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microw
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Posted: Tue Mar 18th, 2008 02:06 |
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In some of my experiments, I have found that fungal metabolites manifest beyond microscopic detection. I have also seen organization of proteins to form higher complexes.
L-forms also go through transformational stages and reconstruction processes.
Has fungal RNA ever been implicated in cellular isolates of persons\hosts in L-form gene profile investigations? Microw
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Dr Trevor Marshall
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Posted: Tue Mar 18th, 2008 02:18 |
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Fungal and Viral co-infections will flourish in the environment created by the Th1 pathogens disabling the innate immune system. Having said that, I am not aware of any fungal DNA surfacing during the shotgun sequencing studies which have already occurred.
Even if such DNA isolates were found, I would argue that their presence is not material to the chronic disease process.
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microw
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Posted: Tue Mar 18th, 2008 03:05 |
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Interesting. I was not sure of the use of the term 'RNA' when decribing these metabolites, because I did not feel they could have acheived status of eucaryote at this stage. Could be a string of nucleic acids at this point, I guess.
The number of factors must be endless, like a "pea soup" {I've heard}.
Since some of these forms have been quantified outside the cellular environment, I assume cultures have been successful. I will be interested to know what mature forms have been discovered. I am sure spirochetes must be one of them----I am still reviewing the material.
Shroom
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Dr Trevor Marshall
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Posted: Tue Mar 18th, 2008 03:27 |
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Cultures are not successful, and spirochetes are not involved (in-vivo).
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jcwat101
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Posted: Tue Mar 18th, 2008 04:23 |
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If you haven't looked at the articles on L-forms at http://www.bacteriality.com you might be interested in doing so. Also among the interviews, are a couple with L-form researchers (including Domingue).
Joyce Waterhouse
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20 yrs with CFS/FM/Lyme/IBS, food sensitivities; 1,25D/25D 8/04:64/11 1/05:22/6 9/05:1,25D=12 10/06:22/8, 4/07:25/<4 chewed Ben. 40mg q8h; Mod. P2: 2/23/05, P2: 4/06; P3: 1/1/07
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microw
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Posted: Tue Mar 18th, 2008 13:10 |
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Hi Joyce. I did review the link you provided, but it does confuse me a little bit.
The link, a work authored by Amy Proal, not only covers in vitro culturing technique, but offers insight into the possibility of of how some L forms are created from the actions of blocking inactivation of some PBP's [penicillin blocking proteins] thus preventing the successful development of complete cell walls in the given bacterium.
In the article, it states that D'Aris team was "also able to come up with a new, more effective protocol for culturing L-form bacteria in the first place".
And, "D'Aris team has broken new ground by discovering a way to culture L-forms using a new advanced technique".
The technique, of course, uses the antibiotic Cefulodin.
So I am left to assume that Dr. Marshall meant the L-forms from affected patients have not been successfully isolated through culture or transfered to animal models through in vivo techniques.
I am sold on the basics of the M protocol, and am satisfied that it is revolutionary albeit not fully understood.
But, I am still unsure about the L-forms. Does the pathogen type have bearing on the illness eg. sarciodosis CFS fibromyalgia etc? And, does knowing the type hold insight into the serendipitous use of other drugs which could speed up the process?
And how does capnine fit into the picture, is it produced by all L-forms, or just just certain strains?
Sorry for all the fuss, but I am very interested with this research; Microw
Last edited on Tue Mar 18th, 2008 13:11 by microw
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Dr Trevor Marshall
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Posted: Tue Mar 18th, 2008 13:38 |
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The primary Th1 pathogens are biofilm-dwelling species. Lysobacter seems to pop up frequently in the studies, along with Staph, Eubacteria, Methylobacter, and others.
The L-forms of species which are not obligate biofilm dwellers, can contribute to the "pea-soup" by contributing their own survival genetics to the metagenomic community with horizontal transfer of their DNA, or by sharing the proteins and enzymes they produce.
L-forms of common pathogens are just a subset of the metagenomic community, and probably not the founding subset.
I hope that helps. Take a look at my presentation at Metagenomics 2007 for more background on this.
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migsies
Member in Phase 3
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Posted: Tue Mar 18th, 2008 23:37 |
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Interestingly, there are some intracellular fungi, and fungi have certainly been found as components of biofilm communities. I am sure Dr. Marshall already knows this from his tireless sleuthing and has good reasons to suspect their role in Th1 disease is negligible. However, to reiterate what Dr. Marhsall has said, because of the confounding factors introduced by lateral gene transfer (not only pathogen-pathogen but also pathogen-host), vague microbial "species" boundaries, and the fact that many regulatory proteins have ancient histories and are thus shared among broadly divergent "species", which means they affect gene expression accross "species", I suspect it will take a long time before this mess is cleared up in a rigorous scientific manner, and well understood, especially given some of the persiting paradigms. Hopefully, a well funtioning immune system should be able to take care of all these critters, which I guess is what we are striving for on the MP.
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Sarcoidosis FM Lyme babesia 25D>7(Feb07) Ph1Aug05 Ph2Oct05 Ph3 Jun06 Valium Lyrica Ambien NoIRs limited outings covered Phase I 8/05, II 10/05, III 6/06.
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microw
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Posted: Wed Mar 19th, 2008 00:11 |
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Hi Migsies,
Thank you for addressing that segment of my inquiry. I would be appreciative if you could provide any information on fungal types which have been clinically documented of having interactions with bacterial biofilm formations.
It does not nessesarily have to do with Th 1 bugs. For example, S. mutans biofilms in oral-pathology situations.
P.S. I am happy you are progressing with the therapy, hope you have a full recovery.
Microw
Last edited on Wed Mar 19th, 2008 00:11 by microw
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jcwat101
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Posted: Wed Mar 19th, 2008 05:21 |
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I would just add that Amy Proal's site has several articles that discuss L-forms. There are two interviews, the D'Ari one you mention, and one on the antibiotics and how they target them, and one on the L-forms themselves. If you go down the right side of the page, you should see several categories with articles within each category. I wasn't sure if you saw the others.
Joyce Waterhouse
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20 yrs with CFS/FM/Lyme/IBS, food sensitivities; 1,25D/25D 8/04:64/11 1/05:22/6 9/05:1,25D=12 10/06:22/8, 4/07:25/<4 chewed Ben. 40mg q8h; Mod. P2: 2/23/05, P2: 4/06; P3: 1/1/07
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microw
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Posted: Thu Mar 20th, 2008 00:05 |
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Hi Joyce. Yes I am aware of those articles, and will reveiw them as I go along.
Right now I am still trying to wrap my brain around the specific bacteria mentioned by Dr. Marshall. Lysobacteria, eubacteria, methylobacter etc., all these species are very ubiquitous, common bacteria. To general. Eubacteria covers a gazzilion types.
If he said mycobacteriaceae, mycoplasmas, rickettsias, chlamydias, species of the cynobacterias or certain endosymbionts, I would feel I had a lead.
But I am certain there is good reason for the mention of the examples given, and this will keep me very busy for a while.  Microw
Last edited on Thu Mar 20th, 2008 00:52 by microw
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migsies
Member in Phase 3
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Posted: Thu Mar 20th, 2008 23:00 |
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Hi microw,
I would like to help you but since becoming ill I have not kept up with filing references and only sporadically with the science. All I can tell you is that there is rapidly growing interest in biofilms and that if you search pubmed, conference abstracts, NIH/NSF and other grant submissions you will find enough to keep you busy for awhile, along with some discussion of their community ecology (species composition), although this is an area that is in its infancy as it is highly dependent on the state of genomic technologies. I get the feeling biofilms are a pretty tough nut to crack, so to speak, from the perspective of both host and researcher. Perhaps someday, if somebody can figure out how to disrupt "quorum sensing" in vivo, and safely, complementary therapies to the MP can be developed.
As for the issue of intracellular fungi, you can look up Histoplasma sp. or Cryptococcus sp. along with macrophages, and you will find some references. There may be other fungal species that can survive inside macrophages but nothing comes to mind. As with bacteria, the advent of widely available and reasonably priced DNA sequencing has revealed a level of genetic diversity in fungi that was previously unimaginable.
Since you appear to have a broad interest in microbiology, I should mention that there are significant efforts currently underway to characterize the biodiversity within and across many basal groups in the tree of life with the aid of DNA sequencing. I understand there have been many surprises, especially within 'protistan' groups. Unfortunately, I have not been able to keep up with the rapidly shifting classification schemes and their biological implications. However, I am glad you are able to pursue this interest. This is a very exiting time for anyone interested in the biodiversity of basal groups (including microbes), and the perfect time for forward thinking people like Dr. Marshall, looking at this from the standpoint of human health, to be pushing some boundaries. Hopefully, we are at a tipping point, in terms of accumulation of knowledge and relevant technologies, that his ideas will catch on without much delay, unlike the other Dr. Marshall (Barry), who had to wait nearly twenty years for his critics to come around (or pass away).
Have fun with your research!
____________________
Sarcoidosis FM Lyme babesia 25D>7(Feb07) Ph1Aug05 Ph2Oct05 Ph3 Jun06 Valium Lyrica Ambien NoIRs limited outings covered Phase I 8/05, II 10/05, III 6/06.
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microw
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Posted: Fri Mar 21st, 2008 00:55 |
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Thanks Migsies. That was a a nice note. I need the encouragement.
My interest in fungi, exists because of my research findings. It appears that my body is producing penicillium in the gut--as I will assume is normal in some people.
One of my annoying symptoms is constant itchy scalp, which turns out to be pink yeast--the same yeast I find in stool cultures.
Stool is very heavy with protozoa, e-coli, klebseila and other gram negs, and catalase +.
Anyway, I disrupted the cell walls of pink yeast and penicillin mold spores, transfered that to culture, and have pink mold. Interesting enough, certain antibiotics produce the same mold.
So this brings home some interesting theories about the role of penicillin in symbiosis with animal physiology. Or, the pitfalls of past antibiotic usage....who knows at this point, more peasoup stuff. Thanks for responding,
Microw
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Dr Trevor Marshall
Research Team
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Posted: Fri Mar 21st, 2008 13:34 |
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Back in 1978 I wrote a paper "Electronic Design Educating for an Uncertain Future" where I wrote about "tackling .. tasks where the starting data may be vague, or incomplete, and where many alternative solutions may be equally valid."
The Idiopathic diseases present us with a very similar set of disparate and incomplete data. We can detect parasitic genomes, in-vitro, but have little data about whether they are active in-vivo, or what their effects might be, in-vivo. Additionally, there are tantalizing hints that other parasitic entities might be present, even though we can't detect them.
The Wirostko TEM micrographs, for example, showed a microbiota totally unknown to Medicine, yet clearly present in the patients Emil and his group were studying. Similarly, there had been many, many studies linking various known pathogens to Sarcoidosis, and CFS, yet none of them were clearly causal, as none of them were present in every individual.
The CFS patients in Australia, for example, who, if seropositive, were usually so for Rickettsia, suffer identically to those in the USA, who are often seropositive for Borrelia. Clearly neither of these pathogens were causal, and there were factors in play which were unknown, interacting in ways which were poorly understood.
That is why I took a different approach back in 1999. Building on my experience dealing with uncertain data and outcomes, I decided that in-vitro testing, the Gold-Standard of Medicine, just had to be missing something important. Similarly, the animal models were not producing results which were portable to human experience, so they, too, had to be set aside.
Thus, having discarded a century of studies, a century of what was thought to be "knowledge," I started to re-examine chronic disease based on the tools and techniques which had been developed for modern genetic biology. Trying to piece together the clues from a tiny subset of available perceptions and data, into a model which would be rigorous, and which would exactly describe the human experience. By its very nature, this study dealt largely with the philosophical. Only in later years did the science fall together into the rigorous mechanistic model we now have elucidated.
It is meaningless to focus on a virus, fungus, or bacterium which can be easily observed. Otherwise the pathogenesis of chronic disease would have been described decades ago. Being able to culture a pathogen, or detect it with PCR, gives no clue as to whether that pathogen is active in-vivo, or whether it is causal in the disease process. It may be persistent as a result of the innate immune system being weakened by some disparate underlying disease process.
I know how tempting it is to apply the lab techniques of yesteryear to the imponderable problems of today. But one needs to start thinking, instead of focusing on observations. The fundamental problem with observational science is that unless you know what you are looking for, you don't know how, or why, to observe it. What is needed in modern medicine is the discipline of Planck and Einstein, the discipline of working with dilemma which defy description, and puzzle out, by sheer philosophical effort, what the inter-relationships might be, in order that the data can then be experimentally observed, ranked, and the model verified.
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microw
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Posted: Sat Mar 22nd, 2008 14:19 |
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I am seeing your point, more than ever as I move further into the ocean of endless possibilities that experimental work provides.
However, in some cases this old school approach can still provide vital clues on what needs prioriety for addressing individual issues.
There are also inherited traits to consider, and health histories etc.
If we are looking for commonality in chronic disease, your approach is proving to be on the right track, but obviously incomplete.
For example the "capnine" lipid, thing still needs more investigation. And, are there other molecules which can be singled out in high percentages of sufferers?
It does appear that, according to anecdotal accounts from patients engaged in your protocol, the LL37 receptor is an intrinsic factor to many chronic disease conditions.
In my personal opinion, I believe something man-made is going on, and we should be trying to find a common chemical factor and microbes which can carry it or produce it.
Microw
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Dr Trevor Marshall
Research Team
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Posted: Sat Mar 22nd, 2008 14:50 |
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Microw,
Science advances not with accusations of being "obviously incomplete" or "needing more investigation" but by somebody actually doing the hard work to get the results which put forward a new, improved, understanding.
I would ask you to focus on constructive thought. In that spirit I will end this 'conversation' between us. In a months time, I will be defending our discoveries (again) before Team Nobel. I need to focus on that task
Trevor
Last edited on Sat Mar 22nd, 2008 15:22 by Dr Trevor Marshall
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