From owner-ageing@net.bio.net Mon Oct 04 23:00:00 1993
Path: biosci!NET.BIO.NET!kristoff
From: kristoff@NET.BIO.NET (Dave Kristofferson)
Newsgroups: bionet.molbio.ageing
Subject: test, please ignore
Message-ID: <CMM.0.90.2.749862273.kristoff@net.bio.net>
Date: 5 Oct 93 23:04:33 GMT
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Test, please ignore.

From owner-ageing@net.bio.net Thu Oct 07 23:00:00 1993
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From: treon@u.washington.edu (Treon Verdery)
Newsgroups: sci.life-extension,sci.med,bionet.molbio.ageing
Subject: mitochondrial DNA therapy for aging
Message-ID: <294mlh$15n@news.u.washington.edu>
Date: 8 Oct 93 21:38:57 GMT
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	*All comments are welcome!*  *Please write!*

A few months ago I had what seemed to be an insight about mitochondrial
DNA therapy, longevity, and cancer.  Other activities in life have kept
me from devoting as much time as I'd like to these ideas.  I post them
now in hopes that they will provide some useful stimulation to real
researchers.  All copyright is reserved, and I specifically claim
ownership of the ideas for patent or other purposes.  Distribution is
set to USA only, please maintain this distribution on any followups.

>> Dr. Patil/Chris - I'll be amending this document with lots of postnotes,
>> indicated by the double >>.  This file consists of three parts:
>> the unsophisticated write up produced a few hours after having the basic
>> ideas.  This section contains some *drastic* inaccuracies, but you will 
>> get the drift of it.  The second part is a letter with some additional 
>> concept refinement, and the third part is a patentistic description of 
>> most of the above, plus many new ideas.  

>> This file is huge, but the crux of it is in the first 2-3K of words
>> so don't despair at the length.

>> I hope you find it thought provoking, and I welcome (a polite way to 
>> say urge!) any comments.

------------------------------------------------------------------------------
anyway, here's the big idea... maybe a BIG idea, sort of section three, 
subparagraph two of the holy grail of Big Ideas...

        A new class of pharmaceutical therapy for keeping       
        mitochondria from accumulating deletions during replication, 

also known throughout Europe and America as...
  
        "Eternal Youth"

(Wow what Severe Hype!  I'm not sure Hype can get any more grandiose than 
that... seriously though, I've been looking though Medline this evening 
trying to pin the idea(s) down and offer real support for some vague 
points.  you will find *many* errors, but read on!)

here goes:

Have you heard of the mitochondrial theory of aging?
As I vaguely remember it goes quite a bit like this:

Mitochondria do not reproduce sexually.  As your cells
divide mitochondria replicate themselves.  In order to create a new cell, 
'about' 100 new mitochondria have to be replicated.   
        
Mitochondrial DNA  is kinda like a 
simple circular plasmid with a Start sequence, an End
sequence and in-between sequences encoding protein
production.  These '100' mitochondria, each with its own mtDNA, 
replicate as individuals.  Each of these '100'
are subject to point mutations and deletions during the life of the cell.  

Mitochondrial DNA  is unusually susceptible to deletion at specific weak 
points.  So much so that while about 100%
of a newborn's mitochondria will be doing their job, only 
20% of a 60 year old's mitochondria will be working.
Each cell has much less energy available for protein synthesis in general.  
This has been specifically linked with changes in tissue behavior and 
senesence.

Particularly exciting is the observation that damaged
(smaller/bearing deletions) mtDNA is replicated
*preferentially* 'simply' because there is less stuff between the Start and 
End sequences of the mtDNA!  
Nonfunctional mutations accumulate in that cell's line with each cell 
division, and with each generation of new cells there is a (modified) 
exponential rise in the number of dysfunctional mitochondria per cell.

AND NOW FOR THE PUNCHLINE

I'm pretty darned sure I've figured out a way to make mtDNA 
(mtDNA specifically) less sensitive to deletions and/or cause the replication 
process to avoid replicating mtDNA that is missing (specific) big chunks.
Perhaps in a pill no less -no viruses or even  nanotechnology ;-)

It'll seem easier to swallow (gulp!), if I describe a couple functioning 
concepts that are commercialized now, and operate using methods I'm going 
to borrow:

Component idea 1)

Zovirax is an anti-viral drug for herpes.  here's how it works:

Viruses that Zovirax targets like to make themselves
out of specific amino acid sequences.  during replication they find these 
sequences floating around and incorporate them into structure.  
People who take zovirax tablets are really taking pills filled with a 
specific amino acid-sequence that the virus wants. ALMOST.  The Zovirax 
sequence contains an amino-acid that is the L-isomer.  (er, maybe) The cell 
produces all the little virus copies, but none of them work - that is, none 
of them can infect a second generation of cells.   The drug
is 'safe' because the rest of the body has little interest in the 
tricked-out amino acid sequence, and because virii reproduce quickly and 
are the preferential uptakers. 

Component idea 2)

In the Bad Old Days there was a class of sedatives called Bromides.  
Essentially, people would take Bromine compounds (KBr) until some of their Cl
had been replaced by Br and the electrical potentials in their nerves had 
changed a bit.  Unfortunately, as the Br built up, eventually all sorts of 
stuff would go out of whack.

and here's component idea 3)

Cellular chemistry is traced with radioactive isotopes.
Scientists have recently taken specific note than some
tritiated proteins (tritium instead of H) diffuse across
mitochondrial membranes much more slowly(increased mass).  The cellular
chemistry that the radiolabelled compounds execute is, however, generally 
the same. At sufficient mass increases however, the chemical 
functionality radically changes.


*******Now, as best as I can explain it so far here's the idea:

Assemble amino acid sequences that have preferential
uptake for mtDNA replication. 

'weight' these sequences so that their total mass
is the same as a naturally occuring sequence, BUT
make some of the individual proteins out of Heavier, 
and also Lighter *stable* isotopes. ((**This is the drug.**))

an example:

normal original protein fragment: CGGACCTAGT
Heavy Gaunidine version: CggACCTAg

(lowercase = deuterium as substitute for H, or perhaps
C13 for C12, or perhaps some O isotope
let's pretend that the T's have some lighter stable isotope(N) so that the 
total mass of this sequence is the same as the normal original.)

I have to pause and add some helpful additional concepts:

One of the reasons mtDNA accumulates deletions is that
some places along the amino acid sequence are fragile, that is,
they like to drop out under replication.  Simplistically, there are some 
weak links in what is otherwise a strong chain.

(NOT! -my how learned this all sounds. free grains of salt: .. . ... )

Bacteria that live in deep sea thermal vents thrive at
temperatures above 212 F.  These bacteria have many of the same enzymes 
and protein chemistry cycles as cool cells, their proteins are almost 
exactly the same, however, some of their proteins are less 'ornate', 
less 'sticky'; with fewer opportunities to pick up thermal motions and 
cross-link.  The rapid folding-and unfolding of hot-cell proteins is 
also somewhat different...

Some scientists speculate that hot bacteria were first, and that 
proteins evolved stickier, more ornate, more-cross-linkable molecular
forms to adapt to cooler environments.  

Just as a floating concept: imagine a partially deuterated enzyme as much 
more sluggish at low temperatures...normal at higher temperatures...
obviously the things the enzyme reacts with would have trouble w/the 
higher temperatures though...

>> sudden thought: is there a dueterated PCR patent enzyme work around?
 
It strikes me that there are possible strategies for using light and heavy 
amino acids to 
        
        1) bog down/break the replication of specific   
            misbegotten (deletion-flagging) amino acid sequences

        2) protect weak spots from damage, but not from
            replication (w/a slight differential of charge 
            potential)

        3)  all kinds of other stuff that messes with RNA

A typical 1) strategy:
A Grungy strategy to bog down shortened mtDNAs is this: After dosing 
the organism with isotopically peculiar amino acid sequences the 
'normal nonmutant' mtDNA has a 'normal' mass and reactivity.  
Those mtDNA that have experienced typical deletions at the 'weak links'
have unusual isotope concentrations that affect the behavior of the 
protein replication:

ok-to-replicate version:
CgAgg + gCTCC = thermodynamically ok to replicate

but:

CgAgggggg + GCTCCCCCC = thermodynamically slow/prohibited as all the heavies 
cluster together and/or  are limited by diffusion speed/availability of 
bits with all those heavy ggggs.

I guess you could call this "putting the wrong size pins on
the zipper" - when you get the big pins, and the big zip
there isn't enough energy/room to pull it any farther - but if you have at 
least 1 small pin it will work.  (Iffy indeed, but I can think of an 
experiment to test it - hoping to find the components of the experiment 
on medline). 

An interesting alternative to "wrong size pins on the zipper" is 
"slower pins on the zipper reduce the risk of speedy accidents", or perhaps, 
"I'm only going to zipper you if your start sequence includes light/heavy 
isotopes - and deletion-prone versions versions lack this 
light or heavy sequence.

In fact, once you begin thinking about it, there are a lot of 
"ordinary" things that could happen to work on this problem - without 
any isotope naughtiness at all.

I guess what is most important from my perspective is the idea that stable 
isotopes, with some degree of clever manipulation, can be used as amino 
acid replication/synthesis modifiers.  
Now I have a lot of reading to do! (Did you notice that I 
didn't mention mRNA hardly at all?)

-Treon


Here are some medline references at the end for background and stuff.  
I should have copied more but they seemed long enough as it was.

you can search medline anytime you want to follow your own fancies - 
(you probably know this address) just:
telnet uwin.u.washington.edu

#1 is an example of Tritiated compounds doing the same chemistry,
but 3-9X slower (within mitochondria (but not reproduction) no less!)

#2-4 are lame, but exploratory examples of mtDNA
 accumulating damage at extreme exponential rates and how this affects 
cellular energy and the respiration cycle.
my info comes from a dimly remembered review article that was much clearer...

P.S.  BOO!!

be my friend!  write back!!
(you are eligible for a medal for reading this far...)

#1
Loss of tritium from a substrate is often used to estimate
                the rate of dehydrogenation.  However, loss of 3H may be much 
		slower than loss of H because of the tritium isotope effect.
                In order to assess the impact of the tritium isotope effect,
                loss of 3H from the C-5 position of proline during
                dehydrogenation by rat liver mitochondria and bacteroids from
                soybean (Glycine max [L.] Merrill) nodules was compared with
                appearance of 14C in products of [14C]proline
                dehydrogenation.  Incubations were carried out in the
                presence of o-aminobenzaldehyde (added to trap the initial
                product, delta 1-pyroline-5-carboxylate).  The fraction of
                total 14C products trapped by o-aminobenzaldehyde varied from
                0.07 to 0.75 depending upon experimental conditions.  With
                rat liver mitochondria, dehydrogenation of [14C]proline was
                between 3.27 and 9.25 times faster than dehydrogenation of 3H
                proline, depending upon assay conditions.  Soybean nodule
                bacteriods dehydrogenated [14C]proline about 5 times faster
                than [3H]proline.  We conclude the following: (i) the rate of 
		proline dehydrogenation may be greatly underestimated by the
                tritium assay because of the tritium isotope effect, and (ii)
                the 14C assay may underestimate the rate of proline
                dehydrogenation if it is assumed that o-aminobenzaldehyde
                quantitatively traps delta 1-pyrroline-5-carboxylate under
                all conditions.  The simplicity of the tritium assay makes it
                attractive for routine use.  However, its use requires
                determination of the tritium isotope effect, under the
                specific conditions of the assay, in order to correct the
                results.  The considerations discussed here have broad
                applicability to any dehydrogenase assay employing tritium
                loss.


#2

The analysis of human skeletal muscle mitochondria revealed aprogressive 
		decline in mitochondrial respiratory chain
                function with age.  The activities affected to the greatest
                extent were those of complexes I and IV which were decreased
                by 59% and 47% respectively between the ages of 20-30 years
                and 60-90 years of age.  Quantitation of the 5 kb 'common'
                deletion of mtDNA using PCR revealed a progressive
                accumulation with age, from approximately 1 in 100,000 at 21
                years to 1 in 10,000 at 56 years and 1 in 5000 at 78 years of
                age.  The low absolute levels of this mutation are unlikely
                to contribute significantly to the observed mitochondrial
                dysfunction.


 Previous theories of aging based on somatic mutation
                neglected mtDNA, which has a high propensity for mutational
                error.  Knowledge of yeast mtDNA mutations and their
                functional effects, and of human mtDNA mutations identified
                in the mitochondrial cytopathies, provides for a concept of
                aging based on the cumulative effect of mutations affecting
                human mtDNA.  An essential feature of this concept is
                heteroplasmy, representing mixtures of normal and mutant
                mtDNA at the cellular and mitochondrial level, resulting in a
                "tissue mosaic" of focal bioenergetic deficits.  Direct
                evidence for the concept is provided by (i) focal loss of
                staining for mitochondrially encoded enzymes, such as
                cytochrome c oxidase, in tissues of aged individuals (humans
                and rats) and (ii) an age-related increase in deletional
                mutations in mtDNA demonstrable by application of the
		polymerase chain reaction to DNA templates from individuals
                of different ages.

Some mutations in mitochondrial DNA (mtDNA) causing a number
                of neuromuscular diseases are suggested to arisespontaneously
		during the life of an individual.  To
                substantiate the extent and the rate of these somatic
                mutations, mtDNA specimens from post-mortem human heart
                muscles of subjects in differing age groups were hydrolyzed.
                8-Hydroxy-deoxyguanosine (8-OH-dG), a hydroxyl-radical adduct
                of deoxyguanosine, in mtDNA, was quantitatively determined
                using a micro high-performance liquid chromatography/mass
                spectrometry system.  In each specimen, the mtDNA with a 7.4
                kilo base-pair deletion was quantified by the kinetic
                polymerase chain reaction method.  In association with age,
                the 8-OH-dG content accumulated exponentially up to 1.5% with
                a correlative increase in the content of the deleted mtDNA up
                to 7%.  Clear correlation between the 8-OH-dG content in
                mtDNA and the population of mtDNA with a deletion (r = 0.93,
                P < 0.01) gives insight into the mechanism for the generation
                of a large deletion.  These results indicate thataccumulation 
		of somatically acquired oxygen damage together
                with age-associated mutations in mtDNA which lead to
                bioenergetic deficiency and the heart muscle weakness are
                inevitable in human life.
-------------------------------------------------------------------------------
End of the email extraction from the first letter.

Here is an extraction from a second letter that I wrote to a friend.  


Anyway, Hello!   Thanks for asking if you could pass the idea on
first - I never bothered to get it notarized so I'll do that today
so that you can pass it on to Peter say Thursday.  It is a building
thrill to have someone else interested and to hopefully add some
explorations and accuracies.  Makes me nervous too!  That version 
I sent you was written about 4 hours after the original inspiration
So, um, it'll read really dumb to someone who knows what they
are talking about.  I think it has been 6-8 weeks since I wrote that,
and have learned all sorts of shoring-up and eroding-down influences
to the central idea:


And now... some inferences from the literature:

Plus:
* There are specific common deletion sites in mtDNA that result in 
  large, unique amino acid sequences suitable as labels 

* the idea is obviously portable to other genetic and protein
 pharmacological things; RE aging, it also has direct application
 to other aging theories/aging markers notably the telomeric
 marker/tape leader theories and what I'd call the 
 psuedocaloric restriction methionine displacer theory

* A similar idea/set of ideas has never appeared in the abstracted
  literature/patent databses I've looked in

* Rats forced to live out their lives on 30% D2O are normal
  (an incredible puzzle there I'd say)

Minus:

* people with progeria, a very unusual rapid aging syndrome do not
  have mtDNA problems at all (secret plus: they do have shortened
  telomeres proportional to the shortening seen in people of their
  apparent physical age!)

* Cancer research suggests that that targeting 
   is very difficult; then again, maybe I've lucked out
   and thought of a harmless-unless-cancerous mechanism.  or even
   a cancer prophylactic of a different nature than antioxidants
   sort of like invisible chemotherapy.
>> -distributed stable isotopes lie in transparent wait until cancer/other
>> bioprocesses concentrate them and 1) retard them 2) signal them.
>> Advantage: minimal/no toxicity excaept at active concentration/comnination
>> sites

(Andrew... the minuses are turning into positive wild speculation!
 This is good - but I started out wanting to write a balanced treatment
 for You and Peter)

More Wild Speculation

* currently existing gene therapies could add another degree
  of 'facility' by influencing the residence times and
  stabilities of introduced genes, as well as marking sites for 
  secondary therapies. The whole idea of tagging, signalling, and modifying
  cellular stuff without active chemical groups just floats there...
  suggesting wild stuff like cellular early-early-early diagnoses
  dianoses based on excretion/assay of oddball Isotope-loaded amino acid
  sequences.  

  The various forms of matching and concentration
  that I know about in cells suggest statistical 'control'(?) of how much
  of what accumulates where.  Nucleic acid dynamics are so bizarre
  that there are many different sorts of active and inactive structures
  to tweak on...

  ...I guess I'm just really turned on by the idea of chemicals that
  in low concentrations mimic perfectly their normal isotope
  cousins, but at times of unusual concentration due to replication,
  or other cellular protein production can influence cellular processes.
------------------------------------------------------------------------------

End of text extraction from letter to Andrew Greenberg.  

Here are some notes, wrtten today, June 23, 1993 about the whole
thing...Ideas not stated here may have been created at an earlier date than 
today, but are in some other paper form I don't have access to right now.

A* Ok, so we've got a stable isotopes incorporated into nucleic acid sequences
or other, even *non-protein* polymers concept going.  I'm going to use the word
stable isotopes generally, but under the right conditions sufficiently 'cool' 
radioactive isotopes might be useful in producing the same kind of 
isotope-effects I'm expecting stable isotopes to be adequate for. 

These stable isotopes, lighter or heavier, or more homogenous-in-percentage 
than as found in a typical situation are instrumental in:

Causing rate of reaction changes 
Influencing thermal lability of proteins/polymers
Creating clines and/or thresholds of reactivity/bonding intensity/membrane 
    transport
Changing the physical spacing/volume dynamics of proteins/polymers
Causing absorption and emmisivity changes in response to light/radiation

These are very general, but combining them we get:

A0*: The facility of slowing/speeding up, stopping, forking, or breaking 
transcription, replication, or expression processes in relation to DNA and 
RNA, or other information containing polymers that are partially or completely 
composed of atypical stable isotopes.

This includes the possibility of creating proteins/polymers of the same 
molecular mass as a typical protein/polymer, but with both atypical heavy and 
light isotopes combining to give the typical mass.

and...

The specific use of A* + A0* to affect the way in which mitochondrial DNA is 
involved in replication, or for that matter nuclear DNA/RNA, esp. telomeres.  
I note here also the idea of atypical isotope biomolecules as differing 
structural elements so that they hold up differently over time - independent 
of replication.  

Isotopes might be introduced as a specific actor in response to an acute 
condition or a specific interest in action.  Alternatively, isotope loading 
could occur prior to an acute interest, perhaps as a baseline, or in the case 
of several paragraphs that follow, as a kind of prophylactic loading action
that would later be brought to the point of activity by significant grouping 
of the isotopes.

Specific uses of A0* to signal, label, or act upon DNA/RNA activities in a 
living organism that are of interest: 

	A disease, cancer, or other bioactivity is associated with the 
transcription, recombination, expression, or concentration of amino acids, 
proteins or amino acid sequences.  Could be a gene thing, or just a protein 
product.  As a result of this process, Numerically variable, 
significant-to-action 
quantities of isotopes are matched and/or otherwise grouped together, either 
within new molecules, or just as a nonbonded percentage. 

A1*: This togetherness or grouping:

	1)could cause a change in A* + A0* as therapy or create an intermediary
	 to to #2:
	
	2)could be noted as some sort of excretion product or other 
detectable/assayable concentration, and used as a label and/or signal as to 
the type or location of the disease/other bioactivity in progress.  These 
might, or might not, contain an element of signal coding to them to reveal 
specifics about the process that caused the grouping.
	
	3) could be used as a signal to an additional compound for binding or 
location information.  In addition to the straightforward case, here is one of 
several plausabilities: weaker bonding by the Isopically different amino acids 
on one side of a paired sequence might allow a different chemical to have 
special reaction/recognition possibilities with the isotopically normal side 
of the paired sequence because of changes in bond strength or shape. 
	
A2*: In a nongrouped, nonactive  situation, information could be noted, or 
accumulated as history in a DNA/RNA/protein product in vivo as a result of the 
isotope exchanges during the cellular process-history.  A plausibility is the 
embedment of data or compressed data for the use of introduced, or induced, 
cellular processes.  Because the coding involves isotope substitution and not 
active chemical groups, it should be essentially transparent to routine 
cellular chemistry.
In addition to activities that read this extra coding, the historical path of 
cellular disease might be specifically backtracked, or mechanisms might be 
used to encode previous in vivo states in the isotopic coding area.  


A3* an  example of isotopic substitution used in a viral therapy might be as 
follows:
	Let's write this part later huh?


B* The use of A* mechanisms in essentially nonbiological, ex vivo applications:

B1* Others have mentioned the use of amino acid sequences as masks and/or 
deposition surfaces or guides for making semiconductors and special micro-scale
machines - mechanical, chemical, electric, or photofunctional.  

By creating amino acid sequences or other polymers with areas of isotopic 
substitution, all of, or areas upon these masks/templates/sites might have an 
additional range of facility in processing that involves temperature, bonding,
or mass-sorting techniques like electrophoresis or centrifugal/acceleration 
effects that can be easily inferred from A* and even the loading mechanisms 
of A0*. Differences in spectral/charge properties as energized by 
light/radiation may be considered an additional area of facility also.  

B2* by creating a standard set of amino acid/polymer sequences with different 
areas of substitution, a kind of shape set is created. 

Example: standard sequence --> PCR for a plurality of identical seeds for 
next step (say 5 seeds for simplicity of example) -->amplification of 
standard sequence; seed one has special light/heavy aminos/mers on one end, 
seed two on the other end, seed three in the middle, seed 4 all heavy, light, 
whatever.  In polymers of width, angle patterning of isotopes might be 
constructed.     

Fabrication can be facilitated by:

Placing elements of this shape set together, most likely on a substrate, and 
then sorting/removing as necessary either the isotopically atypical portions 
or the other portions using the extra facility suggested by A* and  some A0* 
concepts.

B3*: Also, the possibility of using mass-sorting effects to, for example, spin
certain patterns by the facility of mass distribution, or electrophoretically 
draw with/patternize the amino acids/other polymers and create 
templates/masks/deposition sites so that desired designs are created.  

B4*: Photo effects might allow for selective absorption and [ablation or 
fixation] at atypical isotopic sites or molecules.  Photoeffects with 
emission-involving isotopic difference and feedbackto the photosource that 
causes special ablation or fixing may also be used to enhance patternmaking 
or fabrication of devices.

B5: Building up effects like arborization might take place, followed by 
removal or deposition of other active chemicals/semiconductors/etc. by the 
A* facility.

Ok, that's it for now.  It is 11:43 PM on 6/23/93 - Treon Verdery

>> B6: nanotech micromachines that make use of [matching/accumulation etc.]
>> or structural [from erosion to shaping to spacing] concepts, or 
>> photofunctional, or information carrying through isotopes, isotope 
>> laden polymers, or isotope layers, patterns, or tracks.

------------------------------------------------------------------------

Mr. Patil/Chris - thanks for reading all of that. I'd love a response by
email, but since the original text document is so large talking might
be more convenient.  If you like, call me at the University of Washington
at (206) 685-7831, and I'll call you back so it's on my dime.

What do you think?

-Treon

From owner-ageing@net.bio.net Fri Oct 08 23:00:00 1993
Path: biosci!rutgers!uwm.edu!vixen.cso.uiuc.edu!howland.reston.ans.net!agate!darkstar.UCSC.EDU!cats.ucsc.edu!beckman
From: beckman@cats.ucsc.edu (Thomas J Beckman)
Newsgroups: bionet.molbio.ageing
Subject: DNA base pairs/turn and aging?
Summary: DNA base pairs/turn and ageing?
Keywords: DNA ageing
Message-ID: <2970ri$89@darkstar.UCSC.EDU>
Date: 9 Oct 93 18:45:06 GMT
Organization: University of California, Santa Cruz
Lines: 9
NNTP-Posting-Host: am.ucsc.edu


I've heard that the number of base pairs per turn of human
DNA decreases with ageing. I'm looking for references about this.
Thanks for any information.


-- 
Tom Beckman
beckman@cats.ucsc.edu

From owner-ageing@net.bio.net Sun Oct 10 23:00:00 1993
Path: biosci!s.u-tokyo!news.tisn.ad.jp!news.u-tokyo.ac.jp!wnoc-tyo-news!sh.wide!wnoc-kyo!oskgate0.mei!chorus.mei!panasonic.com!newsserver.jvnc.net!udel!darwin.sura.net!spool.mu.edu!sdd.hp.com!elroy.jpl.nasa.gov!decwrl!usenet.coe.montana.edu!netnews.nwnet.net!news.u.washington.edu!treon
From: treon@u.washington.edu (Treon Verdery)
Newsgroups: sci.life-extension,sci.med,bionet.molbio.ageing
Subject: mitochondrial DNA therapy for aging
Message-ID: <294mlh$15n@news.u.washington.edu>
Date: 8 Oct 93 21:38:57 GMT
Distribution: usa
Organization: University of Washington, Seattle
Lines: 568
Xref: biosci sci.life-extension:816 sci.med:24404 bionet.molbio.ageing:510
NNTP-Posting-Host: goren.u.washington.edu


	*All comments are welcome!*  *Please write!*

A few months ago I had what seemed to be an insight about mitochondrial
DNA therapy, longevity, and cancer.  Other activities in life have kept
me from devoting as much time as I'd like to these ideas.  I post them
now in hopes that they will provide some useful stimulation to real
researchers.  All copyright is reserved, and I specifically claim
ownership of the ideas for patent or other purposes.  Distribution is
set to USA only, please maintain this distribution on any followups.

>> Dr. Patil/Chris - I'll be amending this document with lots of postnotes,
>> indicated by the double >>.  This file consists of three parts:
>> the unsophisticated write up produced a few hours after having the basic
>> ideas.  This section contains some *drastic* inaccuracies, but you will 
>> get the drift of it.  The second part is a letter with some additional 
>> concept refinement, and the third part is a patentistic description of 
>> most of the above, plus many new ideas.  

>> This file is huge, but the crux of it is in the first 2-3K of words
>> so don't despair at the length.

>> I hope you find it thought provoking, and I welcome (a polite way to 
>> say urge!) any comments.

------------------------------------------------------------------------------
anyway, here's the big idea... maybe a BIG idea, sort of section three, 
subparagraph two of the holy grail of Big Ideas...

        A new class of pharmaceutical therapy for keeping       
        mitochondria from accumulating deletions during replication, 

also known throughout Europe and America as...
  
        "Eternal Youth"

(Wow what Severe Hype!  I'm not sure Hype can get any more grandiose than 
that... seriously though, I've been looking though Medline this evening 
trying to pin the idea(s) down and offer real support for some vague 
points.  you will find *many* errors, but read on!)

here goes:

Have you heard of the mitochondrial theory of aging?
As I vaguely remember it goes quite a bit like this:

Mitochondria do not reproduce sexually.  As your cells
divide mitochondria replicate themselves.  In order to create a new cell, 
'about' 100 new mitochondria have to be replicated.   
        
Mitochondrial DNA  is kinda like a 
simple circular plasmid with a Start sequence, an End
sequence and in-between sequences encoding protein
production.  These '100' mitochondria, each with its own mtDNA, 
replicate as individuals.  Each of these '100'
are subject to point mutations and deletions during the life of the cell.  

Mitochondrial DNA  is unusually susceptible to deletion at specific weak 
points.  So much so that while about 100%
of a newborn's mitochondria will be doing their job, only 
20% of a 60 year old's mitochondria will be working.
Each cell has much less energy available for protein synthesis in general.  
This has been specifically linked with changes in tissue behavior and 
senesence.

Particularly exciting is the observation that damaged
(smaller/bearing deletions) mtDNA is replicated
*preferentially* 'simply' because there is less stuff between the Start and 
End sequences of the mtDNA!  
Nonfunctional mutations accumulate in that cell's line with each cell 
division, and with each generation of new cells there is a (modified) 
exponential rise in the number of dysfunctional mitochondria per cell.

AND NOW FOR THE PUNCHLINE

I'm pretty darned sure I've figured out a way to make mtDNA 
(mtDNA specifically) less sensitive to deletions and/or cause the replication 
process to avoid replicating mtDNA that is missing (specific) big chunks.
Perhaps in a pill no less -no viruses or even  nanotechnology ;-)

It'll seem easier to swallow (gulp!), if I describe a couple functioning 
concepts that are commercialized now, and operate using methods I'm going 
to borrow:

Component idea 1)

Zovirax is an anti-viral drug for herpes.  here's how it works:

Viruses that Zovirax targets like to make themselves
out of specific amino acid sequences.  during replication they find these 
sequences floating around and incorporate them into structure.  
People who take zovirax tablets are really taking pills filled with a 
specific amino acid-sequence that the virus wants. ALMOST.  The Zovirax 
sequence contains an amino-acid that is the L-isomer.  (er, maybe) The cell 
produces all the little virus copies, but none of them work - that is, none 
of them can infect a second generation of cells.   The drug
is 'safe' because the rest of the body has little interest in the 
tricked-out amino acid sequence, and because virii reproduce quickly and 
are the preferential uptakers. 

Component idea 2)

In the Bad Old Days there was a class of sedatives called Bromides.  
Essentially, people would take Bromine compounds (KBr) until some of their Cl
had been replaced by Br and the electrical potentials in their nerves had 
changed a bit.  Unfortunately, as the Br built up, eventually all sorts of 
stuff would go out of whack.

and here's component idea 3)

Cellular chemistry is traced with radioactive isotopes.
Scientists have recently taken specific note than some
tritiated proteins (tritium instead of H) diffuse across
mitochondrial membranes much more slowly(increased mass).  The cellular
chemistry that the radiolabelled compounds execute is, however, generally 
the same. At sufficient mass increases however, the chemical 
functionality radically changes.


*******Now, as best as I can explain it so far here's the idea:

Assemble amino acid sequences that have preferential
uptake for mtDNA replication. 

'weight' these sequences so that their total mass
is the same as a naturally occuring sequence, BUT
make some of the individual proteins out of Heavier, 
and also Lighter *stable* isotopes. ((**This is the drug.**))

an example:

normal original protein fragment: CGGACCTAGT
Heavy Gaunidine version: CggACCTAg

(lowercase = deuterium as substitute for H, or perhaps
C13 for C12, or perhaps some O isotope
let's pretend that the T's have some lighter stable isotope(N) so that the 
total mass of this sequence is the same as the normal original.)

I have to pause and add some helpful additional concepts:

One of the reasons mtDNA accumulates deletions is that
some places along the amino acid sequence are fragile, that is,
they like to drop out under replication.  Simplistically, there are some 
weak links in what is otherwise a strong chain.

(NOT! -my how learned this all sounds. free grains of salt: .. . ... )

Bacteria that live in deep sea thermal vents thrive at
temperatures above 212 F.  These bacteria have many of the same enzymes 
and protein chemistry cycles as cool cells, their proteins are almost 
exactly the same, however, some of their proteins are less 'ornate', 
less 'sticky'; with fewer opportunities to pick up thermal motions and 
cross-link.  The rapid folding-and unfolding of hot-cell proteins is 
also somewhat different...

Some scientists speculate that hot bacteria were first, and that 
proteins evolved stickier, more ornate, more-cross-linkable molecular
forms to adapt to cooler environments.  

Just as a floating concept: imagine a partially deuterated enzyme as much 
more sluggish at low temperatures...normal at higher temperatures...
obviously the things the enzyme reacts with would have trouble w/the 
higher temperatures though...

>> sudden thought: is there a dueterated PCR patent enzyme work around?
 
It strikes me that there are possible strategies for using light and heavy 
amino acids to 
        
        1) bog down/break the replication of specific   
            misbegotten (deletion-flagging) amino acid sequences

        2) protect weak spots from damage, but not from
            replication (w/a slight differential of charge 
            potential)

        3)  all kinds of other stuff that messes with RNA

A typical 1) strategy:
A Grungy strategy to bog down shortened mtDNAs is this: After dosing 
the organism with isotopically peculiar amino acid sequences the 
'normal nonmutant' mtDNA has a 'normal' mass and reactivity.  
Those mtDNA that have experienced typical deletions at the 'weak links'
have unusual isotope concentrations that affect the behavior of the 
protein replication:

ok-to-replicate version:
CgAgg + gCTCC = thermodynamically ok to replicate

but:

CgAgggggg + GCTCCCCCC = thermodynamically slow/prohibited as all the heavies 
cluster together and/or  are limited by diffusion speed/availability of 
bits with all those heavy ggggs.

I guess you could call this "putting the wrong size pins on
the zipper" - when you get the big pins, and the big zip
there isn't enough energy/room to pull it any farther - but if you have at 
least 1 small pin it will work.  (Iffy indeed, but I can think of an 
experiment to test it - hoping to find the components of the experiment 
on medline). 

An interesting alternative to "wrong size pins on the zipper" is 
"slower pins on the zipper reduce the risk of speedy accidents", or perhaps, 
"I'm only going to zipper you if your start sequence includes light/heavy 
isotopes - and deletion-prone versions versions lack this 
light or heavy sequence.

In fact, once you begin thinking about it, there are a lot of 
"ordinary" things that could happen to work on this problem - without 
any isotope naughtiness at all.

I guess what is most important from my perspective is the idea that stable 
isotopes, with some degree of clever manipulation, can be used as amino 
acid replication/synthesis modifiers.  
Now I have a lot of reading to do! (Did you notice that I 
didn't mention mRNA hardly at all?)

-Treon


Here are some medline references at the end for background and stuff.  
I should have copied more but they seemed long enough as it was.

you can search medline anytime you want to follow your own fancies - 
(you probably know this address) just:
telnet uwin.u.washington.edu

#1 is an example of Tritiated compounds doing the same chemistry,
but 3-9X slower (within mitochondria (but not reproduction) no less!)

#2-4 are lame, but exploratory examples of mtDNA
 accumulating damage at extreme exponential rates and how this affects 
cellular energy and the respiration cycle.
my info comes from a dimly remembered review article that was much clearer...

P.S.  BOO!!

be my friend!  write back!!
(you are eligible for a medal for reading this far...)

#1
Loss of tritium from a substrate is often used to estimate
                the rate of dehydrogenation.  However, loss of 3H may be much 
		slower than loss of H because of the tritium isotope effect.
                In order to assess the impact of the tritium isotope effect,
                loss of 3H from the C-5 position of proline during
                dehydrogenation by rat liver mitochondria and bacteroids from
                soybean (Glycine max [L.] Merrill) nodules was compared with
                appearance of 14C in products of [14C]proline
                dehydrogenation.  Incubations were carried out in the
                presence of o-aminobenzaldehyde (added to trap the initial
                product, delta 1-pyroline-5-carboxylate).  The fraction of
                total 14C products trapped by o-aminobenzaldehyde varied from
                0.07 to 0.75 depending upon experimental conditions.  With
                rat liver mitochondria, dehydrogenation of [14C]proline was
                between 3.27 and 9.25 times faster than dehydrogenation of 3H
                proline, depending upon assay conditions.  Soybean nodule
                bacteriods dehydrogenated [14C]proline about 5 times faster
                than [3H]proline.  We conclude the following: (i) the rate of 
		proline dehydrogenation may be greatly underestimated by the
                tritium assay because of the tritium isotope effect, and (ii)
                the 14C assay may underestimate the rate of proline
                dehydrogenation if it is assumed that o-aminobenzaldehyde
                quantitatively traps delta 1-pyrroline-5-carboxylate under
                all conditions.  The simplicity of the tritium assay makes it
                attractive for routine use.  However, its use requires
                determination of the tritium isotope effect, under the
                specific conditions of the assay, in order to correct the
                results.  The considerations discussed here have broad
                applicability to any dehydrogenase assay employing tritium
                loss.


#2

The analysis of human skeletal muscle mitochondria revealed aprogressive 
		decline in mitochondrial respiratory chain
                function with age.  The activities affected to the greatest
                extent were those of complexes I and IV which were decreased
                by 59% and 47% respectively between the ages of 20-30 years
                and 60-90 years of age.  Quantitation of the 5 kb 'common'
                deletion of mtDNA using PCR revealed a progressive
                accumulation with age, from approximately 1 in 100,000 at 21
                years to 1 in 10,000 at 56 years and 1 in 5000 at 78 years of
                age.  The low absolute levels of this mutation are unlikely
                to contribute significantly to the observed mitochondrial
                dysfunction.


 Previous theories of aging based on somatic mutation
                neglected mtDNA, which has a high propensity for mutational
                error.  Knowledge of yeast mtDNA mutations and their
                functional effects, and of human mtDNA mutations identified
                in the mitochondrial cytopathies, provides for a concept of
                aging based on the cumulative effect of mutations affecting
                human mtDNA.  An essential feature of this concept is
                heteroplasmy, representing mixtures of normal and mutant
                mtDNA at the cellular and mitochondrial level, resulting in a
                "tissue mosaic" of focal bioenergetic deficits.  Direct
                evidence for the concept is provided by (i) focal loss of
                staining for mitochondrially encoded enzymes, such as
                cytochrome c oxidase, in tissues of aged individuals (humans
                and rats) and (ii) an age-related increase in deletional
                mutations in mtDNA demonstrable by application of the
		polymerase chain reaction to DNA templates from individuals
                of different ages.

Some mutations in mitochondrial DNA (mtDNA) causing a number
                of neuromuscular diseases are suggested to arisespontaneously
		during the life of an individual.  To
                substantiate the extent and the rate of these somatic
                mutations, mtDNA specimens from post-mortem human heart
                muscles of subjects in differing age groups were hydrolyzed.
                8-Hydroxy-deoxyguanosine (8-OH-dG), a hydroxyl-radical adduct
                of deoxyguanosine, in mtDNA, was quantitatively determined
                using a micro high-performance liquid chromatography/mass
                spectrometry system.  In each specimen, the mtDNA with a 7.4
                kilo base-pair deletion was quantified by the kinetic
                polymerase chain reaction method.  In association with age,
                the 8-OH-dG content accumulated exponentially up to 1.5% with
                a correlative increase in the content of the deleted mtDNA up
                to 7%.  Clear correlation between the 8-OH-dG content in
                mtDNA and the population of mtDNA with a deletion (r = 0.93,
                P < 0.01) gives insight into the mechanism for the generation
                of a large deletion.  These results indicate thataccumulation 
		of somatically acquired oxygen damage together
                with age-associated mutations in mtDNA which lead to
                bioenergetic deficiency and the heart muscle weakness are
                inevitable in human life.
-------------------------------------------------------------------------------
End of the email extraction from the first letter.

Here is an extraction from a second letter that I wrote to a friend.  


Anyway, Hello!   Thanks for asking if you could pass the idea on
first - I never bothered to get it notarized so I'll do that today
so that you can pass it on to Peter say Thursday.  It is a building
thrill to have someone else interested and to hopefully add some
explorations and accuracies.  Makes me nervous too!  That version 
I sent you was written about 4 hours after the original inspiration
So, um, it'll read really dumb to someone who knows what they
are talking about.  I think it has been 6-8 weeks since I wrote that,
and have learned all sorts of shoring-up and eroding-down influences
to the central idea:


And now... some inferences from the literature:

Plus:
* There are specific common deletion sites in mtDNA that result in 
  large, unique amino acid sequences suitable as labels 

* the idea is obviously portable to other genetic and protein
 pharmacological things; RE aging, it also has direct application
 to other aging theories/aging markers notably the telomeric
 marker/tape leader theories and what I'd call the 
 psuedocaloric restriction methionine displacer theory

* A similar idea/set of ideas has never appeared in the abstracted
  literature/patent databses I've looked in

* Rats forced to live out their lives on 30% D2O are normal
  (an incredible puzzle there I'd say)

Minus:

* people with progeria, a very unusual rapid aging syndrome do not
  have mtDNA problems at all (secret plus: they do have shortened
  telomeres proportional to the shortening seen in people of their
  apparent physical age!)

* Cancer research suggests that that targeting 
   is very difficult; then again, maybe I've lucked out
   and thought of a harmless-unless-cancerous mechanism.  or even
   a cancer prophylactic of a different nature than antioxidants
   sort of like invisible chemotherapy.
>> -distributed stable isotopes lie in transparent wait until cancer/other
>> bioprocesses concentrate them and 1) retard them 2) signal them.
>> Advantage: minimal/no toxicity excaept at active concentration/comnination
>> sites

(Andrew... the minuses are turning into positive wild speculation!
 This is good - but I started out wanting to write a balanced treatment
 for You and Peter)

More Wild Speculation

* currently existing gene therapies could add another degree
  of 'facility' by influencing the residence times and
  stabilities of introduced genes, as well as marking sites for 
  secondary therapies. The whole idea of tagging, signalling, and modifying
  cellular stuff without active chemical groups just floats there...
  suggesting wild stuff like cellular early-early-early diagnoses
  dianoses based on excretion/assay of oddball Isotope-loaded amino acid
  sequences.  

  The various forms of matching and concentration
  that I know about in cells suggest statistical 'control'(?) of how much
  of what accumulates where.  Nucleic acid dynamics are so bizarre
  that there are many different sorts of active and inactive structures
  to tweak on...

  ...I guess I'm just really turned on by the idea of chemicals that
  in low concentrations mimic perfectly their normal isotope
  cousins, but at times of unusual concentration due to replication,
  or other cellular protein production can influence cellular processes.
------------------------------------------------------------------------------

End of text extraction from letter to Andrew Greenberg.  

Here are some notes, wrtten today, June 23, 1993 about the whole
thing...Ideas not stated here may have been created at an earlier date than 
today, but are in some other paper form I don't have access to right now.

A* Ok, so we've got a stable isotopes incorporated into nucleic acid sequences
or other, even *non-protein* polymers concept going.  I'm going to use the word
stable isotopes generally, but under the right conditions sufficiently 'cool' 
radioactive isotopes might be useful in producing the same kind of 
isotope-effects I'm expecting stable isotopes to be adequate for. 

These stable isotopes, lighter or heavier, or more homogenous-in-percentage 
than as found in a typical situation are instrumental in:

Causing rate of reaction changes 
Influencing thermal lability of proteins/polymers
Creating clines and/or thresholds of reactivity/bonding intensity/membrane 
    transport
Changing the physical spacing/volume dynamics of proteins/polymers
Causing absorption and emmisivity changes in response to light/radiation

These are very general, but combining them we get:

A0*: The facility of slowing/speeding up, stopping, forking, or breaking 
transcription, replication, or expression processes in relation to DNA and 
RNA, or other information containing polymers that are partially or completely 
composed of atypical stable isotopes.

This includes the possibility of creating proteins/polymers of the same 
molecular mass as a typical protein/polymer, but with both atypical heavy and 
light isotopes combining to give the typical mass.

and...

The specific use of A* + A0* to affect the way in which mitochondrial DNA is 
involved in replication, or for that matter nuclear DNA/RNA, esp. telomeres.  
I note here also the idea of atypical isotope biomolecules as differing 
structural elements so that they hold up differently over time - independent 
of replication.  

Isotopes might be introduced as a specific actor in response to an acute 
condition or a specific interest in action.  Alternatively, isotope loading 
could occur prior to an acute interest, perhaps as a baseline, or in the case 
of several paragraphs that follow, as a kind of prophylactic loading action
that would later be brought to the point of activity by significant grouping 
of the isotopes.

Specific uses of A0* to signal, label, or act upon DNA/RNA activities in a 
living organism that are of interest: 

	A disease, cancer, or other bioactivity is associated with the 
transcription, recombination, expression, or concentration of amino acids, 
proteins or amino acid sequences.  Could be a gene thing, or just a protein 
product.  As a result of this process, Numerically variable, 
significant-to-action 
quantities of isotopes are matched and/or otherwise grouped together, either 
within new molecules, or just as a nonbonded percentage. 

A1*: This togetherness or grouping:

	1)could cause a change in A* + A0* as therapy or create an intermediary
	 to to #2:
	
	2)could be noted as some sort of excretion product or other 
detectable/assayable concentration, and used as a label and/or signal as to 
the type or location of the disease/other bioactivity in progress.  These 
might, or might not, contain an element of signal coding to them to reveal 
specifics about the process that caused the grouping.
	
	3) could be used as a signal to an additional compound for binding or 
location information.  In addition to the straightforward case, here is one of 
several plausabilities: weaker bonding by the Isopically different amino acids 
on one side of a paired sequence might allow a different chemical to have 
special reaction/recognition possibilities with the isotopically normal side 
of the paired sequence because of changes in bond strength or shape. 
	
A2*: In a nongrouped, nonactive  situation, information could be noted, or 
accumulated as history in a DNA/RNA/protein product in vivo as a result of the 
isotope exchanges during the cellular process-history.  A plausibility is the 
embedment of data or compressed data for the use of introduced, or induced, 
cellular processes.  Because the coding involves isotope substitution and not 
active chemical groups, it should be essentially transparent to routine 
cellular chemistry.
In addition to activities that read this extra coding, the historical path of 
cellular disease might be specifically backtracked, or mechanisms might be 
used to encode previous in vivo states in the isotopic coding area.  


A3* an  example of isotopic substitution used in a viral therapy might be as 
follows:
	Let's write this part later huh?


B* The use of A* mechanisms in essentially nonbiological, ex vivo applications:

B1* Others have mentioned the use of amino acid sequences as masks and/or 
deposition surfaces or guides for making semiconductors and special micro-scale
machines - mechanical, chemical, electric, or photofunctional.  

By creating amino acid sequences or other polymers with areas of isotopic 
substitution, all of, or areas upon these masks/templates/sites might have an 
additional range of facility in processing that involves temperature, bonding,
or mass-sorting techniques like electrophoresis or centrifugal/acceleration 
effects that can be easily inferred from A* and even the loading mechanisms 
of A0*. Differences in spectral/charge properties as energized by 
light/radiation may be considered an additional area of facility also.  

B2* by creating a standard set of amino acid/polymer sequences with different 
areas of substitution, a kind of shape set is created. 

Example: standard sequence --> PCR for a plurality of identical seeds for 
next step (say 5 seeds for simplicity of example) -->amplification of 
standard sequence; seed one has special light/heavy aminos/mers on one end, 
seed two on the other end, seed three in the middle, seed 4 all heavy, light, 
whatever.  In polymers of width, angle patterning of isotopes might be 
constructed.     

Fabrication can be facilitated by:

Placing elements of this shape set together, most likely on a substrate, and 
then sorting/removing as necessary either the isotopically atypical portions 
or the other portions using the extra facility suggested by A* and  some A0* 
concepts.

B3*: Also, the possibility of using mass-sorting effects to, for example, spin
certain patterns by the facility of mass distribution, or electrophoretically 
draw with/patternize the amino acids/other polymers and create 
templates/masks/deposition sites so that desired designs are created.  

B4*: Photo effects might allow for selective absorption and [ablation or 
fixation] at atypical isotopic sites or molecules.  Photoeffects with 
emission-involving isotopic difference and feedbackto the photosource that 
causes special ablation or fixing may also be used to enhance patternmaking 
or fabrication of devices.

B5: Building up effects like arborization might take place, followed by 
removal or deposition of other active chemicals/semiconductors/etc. by the 
A* facility.

Ok, that's it for now.  It is 11:43 PM on 6/23/93 - Treon Verdery

>> B6: nanotech micromachines that make use of [matching/accumulation etc.]
>> or structural [from erosion to shaping to spacing] concepts, or 
>> photofunctional, or information carrying through isotopes, isotope 
>> laden polymers, or isotope layers, patterns, or tracks.

------------------------------------------------------------------------

Mr. Patil/Chris - thanks for reading all of that. I'd love a response by
email, but since the original text document is so large talking might
be more convenient.  If you like, call me at the University of Washington
at (206) 685-7831, and I'll call you back so it's on my dime.

What do you think?

-Treon

From owner-ageing@net.bio.net Tue Oct 12 23:00:00 1993
Path: biosci!uwm.edu!vixen.cso.uiuc.edu!howland.reston.ans.net!agate!darkstar.UCSC.EDU!cats.ucsc.edu!beckman
From: beckman@cats.ucsc.edu (Thomas J Beckman)
Newsgroups: bionet.molbio.ageing
Subject: DNA base pairs/turn and aging?
Summary: DNA base pairs/turn and ageing?
Keywords: DNA ageing
Message-ID: <2970ri$89@darkstar.UCSC.EDU>
Date: 9 Oct 93 18:45:06 GMT
Organization: University of California, Santa Cruz
Lines: 9
NNTP-Posting-Host: am.ucsc.edu


I've heard that the number of base pairs per turn of human
DNA decreases with ageing. I'm looking for references about this.
Thanks for any information.


-- 
Tom Beckman
beckman@cats.ucsc.edu

From owner-ageing@net.bio.net Tue Oct 12 23:00:00 1993
Path: biosci!daresbury!doc.ic.ac.uk!pipex!howland.reston.ans.net!vixen.cso.uiuc.edu!bradley.bradley.edu!cs1.bradley.edu!not-for-mail
From: hexmoon@cs1.bradley.edu (Brett Cloud)
Newsgroups: bionet.molbio.ageing
Subject: A-T, G-C
Keywords: codons, amino acids
Message-ID: <29ftiv$fme@cs1.bradley.edu>
Date: 13 Oct 93 03:44:31 GMT
Organization: Bradley University
Lines: 4
NNTP-Posting-Host: cs1.bradley.edu

I am trying to remember what AAA,AAC,...,TTT map out to what meaning in
amino acid language.  Thanks for any help.

                 Brett

From owner-ageing@net.bio.net Wed Oct 13 23:00:00 1993
Path: biosci!bloom-beacon.mit.edu!usc!howland.reston.ans.net!vixen.cso.uiuc.edu!bradley.bradley.edu!cs1.bradley.edu!not-for-mail
From: hexmoon@cs1.bradley.edu (Brett Cloud)
Newsgroups: bionet.molbio.ageing
Subject: A-T, G-C
Keywords: codons, amino acids
Message-ID: <29ftiv$fme@cs1.bradley.edu>
Date: 13 Oct 93 03:44:31 GMT
Organization: Bradley University
Lines: 4
NNTP-Posting-Host: cs1.bradley.edu

I am trying to remember what AAA,AAC,...,TTT map out to what meaning in
amino acid language.  Thanks for any help.

                 Brett

From owner-ageing@net.bio.net Thu Oct 14 23:00:00 1993
Path: biosci!daresbury!doc.ic.ac.uk!uknet!pipex!uunet!cs.utexas.edu!not-for-mail
From: MEMBP@thcme.indstate.edu ("MARY B. PARAMANATHAN" )
Newsgroups: bionet.immunology,bionet.molbio.ageing,bionet.molbio.methds-reagnts,bionet.neuroscience
Subject: Request antibodies against opioid receptors in mice
Message-ID: <2BB79397595@thcme.indstate.edu>
Date: 15 Oct 93 21:07:44 GMT
Sender: daemon@cs.utexas.edu
Organization: UTexas Mail-to-News Gateway
Lines: 11
Xref: biosci bionet.immunology:631 bionet.molbio.ageing:514 bionet.molbio.methds-reagnts:8208 bionet.neuroscience:1824
NNTP-Posting-Host: cs.utexas.edu

Hi,
    I am a graduate student at Terre Haute center for Medical
education and I am working on the effects of post natal handling on
the immune responsiveness in mice. I am planning to see the
distribution of opioid receptors in various tissues of the immune and
nervous system in these handled animals. I require monoclonal
antibodies for opioid receptors for immunocytochemistry studies.I
request information regarding the availablilty of such antibodies. I
have no direct contact with the news groups, so please send
information to my E mail address MEMBP@thcme.indstate.edu
thanks.

From owner-ageing@net.bio.net Fri Oct 15 23:00:00 1993
Path: biosci!bcm!cs.utexas.edu!sdd.hp.com!spool.mu.edu!agate!darkstar.UCSC.EDU!cats.ucsc.edu!beckman
From: beckman@cats.ucsc.edu (Thomas J Beckman)
Newsgroups: bionet.molbio.ageing
Subject: DNA base pairs/turn and aging?
Summary: DNA base pairs/turn and ageing?
Keywords: DNA ageing
Message-ID: <2970ri$89@darkstar.UCSC.EDU>
Date: 9 Oct 93 18:45:06 GMT
Organization: University of California, Santa Cruz
Lines: 9
NNTP-Posting-Host: am.ucsc.edu


I've heard that the number of base pairs per turn of human
DNA decreases with ageing. I'm looking for references about this.
Thanks for any information.


-- 
Tom Beckman
beckman@cats.ucsc.edu

From owner-ageing@net.bio.net Sat Oct 16 23:00:00 1993
Path: biosci!lhc!paladin.american.edu!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: music@PARCOM.ERNET.IN (Rajeev Upadhye)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: <None>
Message-ID: <9310131311.AA02570@parcom>
Date: 13 Oct 93 16:18:38 GMT
Sender: Geriatric Health Care Discussion Group <GERINET@UBVM.BITNET>
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Lines: 14
Xref: biosci bionet.molbio.ageing:518
To:	IN%"NEWSMGR@muvms6.wvnet.edu"  "Marshall University"
CC:
Subj:
Return-path: <@UBVM.CC.BUFFALO.EDU:owner-gerinet@UBVM.CC.BUFFALO.EDU>
Return-path: music <@UBVM.CC.BUFFALO.EDU,@MITVMA.MIT.EDU:music@PARCOM.ERNET.IN>
To: Marshall University <NEWSMGR@muvms6.wvnet.edu>
Content-transfer-encoding: 7BIT
Organisation: <Centre for Development of Advanced Computing, Pune, INDIA>
X-To:         gerinet@ubvm.bitnet

I would like to subscribe to this discussion group.

_________________________________________________________________________
    Fundamentals of Research Methodology | Centre for Development of

 | Advanced Computing
   "Take roots of some tree                      | Pune University Campus
    Crush them with some thing           | Ganesh Khind, Pune
    Then give it to someone              | Maharashtra, INDIA 411 007
    SOMETHING will definitely happen!!!" | Email: music@parcom.ernet.in
                                         | Fax  : 91 212 337551
           ------ PANCHA TANTRA          | Phone: 91 212 332461
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_________________________________________________________________________

From owner-ageing@net.bio.net Sat Oct 16 23:00:00 1993
Path: biosci!lhc!paladin.american.edu!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: GGRAHAM@PSTCC.CC.TN.US (George Graham)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: discussion
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Ganesh Khind (I don't know how to address you)

I've been on this list for awhile and have heard nothing until I
saw your plea for converstaion.

My name id George Graham and I teach nursing students.  Plus I do
dentistry for the elderly in theior homes or in their nursing
establishment.

My prayers go out ty the families of the people who died in the
natural disaster last week in your country.

If you want to converse you can use this list since noone else
seems to be using it or you can e-mail me direct at

ggraham@pstcc.cc.tn.us

From owner-ageing@net.bio.net Sat Oct 16 23:00:00 1993
Path: biosci!lhc!paladin.american.edu!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: VBSELBY@UALR.EDU (RABBLE ROUSER)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: welcome
Message-ID: <931013155255.25215184@ualr.edu>
Date: 13 Oct 93 20:52:55 GMT
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>
>I would like to subscribe to this discussion group.
>
The net has been quiet for a long time now.

Boyd
bbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbb
??                                                                           ??
??            OLD AGE AND TREACHERY WILL OVERCOME YOUTH AND SKILL            ??
??   When all is said and done...                                            ??
??                               More is said than done!!!!                  ??
??                                                                           ??
??                                             vbselby@ualr.edu              ??
??                                             vbselby@ualr.bitnet           ??
sssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssss

From owner-ageing@net.bio.net Sun Oct 17 23:00:00 1993
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From: VBSELBY@UALR.EDU (RABBLE ROUSER)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: welcome
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>
>I would like to subscribe to this discussion group.
>
The net has been quiet for a long time now.

Boyd
bbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbb
??                                                                           ??
??            OLD AGE AND TREACHERY WILL OVERCOME YOUTH AND SKILL            ??
??   When all is said and done...                                            ??
??                               More is said than done!!!!                  ??
??                                                                           ??
??                                             vbselby@ualr.edu              ??
??                                             vbselby@ualr.bitnet           ??
sssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssssss

From owner-ageing@net.bio.net Sun Oct 17 23:00:00 1993
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From: edemt@TTACS.TTU.EDU
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: Parkinson's readings
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Is there anyone on the list who could cite some sources for readings on
Parkinson's...something written for a *layman* to understand and something
besides the average pamphlet handout (which, of course, tells little above
the very basic)?  Sometimes I come across "updates" into the study of it,
but I've seen very little in the way of "whats" and "whys"--that I can
understand (and *I* have to understand them before I can even begin to
explain it to my dad--diagnosed with it over two years ago).  Certain
changes would not have upset me so, if I'd just had a little forewarning
they would or might appear... things the readings I've seen so far haven't
given a clue to.

Any help would be very much appreciated.  My Internet address is below.
Thanks.

Edie T.
+:::::::::::::::::::::::::::::::::::::::::::::::::::::::::+
 Edith (Edie) Temple    ::
 Computer Doc. Editor   ::  Internet: edemt@ttacs.ttu.edu
 Texas Tech University  ::  Bitnet:   EDEMT@TTACS.BITNET
 Lubbock, Texas         ::
+:::::::::::::::::::::::::::::::::::::::::::::::::::::::::+

From owner-ageing@net.bio.net Sun Oct 17 23:00:00 1993
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From: EDWARDSH@QUT.EDU.AU (qut.edu.au)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: discussion
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Dear George, Ganesh Khind and Edie

I am a new subscriber from a School of Nursing in Australia.  I'd be interested
to hear about research that people are doing.  Currently I am involved in resear
ch in the following:
communication between caregivers and their elderly family members




skin tears in the elderly who reside in nursing homes
communication between alzheimers patients and the nurses who care for them in nu
rsing homes
pain in the elderly
Anybody interested in these areas??
Regards
Helen

From owner-ageing@net.bio.net Sun Oct 17 23:00:00 1993
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From: EDWARDSH@QUT.EDU.AU (qut.edu.au)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: Parkinson's readings
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Dear Edie T
I am a new subscriber to gerinet and I don't personally have anything on Parkins
ons.  Michael Dunne a colleague in my School is doing some work with Parkinsons.
  He may be a useful contact.  His Email is
m.dunne@qut.edu.au
Regards
Helen Edwards

From owner-ageing@net.bio.net Sun Oct 17 23:00:00 1993
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From: ABARE@SMCVAX.BITNET (Amy Abare)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
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I have been wondering the same thing myself.  I've been on the list for
about two months and have received no mail.  I joined the list out of
pure interest.  I am a part-time home care provider, but am considering
entering the geriatric field.  I was hoping to get tons of helpfull
information, but alas, nothing until now.  At the moment, I have to
cut this short but will be doing more E-mail tomorrow, so until
then................

Abare@smcvax.smcvt.edu

From owner-ageing@net.bio.net Sun Oct 17 23:00:00 1993
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From: GGRAHAM@PSTCC.CC.TN.US (George Graham)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: discussion
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Ganesh Khind (I don't know how to address you)

I've been on this list for awhile and have heard nothing until I
saw your plea for converstaion.

My name id George Graham and I teach nursing students.  Plus I do
dentistry for the elderly in theior homes or in their nursing
establishment.

My prayers go out ty the families of the people who died in the
natural disaster last week in your country.

If you want to converse you can use this list since noone else
seems to be using it or you can e-mail me direct at

ggraham@pstcc.cc.tn.us

From owner-ageing@net.bio.net Sun Oct 17 23:00:00 1993
Path: biosci!news.cs.umb.edu!hsdndev!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: music@PARCOM.ERNET.IN (Rajeev Upadhye)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: <None>
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Organisation: <Centre for Development of Advanced Computing, Pune, INDIA>
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I would like to subscribe to this discussion group.

_________________________________________________________________________
    Fundamentals of Research Methodology | Centre for Development of

 | Advanced Computing
   "Take roots of some tree                      | Pune University Campus
    Crush them with some thing           | Ganesh Khind, Pune
    Then give it to someone              | Maharashtra, INDIA 411 007
    SOMETHING will definitely happen!!!" | Email: music@parcom.ernet.in
                                         | Fax  : 91 212 337551
           ------ PANCHA TANTRA          | Phone: 91 212 332461
       (A Sanskrit Book of Fairy Tales)  |
_________________________________________________________________________

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
Path: biosci!daresbury!doc.ic.ac.uk!agate!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: GGRAHAM@PSTCC.CC.TN.US (George Graham)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: discussion
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Date: 15 Oct 93 10:27:31 GMT
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Helen,

I am very interested in the communication between family and acre
caregiver. I deal with that on a daily basis.

george g
p
ggraham@pstcc.cc.tn.us

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
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From: FCM001@UKANVM.BITNET (Mary Hursey)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
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Helen and George regarding communication with  elderly and caregivers - I have
my mother living with me who been diagnosed with Alzhiemers (sp) if you have an
y questions you might want to ask I'll be happy to answer the best I can.

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
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From: GGRAHAM@PSTCC.CC.TN.US (George Graham)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: discussion
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Louella,

Sory for my lack of clarity.

I have two assistants.  My main one was on vacation and my backup
went with me to the patients house.

She had several loose teeth and I was afraid of aspiration so I
wrote a Rx for an antibiotic and made an appointment to come back
in a few days.

In the meantime, the main assistant came home.  So the next time I saw
the patient, the second assistant was with me.  I hadn't paid attention
and neither had the ladies husband.

But the patient o looked up and said .... "You're not the same one "

Unfortunately in most nursing homes they are treated as if they
didn't understand anything.

Don't be cruel ... assume they do ... This is what I bring up at
continuing education classes.  that I do for my nursing homes.

George G
ggraham@pstcc.cc.tn.us

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
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From: ICOOPER@SNYESCVA.BITNET (INDIE)
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Yes--I am also interested in these topic areas.  I am an RN who is currently
working in the longterm setting.  I am pursuing a BS in Community & Human
Services with concentrations in Counseling and Psycho-physiology.  I have a
keen interest in chronic pain and pain in many forms ie physical, emotional &
psychosocial.  I also lost my stepfather on October 2nd.  He was 80 years old
and suffered alzheimers type dementia however just before he died, he was seen
by a neurologist who mentioned Credsfeld Jacobs disease (spelling may be wrong).
I am not familiar with this disease however his symptoms I now understand were
very similar to ones associated with this disease.  His symptoms progressed
very fast--over 2-3 years.
I tend to analyze things along the lines of Erikson's developmental theory &
Family systems theorists however, I recognize the value of other theorists as
well.
Indie

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
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From: DEMERS@SJSUVM1.BITNET (Louella De Mers)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: discussion
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Date: 15 Oct 93 20:01:53 GMT
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George
Spelling doesn't count!!

I, too, believe people with AD can be more aware that
is generally recognized. I helped to care for a wonderful
woman who got a bit stubborn on occasion. She seemed to
be out of touch with reality except for food. And the
best way to elicit her cooperation was to offer her
chocolate. She would instantly open her mouth, get the
chocolate piece, and then cooperate fully.

Would you explain a bit more about your patient being
able "to tell the difference between my assistants
when her husband and I couldn't?" I not sure I understand.

Thanks
Louella
demers@sjsuvm1
demers@sjsuvm1.sjsu.edu

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
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From: vinta@UNR.EDU (Vinta Dobrenen)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: Suggestions
Message-ID: <40868.vinta@equinox.unr.edu>
Date: 15 Oct 93 19:20:58 GMT
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In Message Fri, 15 Oct 1993 09:54:46 -0500,
  Amy Abare <ABARE%SMCVAX.BITNET@UBVM.cc.buffalo.edu> writes:

>I am considering entering the Geriatric field on some level and am wondering
>if people could offer information about their specific fields, specialties,
>interests, or any kind of advise.  Currently I am doing home health care on
>a part-time basis through a nursing agency, but I really want to make a
>move into a full-time career.  I am weighing the options of entering the
>field either through nursing or social work.  Any feedback would be
>greatly appreciated!  Thanks!
>
>Abare@smcvax.smcvt.edu


Amy,
     I was glad to see your messages and also others.  I have been on this
listserve for a little while, but have not seen much action until now.

     I am a Medical, and also Geriatric, Librarian for the Nevada Geriatric
Education Center (NGEC) at the University of Nevada in Reno, Nevada.  My
specialties are geriatric information sources, computer literature
searching, and database development.  I provide information throughout
Nevada mostly to health professionals on any issue in the field of aging.  I
also have developed a speakers/experts database, an Audio-Visual Catalog, a
Directory (and database) of Sources for Seniors, and I am working on a
newsletter if I ever get it past all the people who approve it and keep
wanting to change it.  All of this is for the state of Nevada only.  But I
am a part of several Gerontology/Geriatric interest groups, one connected
with other Geriatric Education Centers throughout the United States, and one
connected with the Medical Librarians Association, and so there is slowly
some connecting going on between people in this field, which is exciting.

     In answer to your inquiry about education, this field is
interdisciplinary and you generally get a degree in some other field like
social work, psychology, nursing, medicine, etc., and then add this to it
as a minor or get a certificate.  It will help in obtaining a job if you
have this education and others don't.  Let me know if there is anything else
that I can help with.

Vinta Dobrenen, M.L.S.
vinta@unr.edu
(702) 784-1805

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
Path: biosci!daresbury!doc.ic.ac.uk!uknet!pipex!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: TKELLY@UGA.CC.UGA.EDU (Tim Kelly)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: Suggestions
Message-ID: <GERINET%93101512593058@UBVM.CC.BUFFALO.EDU>
Date: 15 Oct 93 16:33:42 GMT
Sender: Geriatric Health Care Discussion Group <GERINET@UBVM.BITNET>
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In-reply-to: Message of Fri, 15 Oct 1993 09:54:46 -0500 from <ABARE@SMCVAX>
To: Marshall University <NEWSMGR@muvms6.wvnet.edu>
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Amy:
I am a geriatric social worker so my bias would be for the social work professi
on. I have worked in mental health centers with elderly clients, run day progra
ms for mentally ill older adults, and worked as a social worker in a geriatric
hospital. I love the field. If you want more info please e-mail me.
Thanks!
Tim

Tim Kelly
University of Georgia
School of Social Work
(706) 542-5441

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
Path: biosci!daresbury!doc.ic.ac.uk!pipex!howland.reston.ans.net!europa.eng.gtefsd.com!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: murlakis@POST.ITS.MCW.EDU (Mary Anne Urlakis)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: caregivers & Alzheimer's patients
Message-ID: <Pine.3.05.9310151058.A26457-a100000@post.its.mcw.edu>
Date: 15 Oct 93 15:17:22 GMT
Sender: Geriatric Health Care Discussion Group <GERINET@UBVM.BITNET>
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Helen & George, I too have a mother with Alzheimer's and would be more
than willing to share my experiences. I am also an active member of the
Alzheimer's Suport Group, through the medical center I am employed by. If
you are interested I  may be able to find others  to share
experieces with you.


Mary Anne Urlakis
Program Coordinator-Health Information Technoloogy Center
Health Policy Institute
Medical College of Wisconsin
Phone:  (414) 778-4362
FAX: (414)257-8464
NTERNET: murlakis@post.its.mcw.edu

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
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From: ICOOPER@SNYESCVA.BITNET (INDIE)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: residents & caregivers
Message-ID: <GERINET%93101620123569@UBVM.CC.BUFFALO.EDU>
Date: 17 Oct 93 00:07:00 GMT
Sender: Geriatric Health Care Discussion Group <GERINET@UBVM.BITNET>
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Original_To:  BITNET%"gerinet@ubvm"
Original_cc:  ICOOPER

My husband's grandfather was hospitalized and then sent to a nursing home
following a medication error that left him unresponsive several years ago.
Family was faithful to visit at least 5-7 days a week during the 3-4 months
he was there.  We took him out for rides around the area he grew up in and
farmed many years.  He would just sit staring straight ahead on those rides.
He was fortunately to come out of it and he came home to live for 2 years
before he died.  One day, he said to us "You don't know what it meant to
have you take me out for all of those rides.  I couldn't thank you then but
I can now."  This experience I share with my students to show them that even
though someone may not react to your presence, it doesn't mean they are not
aware of it.  I hope they realize the importance of this.

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
Path: biosci!daresbury!doc.ic.ac.uk!agate!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: phil@WUBIOS.WUSTL.EDU (J. Philip Miller)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: What is Gerinet
Message-ID: <9310161948.AA05087@wubios.wustl.edu>
Date: 16 Oct 93 19:48:17 GMT
Sender: Geriatric Health Care Discussion Group <GERINET@UBVM.BITNET>
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X-To:         Gerinet List <gerinet@ubvm.cc.buffalo.edu>

Recently several subscribers have asked about the purpose of the Gerninet
list.  The official purpose is stated as:

* This is a mailing list of those interested in geriatric
* health care.  It is intended to have multidisciplinary
* representation (e.g. physicians, nurses, social workers,
* physical therapists, occupational therapists, psychologists,
* speech therapists, lawyers, nursing home administrators, etc.) of
* individuals concerned about the well-being of our elderly.

but the reality is that the list can be anything that its subscribers want it
to be!  As owner of the list, if there does not seem to be any interest in the
list, then I will disband it.  Thus I suggest that if you have questions or
information generally about geriatric health care, then please post them!

-phil

--
     J. Philip Miller, Professor, Division of Biostatistics, Box 8067
         Washington University Medical School, St. Louis MO 63110
          phil@wubios.WUstl.edu - (314) 362-3617 [362-2693(FAX)]

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
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From: ABARE@SMCVAX.BITNET (Amy Abare)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: Suggestions
Message-ID: <01H44XYDE5MG8Y8LK6@SMCVAX.SMCVT.EDU>
Date: 15 Oct 93 14:54:46 GMT
Sender: Geriatric Health Care Discussion Group <GERINET@UBVM.BITNET>
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I am considering entering the Geriatric field on some level and am wondering
if people could offer information about their specific fields, specialties,
interests, or any kind of advise.  Currently I am doing home health care on
a part-time basis through a nursing agency, but I really want to make a
move into a full-time career.  I am weighing the options of entering the
field either through nursing or social work.  Any feedback would be
greatly appreciated!  Thanks!

Abare@smcvax.smcvt.edu

From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
Path: biosci!daresbury!doc.ic.ac.uk!uknet!pipex!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: SUPERVISOR@SWEEP.FO.UKANS.EDU (Phil Endacott)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: Gerinet Archives. . .
Message-ID: <30500F1B2C@sweep.fo.ukans.edu>
Date: 15 Oct 93 13:50:01 GMT
Sender: Geriatric Health Care Discussion Group <GERINET@UBVM.BITNET>
Reply-To: Geriatric Health Care Discussion Group <GERINET@UBVM.BITNET>
Organization: UNIVERSITY OF KANSAS
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X-Mailer: Pegasus Mail v2.3 (R5).
X-pmrqc:      1

Subscribers are reminded that GERINET is archived in NOTEBOOKs and
are searchable for topics of interest.  To date, 225 messages have
been posted to GERINET.  The following list points out the importance
of including a proper SUBJECT: line in both posts and replys to the
List--its really hard to tell the content of a message without it!!

Individual items can be retrieved for review.  If you are not
familiar with the retrieval process, send me private mail and I will
try and help.           . . . Phil---


> s * in GERINET
--> Database GERINET, 225 hits.

> index #.5 date.8 sender.30 subject.35
#     DATE     SENDER                         SUBJECT
-     ----     ------                         -------
1     91/12/04 TOSDRST@GE1VM.SCHDY.GE.COM     availability of 'humanly priced h+
2     92/01/25 DFOSTER@UA1VM.UA.EDU
3     92/01/28 vbselby@UALR.EDU               GERINET
4     92/01/28 FMBRUCE@ECUVM1.BITNET          GERINET
5     92/01/28 vbselby@UALR.EDU               RE: GERINET
6     92/01/29 MICHAEL@UNTVAX.BITNET          Re: GERINET
7     92/01/29 OLSON@UMKCVAX1.BITNET          Re: GERINET
8     92/01/29 FMBRUCE@ECUVM1.BITNET          Re: GERINET
9     92/01/29 BRICKEYJ@VTVM1.BITNET          Re: GERINET
10    92/01/29 FMDAUGHE@ECUVM1.BITNET         Re: GERINET
11    92/01/29 KB27508@UAFSYSB.BITNET         Re: GERINET
12    92/01/29 MICHAEL@UNTVAX.BITNET          Re: GERINET
13    92/01/30 FMBRUCE@ECUVM1.BITNET          Re: GERINET
14    92/01/30 BREWERJ@UNCG.BITNET            Re: GERINET
15    92/01/30 MICHAEL@UNTVAX.BITNET          Re: GERINET
16    92/02/01 DFOSTER@UA1VM.BITNET           Feedback(Relief)
17    92/02/01 FRIED@UCONNVM.BITNET           Re: Feedback(Relief)
18    92/02/01 DFOSTER@UA1VM.BITNET           Caregiver, Elders and Living Wills
19    92/02/02 MICHAEL@UNTVAX.BITNET          Re: Feedback(Relief)
20    92/02/03 BREWERJ@UNCG.BITNET            DNR
21    92/02/04 vbselby@UALR.EDU               RE: GERINET
22    92/02/06 BREWERJ@UNCG.BITNET            Re: Caregiver, Elders and Living +
23    92/02/06 BREWERJ@UNCG.BITNET            Re: Caregiver, Elders and Living +
24    92/02/10 FMBRUCE@ECUVM1.BITNET          Re: Feedback(Relief)
25    92/02/10 SASMTS@MVS.SAS.COM             Suggestions for Stroke Victim
26    92/02/10 FRIED@UCONNVM.BITNET           Re: Suggestions for Stroke Victim
27    92/02/10 FRIED@UCONNVM.BITNET           Re: Suggestions for Stroke Victim
28    92/02/11 CEBERLE@UNMCVM.BITNET          pneumonia
29    92/02/12 sawalker@UALR.EDU              gerinet
30    92/02/12 vbselby@UALR.EDU               RE: Suggestions for Stroke Victim
31    92/02/12 FRIED@UCONNVM.BITNET           RE: Suggestions for Stroke Victim
32    92/02/12 U55336@UICVM.BITNET            Response To Mary Serianni
33    92/02/13 SASMTS@MVS.SAS.COM             Thanks!
34    92/02/14 GA0708@SIUCVMB.BITNET          Information about group
35    92/02/15 DFOSTER@UA1VM.BITNET           Caregivers, Elder Abuse and Living
36    92/02/15 DFOSTER@UA1VM.BITNET           Elder Abuse
37    92/02/21 OTCM894@IBMH1.ORL.MMC.COM
38    92/02/23 DFOSTER@UA1VM.BITNET           Cognizance,Alziemers,and questions
39    92/02/23 SUPERVISOR@SWEEP.FO.UKANS.EDU  Re: Cognizance,Alziemers,and ques+
40    92/03/01 DRSTALL@UBVMS.BITNET           Re: Thanks!
41    92/03/01 DRSTALL@UBVMS.BITNET           Rex's dad
42    92/03/04 FMBRUCE@ECUVM1.BITNET          Re: GERINET
43    92/03/05 LLEEPER@NMSUVM1.BITNET         COMMUNICATION & AGEING
44    92/03/07 DFOSTER@UA1VM.BITNET           Communication,Aging, & Other thin+
45    92/03/07 LLEEPER@NMSUVM1.BITNET         Re: Communication,Aging, & Other +
46    92/03/11 sawalker@UALR.EDU
47    92/03/12 JMCDO00@UKCC.UKY.EDU
48    92/03/14 DFOSTER@UA1VM.BITNET           test
49    92/03/14 DFOSTER@UA1VM.BITNET           test
50    92/03/14 DFOSTER@UA1VM.BITNET           :(
51    92/03/14 DFOSTER@UA1VM.BITNET           re-intro
52    92/03/14 DFOSTER@UA1VM.BITNET           old-postn
53    92/03/07 DFOSTER@UA1VM                  Communication,Aging, & Other thin+
54    92/03/14 DFOSTER@UA1VM.BITNET           re-intro
55    92/03/15 LISTMGR@UBVM.BITNET            List owner needed for this list
56    92/03/18 JCOWARD@UVVM.UVIC.CA
57    92/03/18 vbselby@UALR.EDU
58    92/03/21 DFOSTER@UA1VM.BITNET
59    92/03/21 DFOSTER@UA1VM.BITNET           Re-intro
60    92/03/21 dorisann@TENET.EDU             Re: Re-intro
61    92/03/21 DFOSTER@UA1VM.BITNET           Notebook Filelist
62    92/03/21 DFOSTER@UA1VM.BITNET           Thanks
63    92/03/22 LLEEPER@NMSUVM1.BITNET         Re: Re-intro
64    92/03/23 pcallan@UMSA.UMD.EDU           Re: Re-intro
65    92/03/24 kemnitz@PRIMATE.WISC.EDU       membership
66    92/03/24 KVRAO@TRAPPER.BITNET           Forwarded mail
67    92/03/25 LISTMGR@UBVM.BITNET            New list owner found
68    92/03/28 DFOSTER@UA1VM.BITNET
69    92/04/03 DFOSTER@UA1VM.BITNET           Granny Dumping
70    92/04/03 DFOSTER@UA1VM.BITNET           Murder-Suicide-The Burden of Alzh+
71    92/04/05 LLEEPER@NMSUVM1.BITNET         Re: Murder-Suicide-The Burden of +
72    92/04/07 vbselby@UALR.EDU               testing
73    92/04/07 KMEVER01@UKCC.UKY.EDU          Re: testing
74    92/04/07 FISHER_DAL@CTSTATEU.BITNET     test
75    92/04/07 MICHAEL@UNTVAX.BITNET          Re: test
76    92/04/08 HNF@NIHCU.BITNET               Re:  test
77    92/04/21 lpowell@ATL.CALSTATE.EDU       Seniors Using Computers
78    92/04/21 lpowell@ATL.CALSTATE.EDU       Computer Benefits
79    92/04/21 dorisann@TENET.EDU             Re: Computer Benefits
80    92/04/21 HNF@NIHCU.BITNET               Re: Seniors Using Computers
81    92/04/22 FRIED@UCONNVM.BITNET           Re: Computer Benefits
82    92/04/23 OLSON@UMKCVAX1.BITNET          Re: Seniors Using Computers
83    92/04/24 STELLAFU@USCVM.BITNET          Re: Seniors Using Computers
84    92/04/21 SISC92@ITESO.BITNET            3th Week of Computing Systems Eng+
85    92/04/30 JACOBSVJ@VUCTRVAX.BITNET       Re: 3th Week of Computing Systems+
86    92/05/11 BENEDITA@BRUFPB2.BITNET
87    92/07/11 MEDICUR1@GREARN.BITNET
88    92/08/07 HAMIL@BRFUEL.BITNET            Traineeship in Physiotheraphy
89    92/08/20 ICOOPER@SNYESCVA.BITNET
90    92/08/20 GMP@PSUVM.BITNET               Stories needed
91    92/08/21 HCLADM04@UCONNVM.BITNET        Staff motivation
92    92/08/26 ICOOPER@SNYESCVA.BITNET        AJN MED/SURG GERIATRIC CONVENTION
93    92/09/05 DFOSTER@UA1VM.BITNET
94    92/09/08 ICSLG@ASUACAD.BITNET           No Subject
95    92/09/09 DFOSTER@UA1VM.BITNET           Re: No Subject
96    92/09/09 DFOSTER@UA1VM.BITNET           Help
97    92/09/12 DFOSTER@UA1VM.BITNET           Repeat of Posting
98    92/09/22 JCOWARD@UVVM.UVIC.CA           REGISTER NOW FOR ITCH'92
99    92/09/28 gomide@FPSP.FAPESP.BR          Apologies re: InterMeta course
100   92/10/06 MCELWRE@UWEC.BITNET            NATURAL ANTI-cancer Remedies
101   92/10/08 HSSDEAN@OUACCVMB.BITNET
102   92/10/10 DFOSTER@UA1VM.BITNET
103   92/10/12 JAJONE02@UKCC.UKY.EDU          Re: NATURAL ANTI-cancer Remedies
104   92/11/22 DFOSTER@UA1VM.BITNET           Hello
105   92/11/22 DEMERS@SJSUVM1.BITNET          Re: Hello
106   92/11/23 C576814@MIZZOU1.BITNET         Re: Hello
107   92/11/23 DEMERS@SJSUVM1.BITNET          Re: Hello
108   92/11/23 GMP@PSUVM.BITNET               Re: Hello
109   92/11/23 DEMERS@SJSUVM1.BITNET          Re: Minority, Senior?
110   92/11/23 GMP@PSUVM.BITNET               Re: Minority, Senior?
111   92/11/23 DEMERS@SJSUVM1.BITNET          Re: Minority, Senior?
112   92/11/23 DEMERS@SJSUVM1.BITNET          Re: Minority, Senior? cont.
113   92/11/23 DEMERS@SJSUVM1.BITNET          Re: Minority, Senior?
114   92/11/23 GMP@PSUVM.BITNET               Re: Minority, Senior?
115   92/11/23 DEMERS@SJSUVM1.BITNET          Re: Minority, Senior?
116   92/11/23 dorisann@TENET.EDU             Re: Hello
117   92/11/23 DICKG@TEMPLEVM.BITNET          Re: Minority, Senior?
118   92/11/23 DFOSTER@UA1VM.BITNET           Re: Hello
119   92/11/24 GMP@PSUVM.BITNET               Re: Minority, Senior?
120   92/11/24 HCLADM04@UCONNVM.BITNET        Re: Hello
121   92/11/24 GMP@PSUVM.BITNET               Re: Hello
122   92/11/24 vbselby@UALR.EDU               RE: Hello
123   92/11/24 vbselby@UALR.EDU               RE: Hello
124   92/11/28 MAJACOBS@NDSUVM1.BITNET        Re: Minority, Senior?
125   92/12/03 MAJACOBS@NDSUVM1.BITNET        Re: Hello
126   92/12/02 DEMERS@SJSUVM1.BITNET          Re: Hello
127   92/12/02 DEMERS@SJSUVM1.BITNET          Are you there??
128   92/12/03 MAJACOBS@NDSUVM1.BITNET        Re: Hello
129   92/12/03 MAJACOBS@NDSUVM1.BITNET        Re: Are you there??
130   92/12/03 GMP@PSUVM.BITNET               Re: Are you there??
131   92/12/04 OLSON@UMKCVAX1.BITNET          Re: Hello
132   92/12/05 HNF@NIHCU.BITNET               Health services and retired worke+
133   92/12/05 MAJACOBS@NDSUVM1.BITNET        Re: Health services and retired w+
134   92/12/05 DFOSTER@UA1VM.BITNET           :-)
135   92/12/05 DFOSTER@UA1VM.BITNET           Re: Hello
136   92/12/05 DFOSTER@UA1VM.BITNET           Re: Are you there??
137   92/12/08 MAJACOBS@NDSUVM1.BITNET        Re: :-)
138   92/12/08 SSW1.POSTMSTR@TS3.TEALE.CA.GOV Mail Delivery Status
139   92/12/08 DC.OPSD60@TS3.TEALE.CA.GOV     Mail Delivery Status
140   92/12/08 vbselby@UALR.EDU               RE: Health services and retired w+
141   92/12/09 HNF@NIHCU.BITNET               RE: Health services and retired w+
142   92/12/09 GMP@PSUVM.BITNET               RE: Health services and retired w+
143   92/12/09 vbselby@UALR.EDU               RE: Health services and retired w+
144   92/12/10 DFOSTER@UA1VM.BITNET           RE: Health services and retired w+
145   92/12/15 vbselby@UALR.EDU               RE: Health services and retired w+
146   92/12/16 DEMERS@SJSUVM1.BITNET          RE: Health services and retired w+
147   92/12/18 MAJACOBS@NDSUVM1.BITNET        RE: Health services and retired w+
148   92/12/18 SUPERVISOR@SWEEP.FO.UKANS.EDU  RE: Health services and retired w+
149   92/12/19 DICKG@TEMPLEVM.BITNET          RE: Health services and retired w+
150   92/12/19 GMP@PSUVM.BITNET               RE: Health services and retired w+
151   92/12/19 DICKG@TEMPLEVM.BITNET          RE: Health services and retired w+
152   92/12/19 GMP@PSUVM.BITNET               RE: Health services and retired w+
153   92/12/22 MAJACOBS@NDSUVM1.BITNET        RE: Health services and retired w+
154   92/12/22 MAJACOBS@NDSUVM1.BITNET        RE: Health services and retired w+
155   92/12/22 GMP@PSUVM.BITNET               RE: Health services and retired w+
156   92/12/22 MAJACOBS@NDSUVM1.BITNET        RE: Health services and retired w+
157   92/12/22 DICKG@TEMPLEVM.BITNET          RE: Health services and retired w+
158   92/12/18 WKJ%NIHCU.BITNET@SCI.CCNY.CUNY+Dr. Glaser
159   92/12/31 ICOOPER@SNYESCVA.BITNET        decubitus care
160   93/01/03 KB27508@UAFSYSB.BITNET         Re: decubitus care
161   93/01/06 vbselby@UALR.EDU               RE: Health services and retired w+
162   93/01/06 GMP@PSUVM.BITNET               RE: Health services and retired w+
163   93/01/06 C576814@MIZZOU1.BITNET         Re: RE: Health services and retir+
164   93/01/06 GMP@PSUVM.BITNET               Re: RE: Health services and retir+
165   93/01/06 DEMERS@SJSUVM1.BITNET          Re: RE: Health services and retir+
166   93/01/07 MAJACOBS@NDSUVM1.BITNET        Re: RE: Health services and retir+
167   93/01/07 GMP@PSUVM.BITNET               Re: RE: Health services and retir+
168   93/01/08 MAJACOBS@NDSUVM1.BITNET        Re: RE: Health services and retir+
169   93/01/09 DFOSTER@UA1VM.BITNET
170   93/01/12 MAJACOBS@NDSUVM1.BITNET
171   93/01/21 Linda_M_SAHIN@UMAIL.UMD.EDU
172   93/01/22 Linda_M_SAHIN@UMAIL.UMD.EDU    subscribe
173   93/02/02 MAJACOBS@NDSUVM1.BITNET
174   93/02/02 MAJACOBS@NDSUVM1.BITNET
175   93/02/08 LWROTEN@RN1.NURSING.ARIZONA.ED+reply
176   93/02/08 kraitch@ARGON.BERKELEY.EDU     Info request
177   93/02/13 MAJACOBS@NDSUVM1.BITNET        Re: Info request
178   93/02/13 MAJACOBS@NDSUVM1.BITNET        Re: reply
179   93/02/15 FCM001@UKANVM.BITNET           Re: Info request
180   93/02/15 FCM001@UKANVM.BITNET           Re: reply
181   93/02/15 MAJACOBS@NDSUVM1.BITNET        Re: Info request
182   93/03/07 MAJACOBS@NDSUVM1.BITNET        Re: Info request
183   93/03/07 eprince@LYNX.DAC.NORTHEASTERN.+Re: Info request
184   93/03/07 DFOSTER@UA1VM.BITNET           Re: Info request
185   93/03/07 GMP@PSUVM.BITNET               Re: Info request
186   93/03/07 BISCHOFF@UHUNIX.BITNET         Re: Info request
187   93/03/09 vbselby@UALR.EDU               RE: Info request
188   93/03/13 MAJACOBS@NDSUVM1.BITNET        RE: Info request
189   93/03/27 KIRSHENBLATT@NYUACF.BITNET     From Womb to Tomb in Film and Vid+
190   93/04/02 shirlee@U.WASHINGTON.EDU       Women's Health
191   93/04/10 astull@U.WASHINGTON.EDU        Agenet Database?
192   93/04/28 abcnews@CLASS.ORG              ABC News Request
193   93/05/11 MAJACOBS@NDSUVM1.BITNET        Re: reply
194   93/06/07 leone@OHSU.EDU                 Childhood immunization list
195   93/06/10 georgeb@CSN.ORG                Fall Prevention Training
196   93/06/22 jwhitesi@ACAD.BRYANT.EDU       Budget Cuts in Rhode Island (fwd)
197   93/06/28 gdfb@TROI.CC.ROCHESTER.EDU     Medical/HealthCare Hypermedia Exh+
198   93/06/30 samajane@ATHENA.MIT.EDU
199   93/07/06 JSMIT@UKANVM.BITNET
200   93/07/07 mmg@CAMIS.STANFORD.EDU
201   93/07/07 kristoff@NET.BIO.NET           Re: <None>
202   93/07/12 georgeb@CSN.ORG                Reimbursement for Fall Prevention+
203   93/07/15 HECKERSL@TEMPLEVM.BITNET       subscription
204   93/07/19 mwitten@HERMES.CHPC.UTEXAS.EDU COMPUTATIONAL HEALTH (long)
205   93/08/23 netad@UDS01.UNIX.ST.IT         The Net ADvertiser
206   93/08/25 WMILHEIM@PSUGV.PSU.EDU         Internet Survey
207   93/08/27 vinta@UNR.EDU                  Re: Internet Survey
208   93/09/14 mwitten@HERMES.CHPC.UTEXAS.EDU CONGRESS: COMPUTATIONAL MEDICINE +
209   93/09/14 KUCHTA@TCUCVMS.BITNET          Upcoming Gerontological Symposium
210   93/09/15 GDEKKER@MED.RUU.NL             oproep kontakt en informatie
211   93/09/16 BROW7242@SNYPLAVA.BITNET
212   93/09/17 ABARE@SMCVAX.BITNET
213   93/09/23 FWR10@PHOENIX.CAMBRIDGE.AC.UK  Info resources
214   93/09/23 gerritf@HACKTIC.NL             Re: Info resources
215   93/09/23 mmg@CAMIS.STANFORD.EDU         Re: Info resources
216   93/09/29 goes@CHIMERA.SPH.UMN.EDU       Announcing HEALTHMGMT
217   93/10/13 music@PARCOM.ERNET.IN
218   93/10/13 VBSELBY@UALR.EDU               welcome
219   93/10/13 GGRAHAM@PSTCC.CC.TN.US         discussion
220   93/10/14 edemt@TTACS.TTU.EDU            Parkinson's readings
221   93/10/14 ABARE@SMCVAX.BITNET            Re: discussion
222   93/10/15 EDWARDSH@QUT.EDU.AU            Re: Parkinson's readings
223   93/10/15 EDWARDSH@QUT.EDU.AU            Re: discussion
224   93/10/15 GGRAHAM@PSTCC.CC.TN.US         Re: discussion
225   93/10/15 FCM001@UKANVM.BITNET           Re: discussion

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From owner-ageing@net.bio.net Mon Oct 18 23:00:00 1993
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From: GGRAHAM@PSTCC.CC.TN.US (George Graham)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: discussion
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===============================================

Mary,

I treat a lot of Alzheimer's.  And would love to discuss your
dealings.

The one thing that striked me more than anuything is the fact taht
they are more aware than we thnink. (oops)

I had one peatient that I see in her home who could tell the
diffrernce between my assistants when her husband and I couldm't.

Please excuse my typing. I'm not very good at it and this program
doesn't allow for correcting it.

George G
ggraham@pstcc.cc.tn.us

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
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From: GGRAHAM@PSTCC.CC.TN.US (George Graham)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: discussion
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Helen, et al ...

I think that most of my time with patients is just talking.  In some
cases I think that I'm the closest thing they have to a family.

I look at pictures, talk about grandkids etc most of the time.

I had one emphysema patient who called me one Saturday that he
had an emergency.  I drove to his home just to find out that his
kids came in for his anniversatry and he wanted them to meet me.

I have forgeooten how many VCR movies I have sat through just keeping
a patient company.

Talk is the best BEST medicine.

George G
ggraham@pstcc.cc.tn.us

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
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From: EDWARDSH@QUT.EDU.AU (qut.edu.au)
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Subject: RE: discussion
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Dear George, Indie, Louella, Mary
          Hi!  I agree with all the comments made.  My greatest
          passion and research interest at present is that it is the
          talk that we have with older people, especially ADs, that
          has the greatest impact on their health and well-being.
          Amy comments????
          Helen

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
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From: EDWARDSH@QUT.EDU.AU (qut.edu.au)
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Subject: RE: discussion
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Amy, I am a nurse and therefore biased also.  If I was entering aged care I woul
d consider long term care units - we have to improve care there.  This is an Aus
tralian perspective so I hope it is helpful.   Helen

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
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From: phil@WUBIOS.WUSTL.EDU (J. Philip Miller)
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 <EDWARDSH@QUT.EDU.AU> writes:
>
> Dear George, Indie, Louella, Mary
>           Hi!  I agree with all the comments made.  My greatest
>           passion and research interest at present is that it is the
>           talk that we have with older people, especially ADs, that
>           has the greatest impact on their health and well-being.
>           Amy comments????

At the later stage of AD where little activity other than listening is
possible, undoubtedly you are correct.  At less sever stages of the disease,
then you are probably correct if you include in your "talk" our exortations to
other usefule behavior, e.g. to "get up out of bed and interact with others on
the unit."

What type of "talk" are you thinking about?

-phil

>           Helen
>


--
     J. Philip Miller, Professor, Division of Biostatistics, Box 8067
         Washington University Medical School, St. Louis MO 63110
          phil@wubios.WUstl.edu - (314) 362-3617 [362-2693(FAX)]

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
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From: EDWARDSH@QUT.EDU.AU (qut.edu.au)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: Parkinson's readings
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Edie
          I sent you a message the other day but I'm not sure you got
          it - my system was playing up.  I have a colleague at my
          university who is interested and researching PD.  You can
          reach him on this e-mail  m.dunne.@qut.edu.au
          Hope this is useful
          Helen Edwards

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
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From: caron001@MAROON.TC.UMN.EDU (Wayne A. Caron)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: Talking with AD patients
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I am very happy to see some activity on this list. I am a family therapist on
the clinical faculty of the geriatrics family practice program. My general focus
has been on caregiving and chronic illness with a specific focus on Alzheimer's
disease. Whereas up until about two years ago I worked primarily with caregivers
and other family members, I was asked by our local Alzheimer's Association
chapter to pilot a support group for AD patients. They were unsure how feasible
such a group would be. I was also,but decided to give it a shot. I spent the
first five of weekly sessions with a very rigid structure of topics and format
on the belief that persons with dementia wouldn't be able to handle group
process without this support. On the sixth session, my group members politely
informed me they wanted to talk about what they wanted to talk about - not what
I had listed on the agenda. This was the beginning of a real group experience. I
found that with patience and an atmosphere of acceptance, even AD patients with
moderate to moderate/severe levels of impairment (Folstein score of 12/30) could
talk about their experience share feelings, and support each other. My core
group of three stayed with the group for about a year, while four or five others
moved in and out of the group during that time. I learned a lot and changed many
of my views about what persons with AD can and cannot do. We're currently
working on a three year project studying a combined patient - family group
intervention.

I'd be curious to hear from others who may have had experience in these areas.


--------------------------------
Wayne Caron, Ph.D. LMFT              | caron001@maroon.tc.umn.edu
Family Practice & Community Health   | Voice: 612-627-4941
Univerity of Minnesota               | Fax: 612-627-4314

---------------------------------

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
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From: TKELLY@UGA.CC.UGA.EDU (Tim Kelly)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: Talking with AD patients
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Wayne:
Wesley Woods Geriatric Hospital in Atlanta is running a group for AD patients
and a concurrent group for family members. Susan Peterson might be able to give

 you information on their group.

Tim Kelly
University of Georgia
School of Social Work
(706) 542-5441

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
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Helen,

Yes I am a practitioner ... a dentsit (dentist).  You can see I'm
not a typist.

I am presently teaching anatomy to nursing students as well as doing
dentistry.  I see physically/mentally compromised patients inthier
homes/nursing homes.  I take the treatmemnt tp them since the cost
of taking them to an office is costly.

I had a lady fall in a nursing home and I was worried about a fracture
of the mandible.  I had to send her for a panoramic x-ray (I can't
transport one of those machines).  The x-ray cost her $35 ... the
ambulance trip to the office cost $350.

Plus in addition to taeching and dentsitry.  I'm writing (actually
its finished) a manual on how to do dental treatment without the
dentsit.  This is for nursing/family personnel.

I was asked to publish it with the comapny that I have mentioned
earlier ... the company which set the parts of the body to music
to make memorizing the parts easier.

I'm obviously a workaholic.

Plus I'm in the early stages of getting a research grant to study
something which I have noticed in nursing homes ....

That is that if you correect the gum infections in residents ...
their UTIs go away .... HHHhhhhhhh,mmmmmmmm  !!!!!?????


george g
ggraham@pstcc.cc.tn.us

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
Path: biosci!bcm!cs.utexas.edu!usc!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: ICOOPER@SNYESCVA.BITNET (INDIE)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: Suggestions
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Date: 19 Oct 93 02:48:00 GMT
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I am an RN who would rather focus on psychosocial needs of people.  I currently
work in a nursing home and am frustrated because most RNs focus on physical
symptoms until a behavioral problem arises and then the subject turns toward
possibly trying a medication.  When I try to say hey lets look behind the
behavior and see if we can find out why this resident feels a need to act out.
I don
t get much feedback.  I also have interviewed prospective employers to see
what degrees they preferred.  In the mental health field, the preference was
mainly toward an MSW however they felt having an RN degree was a real plus.
Of course this was the case in a very small sample and could be coincidental.
I personally have decided to go the MSW route.  It was not an easy decision as
I plan to use my nursing skills as an allied health professional. I wish you
the best!

From owner-ageing@net.bio.net Fri Oct 22 23:00:00 1993
Path: biosci!bcm!cs.utexas.edu!usc!howland.reston.ans.net!darwin.sura.net!wvnvms.wvnet.edu!marshall.wvnet.edu!newsmgr
From: EDWARDSH@QUT.EDU.AU (qut.edu.au)
Newsgroups: bionet.molbio.ageing,bit.listserv.gerinet
Subject: RE: Talking with AD patients
Message-ID: <BC10186D5F9F605B06@qut.edu.au>
Date: 19 Oct 93 00:05:00 GMT
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Wayne
          Great to hear of your work.  For a while here in Australia
          I have been trying to get people to acknowledge the other
          side of caregiver burden "carereceiver burden".  I believe
          that the carereceivers also have concerns, problems and
          issues that can be addressed through education and
          counselling.  I have started a clinic thru my university
          for education, support and counselling for older people
          (and their caregivers).  It's been hard to get it off the
          ground because the perception seems to be that the older
          people couldn't or wouldn't want to talk about their
          concerns - it's even hard for some people to acknowledge
          that the carereceivers might have some problems with being
          cared for!!  Another problem is that frequently the
    