot of research and so far he has succeeded in prolonging the life of monkees by some 20%. I'd like to have some more info about this research, as I can't find anything on it on the WWW. From owner-ageing@net.bio.net Sat Jun 29 23:00:00 1996 Path: biosci!galaxy.ucr.edu!ihnp4.ucsd.edu!swrinde!howland.reston.ans.net!agate!cgl!itssrv1.ucsf.edu!itsa!cpatil From: cpatil@itsa.ucsf.edu (Chris Patil) Newsgroups: bionet.molbio.ageing Subject: Re: Immortality research Date: 30 Jun 1996 21:36:22 GMT Organization: UCSF, ITS Computing Facility Lines: 17 Message-ID: <4r6s0m$lh4@itssrv1.ucsf.edu> References: <4r5llv$aca@aladdin.rotterdam.luna.net> NNTP-Posting-Host: itsa.ucsf.edu In article <4r5llv$aca@aladdin.rotterdam.luna.net> peck@luna.nl (Mischa Coster) writes: >I have a question. Has anyone ever heard about telosomes? I read an >newspaper-article about half a year ago about some guy doin a lot of >research and so far he has succeeded in prolonging the life of monkees >by some 20%. I'd like to have some more info about this research, as I >can't find anything on it on the WWW. That's probably because they're called "telomeres." No telomere research has extended the life of a higher organism by any amount, certainly not 20%. A better place to look than Web searches would be literature databases like Medline. Hope this helps. From owner-ageing@net.bio.net Sun Jun 30 23:00:00 1996 Path: biosci!daresbury!not-for-mail From: samuelc@max.roehampton.ac.uk (Samuel Cronin) Newsgroups: bionet.molbio.ageing Subject: Re: Immortality research Date: 1 Jul 1996 09:32:37 +0100 Lines: 20 Sender: lpddist@mserv1.dl.ac.uk Distribution: bionet Message-ID: <4r82f5$o4@mserv1.dl.ac.uk> Fcc: outgoing Security: None Original-To: ageing@dl