Re: where have I heard of Luther Lindner?

[Guest guest]

This patent has 6 micrographs I'd love to look at, which I think should

be here:

http://tinyurl.com/l6vvd

Apparantly these university computers cant read TIFFs, and of course I

cant install a plug-in on them. (I also dont have a computer at home

anymore.) Is anyone in the mood to convert these things to JPGs or

something?

> Heres Linders patent: http://tinyurl.com/mn7oq

[Guest guest]

From the patent:

> There is some overlap between the levels of [the] bacteria in the

normal population and those with the chronic fatigue syndrome and

multiple sclerosis, but there is a correlation between elevated levels

of the bacterium and the presence of active symptoms of these diseases.

Hmmm, overlap eh. Bummer. In that case you have to resort to:

1. immune overreactivity to the organism in sickies, which

paradoxically increases the bacterial load in addition to causing

symptoms

or

2. there is *not* overlap in some other compartment other than the

blood, and the population in that compartment is the one creating the

disease

or

3. they are not the cause of the diseases, but an effect

[Guest guest]

, Hmmm, this is odd. Never heard of it and the original research company appears to have gone out of business. But in this 2000 article, the working name for the new bacterium was "Luey". http://www.newsrx.com/newsletters/Biotech-Week/2000-01-12/2000011233334UW.html How weird. Here are links to research that he's co-authored. Maybe this will help you place him. http://scholar.google.com/scholar?hl=en & lr= & q=%22L.+E.+Lindner%22 & btnG=Search penny <usenethod@...> wrote: I was just looking at some veterinary papers by Tarello. Got wind of a new investigative thread. Apparantly a single group of bacteria found in the bloodstream in MS, lupus, CFS, and (lower levels) healthies. Heres Linders patent: http://tinyurl.com/mn7oqHeres an write up on him, containing some quotes from him:http://www.ottem.org/ccca/news/newsletters/vol16-1.htmFound other pages suggesting this work is ongoing. But, nothing having been published after some years, I have to wonder whether they are getting any consistent results.Hes apparantly on the Pathology faculty at Texas A & M. Name sounds really familiar.

[Guest guest]

I can open it, but it's 30 pages. penny <usenethod@...> wrote: This patent has 6 micrographs I'd love to look at, which I think should be here:http://tinyurl.com/l6vvdApparantly these university computers cant read TIFFs, and of course I cant install a plug-in on them. (I also dont have a computer at home anymore.) Is anyone in the mood to convert these things to JPGs or something?> Heres Linders patent: http://tinyurl.com/mn7oq

[Guest guest]

Interesting. He and allied physicians treated a rather large number

of patients with combo abx. Using binary judgements (improved vs

unimproved, bacterial blood load reduced vs unreduced), he claims

100% correlation between clinical improvement and bacteriologic

improvement.

I'd much rather see actual data, of course, and preferably data that

is much more quantitative. But this is interesting at least.

He also asserts that application of abx to which the organisms are

resistant actually stimulates their growth.

=================

The 66 patients for whom follow-up was adequate are summarized below

by diagnosis: Chronic fatigue syndrome: 41 patients total; 30

patients improved, 11 patients did not improve. Reduced levels of HBB

were seen in all improved patients and HBB levels were not reduced in

unimproved patients. Multiple sclerosis (typical): 7 patients total;

4 patients improved; 3 patients did not improve. Two of the four

improved patients had marked functional improvement, for example,

were able to walk with a cane where a wheelchair had been previously

required. There were reduced levels of HBB in three of the improved

patients, with an insufficient culture follow-up in the remaining

improved patient. There was no reduction in HBB in the patients that

remained unimproved. Atypical multiple sclerosis: One patient was

tested and was markedly and objectively improved for five months

before developing antibiotic resistance (resistance later documented

with sensitivity testing). There was a reduced level of HBB during

the period of improvement and a marked increase in HBB during

relapse. Borderline diagnosis (either chronic fatigue syndrome or

multiple sclerosis): Three patients were tested. All three patients

improved, with reduced levels of HBB. Fibromyalgia (pure or

associated with chronic fatigue): Three patients were tested, and all

patients improved, with corresponding, reduced levels of HBB in the

blood. Arthritis (rheumatoid or other): Five patients were tested;

four improved and one did not improve. All improved patients

demonstrated reduced levels of HBB in their blood, with no reduction

in the level of HBB in the unimproved patient. Behcet's syndrome: One

patient was tested and did not improve, and there was no reduction in

the level of HBB in this patient's blood.

The striking feature of the treatment of these patients was that

there was a 100% correlation between clinical improvement in the

patient and reduction of the levels of HBB in the patient's

bloodstream. This was true even though the improvement resulted from

treatment with antibiotics--despite these illnesses never having been

associated with a bacterial cause in the prior art.

Subsequent to this study, laboratory support has been supplied to

various physicians treating patients. Results have been similar,

except that the percentage of responding multiple sclerosis patients

has appeared to be lower than the level that was seen in the small,

initial group. Furthermore, one collaborator who has been treating

chronic fatigue syndrome patients with penicillin and probenecid has

reported about 100 patients who are in complete remission from

symptoms. This correlates to about a 20% cure rate.

Clearly, the improvement in symptoms correlates with reduction in HBB

in the bloodstream. Long-term follow-up has shown that for some of

the responding patients of the original study, antibiotic resistance

has developed, though each patient benefited greatly overall from

treatment. Lately, study has also demonstrated an important

phenomenon, that is, frequently when antibiotic resistance is

present, the antibiotics can actually stimulate the growth of the

bacteria. The mechanism for this effect is unknown, but it has been

seen repeatedly both in culture and in patients. The increases in HBB

when resistance is present have correlated with increased symptoms.

[Guest guest]

Geez, why is this the first we're hearing of this? Lindner is describing my life! penny <usenethod@...> wrote: Interesting. He and allied physicians treated a rather large number of patients with combo abx. Using binary judgements (improved vs unimproved, bacterial blood load reduced vs unreduced), he claims 100% correlation between clinical improvement and bacteriologic improvement. I'd much rather see actual data, of course, and preferably data that is much more quantitative. But this is interesting at least.He also asserts that application of abx to which the organisms are resistant actually stimulates their growth.=================The 66 patients for whom follow-up was adequate are summarized below by diagnosis:

Chronic fatigue syndrome: 41 patients total; 30 patients improved, 11 patients did not improve. Reduced levels of HBB were seen in all improved patients and HBB levels were not reduced in unimproved patients. Multiple sclerosis (typical): 7 patients total; 4 patients improved; 3 patients did not improve. Two of the four improved patients had marked functional improvement, for example, were able to walk with a cane where a wheelchair had been previously required. There were reduced levels of HBB in three of the improved patients, with an insufficient culture follow-up in the remaining improved patient. There was no reduction in HBB in the patients that remained unimproved. Atypical multiple sclerosis: One patient was tested and was markedly and objectively improved for five months before developing antibiotic resistance (resistance later documented with sensitivity testing). There was a reduced level of HBB during the

period of improvement and a marked increase in HBB during relapse. Borderline diagnosis (either chronic fatigue syndrome or multiple sclerosis): Three patients were tested. All three patients improved, with reduced levels of HBB. Fibromyalgia (pure or associated with chronic fatigue): Three patients were tested, and all patients improved, with corresponding, reduced levels of HBB in the blood. Arthritis (rheumatoid or other): Five patients were tested; four improved and one did not improve. All improved patients demonstrated reduced levels of HBB in their blood, with no reduction in the level of HBB in the unimproved patient. Behcet's syndrome: One patient was tested and did not improve, and there was no reduction in the level of HBB in this patient's blood.The striking feature of the treatment of these patients was that there was a 100% correlation between clinical improvement in the patient and reduction of the

levels of HBB in the patient's bloodstream. This was true even though the improvement resulted from treatment with antibiotics--despite these illnesses never having been associated with a bacterial cause in the prior art.Subsequent to this study, laboratory support has been supplied to various physicians treating patients. Results have been similar, except that the percentage of responding multiple sclerosis patients has appeared to be lower than the level that was seen in the small, initial group. Furthermore, one collaborator who has been treating chronic fatigue syndrome patients with penicillin and probenecid has reported about 100 patients who are in complete remission from symptoms. This correlates to about a 20% cure rate.Clearly, the improvement in symptoms correlates with reduction in HBB in the bloodstream. Long-term follow-up has shown that for some of the responding patients of the original study,

antibiotic resistance has developed, though each patient benefited greatly overall from treatment. Lately, study has also demonstrated an important phenomenon, that is, frequently when antibiotic resistance is present, the antibiotics can actually stimulate the growth of the bacteria. The mechanism for this effect is unknown, but it has been seen repeatedly both in culture and in patients. The increases in HBB when resistance is present have correlated with increased symptoms.

[Guest guest]

, can you access this paper he co-authored on "infectious and inflammatory diseases?" http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=2109317 & query_hl=7 & itool=pubmed_docsumPlus, this is interesting. It's another article written by Pamela Weintraub, who wrote the article you quoted about Lindner. It almost seemed as if she were in partnership or perhaps is a medical publicity/writer for hire? It's unclear. but check out the link to Siga Technologies and their antibiotic research. And check at the very end of the article for a bunch of articles on bacteria, antibiotic resistance, etc. http://www.astralgia.com/magazine/sticky.htm Also, it appears that the original company, Pathobiotek, that was involved with researching the HBB patent changed its name to Adesy Inc. but there's not much available on that company either. A lot of biotechs went under in the late 90s. penny <usenethod@...> wrote: Interesting. He and allied physicians treated a rather large number of patients with combo abx. Using binary judgements (improved vs unimproved, bacterial blood load reduced vs unreduced), he claims 100% correlation between clinical improvement and bacteriologic improvement. I'd much rather

see actual data, of course, and preferably data that is much more quantitative. But this is interesting at least.He also asserts that application of abx to which the organisms are resistant actually stimulates their growth.=================The 66 patients for whom follow-up was adequate are summarized below by diagnosis: Chronic fatigue syndrome: 41 patients total; 30 patients improved, 11 patients did not improve. Reduced levels of HBB were seen in all improved patients and HBB levels were not reduced in unimproved patients. Multiple sclerosis (typical): 7 patients total; 4 patients improved; 3 patients did not improve. Two of the four improved patients had marked functional improvement, for example, were able to walk with a cane where a wheelchair had been previously required. There were reduced levels of HBB in three of the improved patients, with an insufficient culture follow-up in the remaining

improved patient. There was no reduction in HBB in the patients that remained unimproved. Atypical multiple sclerosis: One patient was tested and was markedly and objectively improved for five months before developing antibiotic resistance (resistance later documented with sensitivity testing). There was a reduced level of HBB during the period of improvement and a marked increase in HBB during relapse. Borderline diagnosis (either chronic fatigue syndrome or multiple sclerosis): Three patients were tested. All three patients improved, with reduced levels of HBB. Fibromyalgia (pure or associated with chronic fatigue): Three patients were tested, and all patients improved, with corresponding, reduced levels of HBB in the blood. Arthritis (rheumatoid or other): Five patients were tested; four improved and one did not improve. All improved patients demonstrated reduced levels of HBB in their blood, with no reduction

in the level of HBB in the unimproved patient. Behcet's syndrome: One patient was tested and did not improve, and there was no reduction in the level of HBB in this patient's blood.The striking feature of the treatment of these patients was that there was a 100% correlation between clinical improvement in the patient and reduction of the levels of HBB in the patient's bloodstream. This was true even though the improvement resulted from treatment with antibiotics--despite these illnesses never having been associated with a bacterial cause in the prior art.Subsequent to this study, laboratory support has been supplied to various physicians treating patients. Results have been similar, except that the percentage of responding multiple sclerosis patients has appeared to be lower than the level that was seen in the small, initial group. Furthermore, one collaborator who has been treating chronic fatigue

syndrome patients with penicillin and probenecid has reported about 100 patients who are in complete remission from symptoms. This correlates to about a 20% cure rate.Clearly, the improvement in symptoms correlates with reduction in HBB in the bloodstream. Long-term follow-up has shown that for some of the responding patients of the original study, antibiotic resistance has developed, though each patient benefited greatly overall from treatment. Lately, study has also demonstrated an important phenomenon, that is, frequently when antibiotic resistance is present, the antibiotics can actually stimulate the growth of the bacteria. The mechanism for this effect is unknown, but it has been seen repeatedly both in culture and in patients. The increases in HBB when resistance is present have correlated with increased symptoms.

[Guest guest]

You have a PM where to fetch jpg

/Per

wrote:

>This patent has 6 micrographs I'd love to look at, which I think should

>be here:

>

>http://tinyurl.com/l6vvd

>

>

[Guest guest]

Thanks Per.

I saved the six micrographs and went thru them and their captions.

The TEMs are neat. Ive never seen bacteria with " holes " like fig 4.

>

> >This patent has 6 micrographs I'd love to look at, which I think

should

> >be here:

> >

> >http://tinyurl.com/l6vvd

> >

> >

>

[Guest guest]

> But the big point here is, there's a disconnect between researchers

and doctors. And I'm not sure how that gap can be bridged. So much

research is out there, but if it doesn't have some kind of monetary

value, no one hears about it, especially not our doctors who are mainly

taking their direction from pharmaceutical companies.

I dont think its that. Researchers just dont agree on any of these

diseases being caused by infection. To have those views is *at best*

whats called " barely respectable " in the research mainstream.

[Guest guest]

yea they soon perk up though when they have something in the family or

in person..

Personally, I think, as in all sectors, 90% of people are: 'shall we be

kind and say - not genus'.

bleu

On 19 May 2006, at 03:58, wrote:

>

> >   But the big point here is, there's a disconnect between

> researchers

> and doctors. And I'm not sure how that gap can be bridged. So much

> research is out there, but if it doesn't have some kind of monetary

> value, no one hears about it, especially not our doctors who are

> mainly

> taking their direction from pharmaceutical companies.

>

>

> I dont think its that. Researchers just dont agree on any of these

> diseases being caused by infection. To have those views is *at best*

> whats called " barely respectable " in the research mainstream.

>

>

>

>

>

>

[Guest guest]

I'm not so sure really. I think the people with the bucks who support the research have given up on treating infection because they see it as a losing battle. That's why most major drug companies are no longer creating new antibiotics. But there's still all this related research that could support our position, but docotrs turn a blind eye. I understand there's a lot out there for a doctor to digest just to try to stay current, but what I don't understand is that they're presented with so much evidence every day and still fail to acknowledge a problem. They're in denial mode if you ask me, because there are a few docs who get it and do admit it, but they also, for the most part, feel incapable of dealing with the problem. So until the pharmaceutical companies push a new drug OR we stand up and make a big enough noise to not be ignored, the status quo remains. penny <usenethod@...> wrote: > But the big point here is, there's a disconnect between researchers and doctors. And I'm not sure how that gap can be bridged. So much research is out there, but if it doesn't have some kind of monetary value, no one hears about it, especially not our doctors who are mainly taking their direction from pharmaceutical companies. I dont think its that. Researchers just dont agree on any of these diseases being caused by infection. To have those views is *at best* whats called "barely respectable" in the research mainstream.