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No. in this case, they knew it was differences in the patients.

infecting strains were identified at the start.

Barb

> > > >

> > > >

> > > > > Biofilms, maybe in some cases.

> > > >

> > > > True.

> > > >

> > > > > Evolution thru selective pressure in other cases.

> > > >

> > > > I dont think this is an important factor, at least not on on

a

> > > month-

> > > > to-month scale:

> > > >

> > > > ==========================

> > > >

> > > > Antimicrob Agents Chemother. 2005 Apr;49(4):1294-301.

> > > >

> > > > In vitro susceptibility testing of Borrelia burgdorferi sensu

> > lato

> > > > isolates cultured from patients with erythema migrans before

> and

> > > > after antimicrobial chemotherapy.

> > > >

> > > > Hunfeld KP, Ruzic-Sabljic E, Norris DE, Kraiczy P, Strle F.

> > > >

> > > > Institute of Medical Microbiology, University Hospital of

> > > furt,

> > > > -Ehrlich Str. 40, D-60596 furt/Main, Germany.

> > > > K.Hunfeld@e...

> > > >

> > > > Clinical treatment failures have been reported to occur in

> early

> > > Lyme

> > > > borreliosis (LB) for many suitable antimicrobial agents.

> > > > Investigations of possible resistance mechanisms of the

> Borrelia

> > > > burgdorferi complex must analyze clinical isolates obtained

> from

> > LB

> > > > patients, despite their receiving antibiotic treatment. Here,

> > > > borrelial isolates obtained from five patients with erythema

> > > migrans

> > > > (EM) before the start of antibiotic therapy and again after

the

> > > > conclusion of treatment were investigated. The 10 isolates

were

> > > > characterized by restriction fragment length polymorphism

> > analysis

> > > > and plasmid profile analysis and subjected to susceptibility

> > > testing

> > > > against a variety of antimicrobial agents including those

used

> > for

> > > > initial chemotherapy. Four out of five patients were infected

> by

> > > the

> > > > same genospecies (Borrelia afzelii, n = 3; Borrelia garinii,

n

> =

> > 1)

> > > > at the site of the EM lesion before and after antimicrobial

> > > therapy.

> > > > In one patient the genospecies of the initial isolate (B.

> > afzelii)

> > > > differed from that of the follow-up isolate (B. garinii). No

> > > > significant changes in the in vitro susceptibilities became

> > obvious

> > > > for corresponding clinical isolates before the start and

after

> > the

> > > > conclusion of antimicrobial therapy. This holds true for the

> > > > antimicrobial agents used for specific chemotherapy of the

> > > patients,

> > > > as well as for any of the additional agents tested in vitro.

> Our

> > > > study substantiates borrelial persistence in some EM patients

> at

> > > the

> > > > site of the infectious lesion despite antibiotic treatment

over

> a

> > > > reasonable time period. Borrelial persistence, however, was

not

> > > > caused by increasing MICs or minimal borreliacidal

> concentrations

> > > in

> > > > these isolates. Therefore, resistance mechanisms other than

> > > acquired

> > > > resistance to antimicrobial agents should be considered in

> > patients

> > > > with LB resistant to treatment.

> > > >

> > > > Publication Types:

> > > > Clinical Trial

> > > >

> > > > PMID: 15793100 [PubMed - indexed for MEDLINE]

> > > >

> > >

> >

>

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shredded cheese on a flour tortilla, in the toaster oven till the

edges are brown and crispy.

Topped with some salsa, or better, guacamole and salsa.

*S*

> > > > > >

> > > > > > Good luck with your abx eating.

> > > > > >

> > > > > > These bacteria have almost all the same ribosomal

targets,

> > the

> > > > same

> > > > > > enzymatic targets, all the same drug targets as an E.

coli

> > > > bladder

> > > > > > infection has. Ergo, either

> > > > > >

> > > > > > A. bacteriostasis due to drugs does not cause them to be

> > > > eliminated

> > > > > by

> > > > > > the host (somewhat unlikely), or

> > > > > >

> > > > > > B. bacteriostasis due to drugs is an elective stress

> response

> > > > that

> > > > > > doesnt occur in all bacteria in all circumstances (rather

> > > > > unlikely), or

> > > > > >

> > > > > > C. the drugs arent getting to their targets, for some

> > > particular

> > > > > > molecular reason. Which is what I've focused on.

> > > > > >

> > > > > > Its not necessarily some impenetrable mystery. As of now

> > theres

> > > > no

> > > > > > particular reason to suspect that it probably cant be

> solved.

> > > > > >

> > > > >

> > > >

> > >

> >

>

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  • 1 month later...

Thanks for posting this Tom. Its not far from me. I wasn't sure what

I should or could post here.

Take Care

>

> Ottawa team unravelling brain damage in multiple sclerosis

>

> Last Updated Wed, 21 Dec 2005 13:47:38 EST

> CBC News

>

> The puzzle of how nerve coatings are damaged in the

brains of people with multiple sclerosis may have been solved by a

Canadian-led research team.

>

>

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  • 1 year later...
Guest guest

Members,

Sharon & I have already spoken to and did the telephone

interview. This was all handled in a very nice professional manner and

I would highly advise anyone that has dealt with an employer or

employees to take this interview. The questions are nonevasive.

Hopefully 's research will help teach the employer and employees

to work together and to find a solution that benefits both parties.

Thank you for your interest.

KC

--- In , " Ellsworth " <eellswor@...>

wrote:

>

> Hello, I am a graduate student at the University of Kansas who is

> interested in how people approach their employer when they need a

> change in their work schedule or work environment due to a health

> reason. With permission from KC and Sharon, I am posting in search

> of research participants. If you have asked for a change in your

> schedule or work environment because of health reasons (or if you can

> recommend someone who has) and are willing to participate, please

> contact me at eellswor@... My research is done through a

> telephone interview that lasts between 30 and 45 minutes. Thank you

> very much!!!

> Ellsworth

>

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Guest guest

--- In , " Ellsworth " <eellswor@...>

wrote:

>

> Hello, I am a graduate student at the University of Kansas who is

> interested in how people approach their employer when they need a

> change in their work schedule or work environment due to a health

> reason. With permission from KC and Sharon, I am posting in search

> of research participants. If you have asked for a change in your

> schedule or work environment because of health reasons (or if you can

> recommend someone who has) and are willing to participate, please

> contact me at eellswor@... My research is done through a

> telephone interview that lasts between 30 and 45 minutes. Thank you

> very much!!!

> Ellsworth

>

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  • 3 months later...
Guest guest

> One of the most bogus studies out there regarding CFS, in my view, is

> the " twins study " that tries to draw conclusions about CFS by starting

> from the misleading assumption that identical twins completely

> eliminates genetic influences.

Doesn't it though? Maybe not epigenetic influences (I don't really know).

> To me, the problem with genetic research is not that it's looking at

the

> wrong thing, but that the field way under-estimates the complexity of

> the problems they are tackling. The mentality seems to be that it's

> possible to find one defective gene, enzyme or protein that corresponds

> to one disease state. As if diseases were nice, cooperative little

guys

> with single causes.

Many diseases are like that: sickle cell, Down syndrome, cystic

fibrosis (to a large extent), familial forms of Alzheimer's and ALS...

I can't really agree with your picture; I feel like most researchers

into CFS, lupus, etc are expecting to find bewildering complexity at

the headwaters of each of the immune diseases. In fact, the

introductions of their papers almost ritually state that the disease

is " extremely complex, " although there's usually not significant

evidence to support that statement.

As I see it the main problem with research is faith in models. I can't

even express my outrage and disbelief at the fact that people actually

assume that EAE = multiple sclerosis. Fortunately, this guy can:

" Does the use of animal models of disease take us any closer to

understanding human disease? With rare exceptions, the answer to this

question is likely to be negative. The reasoning is simple. An animal

model of disease can be said to be congruent with the human disease

only when three conditions have been met: we fully understand the

animal model, we fully understand the human disease and we have

examined the two cases and found them to be substantially congruent in

all important respects.

[...]

" All the other animal models — including those of inflammation,

vascular disease, nervous system diseases and so on — represent

nothing more than an extraordinary, and in most cases irrational, leap

of faith. We have a human disease, and we have an animal model which

in some vague and almost certainly superficial way reflects the human

disease. We operate on the unjustified assumption that the two are

congruent, and then we spend vast amounts of money trying to

investigate the animal model, often without bothering to test our

assumptions by constantly referring back to the original disease in

humans. "

This rather acid editorial is found at:

http://www.nature.com/nrd/journal/v2/n2/full/nrd1012_fs.html

It may even be far too harsh. I can't deny that I enjoy reading it,

though.

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Guest guest

wrote:

> Doesn't it though? Maybe not epigenetic influences (I don't really

know).

>

Many diseases are like that: sickle cell, Down syndrome, cystic

fibrosis (to a large extent), familial forms of Alzheimer's and ALS...

Maybe those are the diseases where twin studies would be a good tool

.... in the case of CFS, I think they are using a hammer to tighten a

screw ... and that's a charitable way to put it. Besides, there was

anecdotal evidence that it was a poorly-conducted study anyway ... in

one case I heard of, the twins were mixed up in the study and the

"well" twin could not convince them of their error.

I would call sickle cell, Down's, etc., the "low hanging fruit" of

genetics. The public, I suspect, has made the mistake of extrapolating

those easy wins into a general principle that all disease states are

easy to get everyone to agree on a simple definition, and that they

have single causes that are amenable to single fixes. And at any rate

.... even those aren't "easy wins" in that I don't recall cures even for

those diseases you listed.

Then there was all the hoo-raw surrounding the sequencing of the human

genome ... that turned out to be overblown and now we realize that the

proteome is where the action is at and that will be a much bigger job

to decode and understand, much less do anything about.

But I ramble. At any rate ... I am glad to hear that geneticists at

least understand that CFS will not be an "easy win".

--Bob

wrote:

> One of the most bogus studies out there regarding CFS, in my view,

is

> the "twins study" that tries to draw conclusions about CFS by

starting

> from the misleading assumption that identical twins completely

> eliminates genetic influences.

Doesn't it though? Maybe not epigenetic influences (I don't really

know).

> To me, the problem with genetic research is not that it's looking

at

the

> wrong thing, but that the field way under-estimates the complexity

of

> the problems they are tackling. The mentality seems to be that

it's

> possible to find one defective gene, enzyme or protein that

corresponds

> to one disease state. As if diseases were nice, cooperative little

guys

> with single causes.

Many diseases are like that: sickle cell, Down syndrome, cystic

fibrosis (to a large extent), familial forms of Alzheimer's and ALS...

I can't really agree with your picture; I feel like most researchers

into CFS, lupus, etc are expecting to find bewildering complexity at

the headwaters of each of the immune diseases. In fact, the

introductions of their papers almost ritually state that the disease

is "extremely complex," although there's usually not significant

evidence to support that statement.

As I see it the main problem with research is faith in models. I can't

even express my outrage and disbelief at the fact that people actually

assume that EAE = multiple sclerosis. Fortunately, this guy can:

"Does the use of animal models of disease take us any closer to

understanding human disease? With rare exceptions, the answer to this

question is likely to be negative. The reasoning is simple. An animal

model of disease can be said to be congruent with the human disease

only when three conditions have been met: we fully understand the

animal model, we fully understand the human disease and we have

examined the two cases and found them to be substantially congruent in

all important respects.

[...]

"All the other animal models — including those of inflammation,

vascular disease, nervous system diseases and so on — represent

nothing more than an extraordinary, and in most cases irrational, leap

of faith. We have a human disease, and we have an animal model which

in some vague and almost certainly superficial way reflects the human

disease. We operate on the unjustified assumption that the two are

congruent, and then we spend vast amounts of money trying to

investigate the animal model, often without bothering to test our

assumptions by constantly referring back to the original disease in

humans."

This rather acid editorial is found at:

http://www.nature.com/nrd/journal/v2/n2/full/nrd1012_fs.html

It may even be far too harsh. I can't deny that I enjoy reading it,

though.

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Guest guest

> Maybe those are the diseases where twin studies would be a good tool

I think it's very enlightening to get an upper limit on the genetic

component, for any disease. Twin studies deliver that.

> I would call sickle cell, Down's, etc., the " low hanging fruit " of

genetics.

For sure. Especially the causation of Down by trisomy 21. That's a

discovery that was made (I'm pretty sure) with an optical mircoscope,

just by looking at the number of chromosomes in cells. Could have been

done in a middle school science lab. All it took was to look at the

right thing.

> Then there was all the hoo-raw surrounding the sequencing of the

human genome ... that turned out to be overblown

Yeah, a lot of it seems very exaggerated to me and can be a bit

repulsive. But it garners more money for medical research. So, I'd

probably say the same stuff, if I were the bigshot with the media's

ear. A billion spent on research probably does more good than a

billion spent on most of the stuff that a billion gets spent on.

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  • 1 year later...

Please look on my web site under Why ABA: research

www.learnerscompass.com<http://www.learnerscompass.com/>

[ ] research

Can anyone send me any research to support intensive ABA for young children

with autism that also specify number of hours. I have the Lovaas article but

having trouble finding other articles online, thanks

Kowalski, M.A., BCBA

Certified RDI Consultant

lak214@...<mailto:lak214@...>

610-659-5344

42 Union Street

Norristown, PA 19403

www.connectingpieces.comGet<http://www.connectingpieces.comget/> more from the

Web. FREE MSN Explorer download :

http://explorer.msn.com<http://explorer.msn.com/>

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  • 1 year later...

Dear Pat,

If I remember correctly, even Novartis was skeptical and was going to

shelve STI571, until Dr. Druker asked to buy the patent. He recognized its

potential and went for it. We are the beneficiaries of medical history and his

dream. I want all the researchers to follow their dream, we never know where it

will take us, but I feel positive that someone is on to something that will

eventually become a cure. Let's all keep a positive attitude that in due time,

there will be a cure pronouncement. Thank you to all who keep holding us up

when we are down and holding on to the dream. Haven't we all witnessed members

who were really sick, recover by being patient and changing treatments? I can

think of quite a few right off the bat. It would be interesting to hear part of

their stories posted as a reminder of how fortunate we are to be living in this

time. How many of you have changed from Gleevec to another drug, but at least

credit Gleevec with saving your life?

Hands & hearts,

Lottie Duthu

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You can count me in on that group!

On Wed, Jan 13, 2010 at 1:25 PM, Lottie Duthu <lotajam@...> wrote:

>

>

> Dear Pat,

> If I remember correctly, even Novartis was skeptical and was going to

> shelve STI571, until Dr. Druker asked to buy the patent. He recognized its

> potential and went for it. We are the beneficiaries of medical history and

> his dream. I want all the researchers to follow their dream, we never know

> where it will take us, but I feel positive that someone is on to something

> that will eventually become a cure. Let's all keep a positive attitude that

> in due time, there will be a cure pronouncement. Thank you to all who keep

> holding us up when we are down and holding on to the dream. Haven't we all

> witnessed members who were really sick, recover by being patient and

> changing treatments? I can think of quite a few right off the bat. It would

> be interesting to hear part of their stories posted as a reminder of how

> fortunate we are to be living in this time. How many of you have changed

> from Gleevec to another drug, but at least credit Gleevec with saving your

> life?

> Hands & hearts,

> Lottie Duthu

>

>

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Hello Group..

on research, I hope that all who are now on the newer drugs,  that they hold for

a lifetime.

the unfortunate part of this is, I attend the hospital twice week, and see more

and more of

CML (aml) in younger and younger people.  When I first was dx with my Leukemia

It was

not even called CML and is was very very rare. It was later that I started to

note that

there were more and more people over the age of 40.  Now it seems that young

people

in their 20 and 30's have it.  I have even heard of younger people than that.

So my prayer is that this group and other groups do not let up on the search

for a cure..  I have failed Imatinib, Dasatinib and Nilotnib .  I wonder if the

drugs

they now have will last for a long long time. 

Be safe all

Skip DXed 32 + years

Re: [ ] Research

You can count me in on that group!

On Wed, Jan 13, 2010 at 1:25 PM, Lottie Duthu <lotajam@...> wrote:

>

>

> Dear Pat,

> If I remember correctly, even Novartis was skeptical and was going to

> shelve STI571, until Dr. Druker asked to buy the patent. He recognized its

> potential and went for it. We are the beneficiaries of medical history and

> his dream. I want all the researchers to follow their dream, we never know

> where it will take us, but I feel positive that someone is on to something

> that will eventually become a cure. Let's all keep a positive attitude that

> in due time, there will be a cure pronouncement. Thank you to all who keep

> holding us up when we are down and holding on to the dream. Haven't we all

> witnessed members who were really sick, recover by being patient and

> changing treatments? I can think of quite a few right off the bat. It would

> be interesting to hear part of their stories posted as a reminder of how

> fortunate we are to be living in this time. How many of you have changed

> from Gleevec to another drug, but at least credit Gleevec with saving your

> life?

> Hands & hearts,

> Lottie Duthu

>

>

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Skip,

I agree with you fully.  As a 26 year old new CML-er,  I hope that not only a

cure can be found, but also a cause.  If more and more people are getting this

than ever before... It just makes ya wonder what's going on.

Working toward Zero,

Danny

-- Sent from my Palm Prē

Skip Duffie wrote:

 

Hello Group..

on research, I hope that all who are now on the newer drugs,  that they hold

for a lifetime.

the unfortunate part of this is, I attend the hospital twice week, and see more

and more of

CML (aml) in younger and younger people.  When I first was dx with my Leukemia

It was

not even called CML and is was very very rare. It was later that I started to

note that

there were more and more people over the age of 40.  Now it seems that young

people

in their 20 and 30's have it.  I have even heard of younger people than that.

So my prayer is that this group and other groups do not let up on the search

for a cure..  I have failed Imatinib, Dasatinib and Nilotnib .  I wonder if

the drugs

they now have will last for a long long time. 

Be safe all

Skip DXed 32 + years

Re: [ ] Research

You can count me in on that group!

On Wed, Jan 13, 2010 at 1:25 PM, Lottie Duthu & lt;lotajam@...> wrote:

>

>

> Dear Pat,

> If I remember correctly, even Novartis was skeptical and was going to

> shelve STI571, until Dr. Druker asked to buy the patent. He recognized its

> potential and went for it. We are the beneficiaries of medical history and

> his dream. I want all the researchers to follow their dream, we never know

> where it will take us, but I feel positive that someone is on to something

> that will eventually become a cure. Let's all keep a positive attitude that

> in due time, there will be a cure pronouncement. Thank you to all who keep

> holding us up when we are down and holding on to the dream. Haven't we all

> witnessed members who were really sick, recover by being patient and

> changing treatments? I can think of quite a few right off the bat. It would

> be interesting to hear part of their stories posted as a reminder of how

> fortunate we are to be living in this time. How many of you have changed

> from Gleevec to another drug, but at least credit Gleevec with saving your

> life?

> Hands & amp; hearts,

> Lottie Duthu

>

>

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Yes I agree also a cure and a cause would be fantastic :-)

I am 28 years and have been on Gleevec since Nov. 2003. I cant stop thinking

that I know Gleevec is fighting the CML but what else is it doing? Can it harm

your body after so many years?

>

>

> Dear Pat,

> If I remember correctly, even Novartis was skeptical and was going to

> shelve STI571, until Dr. Druker asked to buy the patent. He recognized its

> potential and went for it. We are the beneficiaries of medical history and

> his dream. I want all the researchers to follow their dream, we never know

> where it will take us, but I feel positive that someone is on to something

> that will eventually become a cure. Let's all keep a positive attitude that

> in due time, there will be a cure pronouncement. Thank you to all who keep

> holding us up when we are down and holding on to the dream. Haven't we all

> witnessed members who were really sick, recover by being patient and

> changing treatments? I can think of quite a few right off the bat. It would

> be interesting to hear part of their stories posted as a reminder of how

> fortunate we are to be living in this time. How many of you have changed

> from Gleevec to another drug, but at least credit Gleevec with saving your

> life?

> Hands & amp; hearts,

> Lottie Duthu

>

>

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  • 1 year later...

Nope - I am not an official researcher. If you are - great!

>

> I am intending a virtual seminar next week, Feb 17th, titled " Beyond the

Bench: The Perceived Price of Activism " . I wanted to get some comments from

others here before I see the talk.

> http://www.sefora.org/feb-2011-seminar/

>

> I am interested to know how many of those in are directly involved in

researching CMT. If you are researching, are you active in other ways in the CMT

community? Why/Why not? Would you be researching it if you could? Do you feel

that creating awareness/raising money is enough? What kind of credit do you give

to those who do the " real work " ? If you neither raise awareness or research,

what are your reasons for doing so?

>

> I feel like this debate is like all those pink ribbons and fund-raisers you

see for cancer research, while all the scientists behind their respective

benches don't really get very much credit from the community.

>

> Any comments will probably help figure out how I feel about doing my own

research and my position in the community.

>

> Thanks,

>

>

>

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