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Dr Trevor Marshall
Research Team
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Posted: Thu Jul 24th, 2008 09:31 |
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Well, yes, except please remember that at Karolinska we we told (effectively) that prions are probably not the infectious agents, and that the Th1 metagenomic microbiota are the agents which are infectious
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Frans
Member in Phase 2
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Posted: Sun Jul 27th, 2008 18:20 |
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Trevor, when looking through the schedule on page 2 of
http://www.ncbi.nlm.nih.gov/pubmed/18324309
under the schedule they state that they have omitted an ellipse with Biofilm formation... which is of interest for us I think
Secondly, unfortunately, I cannot follow mr Arkin in detail in his presentation, so I am not entirely sure what exactly happens during sporulation. I don't hear him saying that they shed their cell walls, but somehow layer it with proteins?
Another thing (I think) he says is that the bacteria dehydrate ?
What would that mean for their size ? I would think this explains why they get so extremely small ? Did mr Arkin say how small they actually get ?
This review on sporulation (PMID 16907804) might be of interest for Ames. They actually allowed the bacteria to form Biofilms, since they theorize that competition for food within biofilms will actually lead to sporulation of members of the commmunity.
I have been looking for an in detail review of what exactly happens during sporulation, but haven't found one yet. Anyone else find something like it?
Best, Frans
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Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
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Frans
Member in Phase 2
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Posted: Fri Aug 1st, 2008 20:56 |
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| bumpy ?
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Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
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inge
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Posted: Mon Aug 4th, 2008 14:39 |
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Sorry if this is posted at the wrong place, and I know that few hours of reading on the site could probably have provided me an answer, but here goes:
Some 300 ME sick patients, me included, have filed a lawsuit against the state of Norway because of a possible connection with a vaccine project we took part in some 16 years ago. Now that I now that the most likely connection is bacteria contaminated vaccines, how easy would it be to find bacteria DNA or viable bacteria in these vaccines? (They may still have samples of the vaccine left).
I know that although one could find bacterial DNA this would perhaps not help our case anyhow, because they would not understand the significance of this.
Inge
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CFS/ME 125D64 25D12(dec 07) Ph1De06 daily lite exp NoIR use Ph2Mar07 ModPh2 Jun07 abx brkOct 07 r//t KFTs freq abx chg to control kidney IP Apr 08 phase 2 abx
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Dr Trevor Marshall
Research Team
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Posted: Mon Aug 4th, 2008 15:01 |
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because they would not understand the significance of this
I don't think I understand the significance of vaccines at this point. The ones using live microbes, like BCG, are clearly going to contribute to the pathogenic load, but it is not possible to generalize about the effect of the others on the immune system.
If I had to make an educated hypothesis, it would be along the lines that if you give 'killed' vaccines to people who are already sick it is likely to place a heavy load upon their immune system, and potentially make them sicker. However, the real problem is the increasing percentage of the population who have heavily compromised immune systems so early in life.
IMO, Cod liver oil is a factor in Norway, and there are probably others which only a detailed study could properly elucidate. IMO, only after looking at all the factors, could blame be properly apportioned.
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Claudia
Member in Phase 3
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Posted: Tue Aug 5th, 2008 17:54 |
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Frans,
I don't know about the heavy science, molecular biology type papers, if that's what you want to read, but if you or anyone wants clear illustrations and plain english, try reading "Sex and the Origins of Death" by William R Clark (1996, Oxford University Press) for a very good explanation of sporulation and a whole lot more about cell biology. I found it to be the best book on the subject for myself, as a layperson, as it had so much info that "clicked" with what I was trying to understand about the MP. Don't be put off by the title - it is a reference to the persistence/immortality of asexually reproducing organisms (like bacteria). This is what we gave up to gain the advantages of sexual reproduction. A must-read.
 Claudia
Last edited on Tue Aug 5th, 2008 17:58 by Claudia
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MP Phase1 23Mar_06; Phase2 July 10_06; Phase3 Nov 4_06. Dx Thyroiditis (Thyroxine); arthritis; glaucoma; CFS (1988-92);Kidney & bladder probs. Feb06 1,25D=43.3; Aug07 1,25D=27.5; Feb06 25D=44; Aug07 25D=28; Nov07 25D=36; Mar08 25D=16.4
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Tll6
Member in Phase 3
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Posted: Wed Aug 6th, 2008 00:41 |
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| Do we not have to make a distinction between spores (endospores) and L-forms. According to one of my text books on bacteriology endospores are formed by only 2 genera of bacteria both of which are gram positive: the aerobic Bacillus and the anaerobic Clostridium. Endospores (as in the anthrax spores) have a layered protective coat consisting of: a cell membrane, a thick peptidoglycan mesh, another cell membrane, a wall of keratin-like protein, and an outer layer called the exosporium. Does that not makes spores very different from L-forms.
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hypothyroid (take thyroid), joint pain, CFS, heart block, GI problems, food intolerances, tinnitus, other symptoms, Ph1Apr08, 25D10 D3:9ng/mL 2009/10/19.
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Dr Trevor Marshall
Research Team
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Posted: Wed Aug 6th, 2008 01:55 |
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W. Ford Doolittle argues cogently against the concept of species at this URL:
http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/doolittle.rm
Anthrax spores are commonly referred to as L-forms. I think that it is likely any text which divides the phylogroup up so tightly into just a couple of species is bound to be overlooking the big picture. On the other hand, studies that only look at genera, such as the human skin study
http://genome.cshlp.org/cgi/content/abstract/18/7/1043
tend to leave the feeling in this reader that they were not precise enough, even though that feeling is totally without basis
In our case, the focus is on the microbiota itself, and the power of its metagenome. That environment tends to make me a little less concerned about physical attributes than I am about individual genes in the metagenome, and how those genes map to to the human genome, with the potential for interference with the mechanisms by which the human genome repairs and replicates itself.
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Tll6
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Posted: Thu Aug 7th, 2008 04:55 |
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I will defer discussion for the time being about what is or isn't a L-form because:
Has anyone connected with the MP looked at or read the National Academy Press document "Size Limits of Very Small Microorganisms. Proceedings of a Workshop". This document is a mind blower. This document could be required reading for anyone who wishes to explore what might be the nature of Dr. Marshall's "pea soup" of intracellular organisms. It considers many things from sizes of various components of cells, RNA, DNA, ribosomes, cell membranes, osmotic pressure, nr of proteins, metabolism, biophysical constraints, nrs of genes, genome size, free living organisms, non free living organisms, and many other subjects. There is even a postulate of a kind of living in consortia rather like Dr. Marshall's "pea soup".
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hypothyroid (take thyroid), joint pain, CFS, heart block, GI problems, food intolerances, tinnitus, other symptoms, Ph1Apr08, 25D10 D3:9ng/mL 2009/10/19.
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geirf
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Posted: Sun Dec 21st, 2008 22:47 |
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According to Andrew Wakefield there have not been made any long term studies on safety of MMR vaccines.
According to prof Tore Midtvedt , Karolinska Institute Stockholm, when MMR (three live viruses) was to be introduced to Sweden , they opposed to use the vaccine, as they were sure the vaccine was not safe, and could be containing Mycoplasmas and / or Chlamydias.
During a foreign trip of the head of Karolinska the MMR vaccine was introduced, he cried when he came back and got to hear they were now using the MMR vaccine.
Vaccine Measles virus is a good candidate to explain Autism, but of course , also here the virus might well only be a coinfectant , or of course be a co cause together with a L-bacteria. ?
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Geir Flatabø
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Dr Trevor Marshall
Research Team
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Posted: Sun Dec 21st, 2008 23:29 |
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Gier,
As I have already said in another topic, Autism Spectrum Disorders result from the same metagenomic microbiota as all the other chronic diagnoses. Forget about viruses - their genomes are not big enough to cause the widespread havoc evident in these diseases. They are just co-infections. The metagenomic microbiota is the root cause, and I now know how it evades the innate immune system, and therefore how to beat it.
Take a look at those videos of my presentations I keep pointing you towards...
Especially the Keynote I gave in China two weeks ago...
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vwmusum
Member
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Posted: Sat Dec 27th, 2008 19:19 |
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Hi Dr. Marshall - In one of our conversations, I recall you saying something to the effect of, "the overemphasized focus on just tics as the sole, root cause for Lyme is foolish."
I hope I am paraphrasing you correctly.
I have been unable to get your powerful comments out of my mind on many levels. I have long suspected Lyme is much bigger than the simplistic focus on just tics. We now know there are MANY more animal vectors (chipmunks, lizards, etc.) from the work of Dr. Kerry Clark, et. al.
I believe (as does renowned epidemiologist, Dr. Tom Kollars at Georgia Southern University whom I have spoken to and has intense interest in researching here in the US) there are indeed many other insect vectors also. I recall a recent study out of Europe that showed 4% of the mosquitoes were carrying Bb.
However, though I am VERY interested in understanding the FULL scope of the vectors carrying Bb and other related pathogens, my question is deeper based on the comment you made to me above.
What do you believe is the full magnitude of the Bb transmission? We know, once bitten, we are likely to get a full 'soup' of pathogens and mycoplasm in addition to just Bb. However, as I and many others strongly suspect, are there OTHER ways of getting Lyme than just insect bites (congenital, sexual, salivary, transfusion, food supply transmission, etc.)?
Moreover, is it possible that virtually EVERYONE to one level or another has some degree of Inter Phagocytic, Metagenomic, Microbiota? I know the implications of this question are staggering, yet science facing the full answer is imperative.
If so or not, what is the BEST BLOOD TEST to see if someone is in need of the MP? Is it just a test of the Vitamin D and the 1, 25 D levels as Dr. Fein did (along w/a whole other battery of tests) on me and also mentioned in Bryan Rosner’s book, The Top Ten Lyme Disease Treatments?
Finally, when we spoke of CWD forms and Mattman's groundbreaking book on them you made a comment I do not even wish to try to paraphrase, but I sensed it was very important. What is the latest understanding of her work and the CWD forms for the lay person? I take it the CWD forms, while critical, are far from the whole current story on chronic illness.
What are there differences for the lay person between Inter Phagocytic, Metagenomic, Microbiota and CWD L-forms, mycoplasm and other rarely understood In-Vivo bacteria?
FYI, when I met last year one on one w/Dr. John Halperin on the board of the IDSA at his hospital - Overlook, Summit, NJ - we had a rather lengthy and pointed "discussion" on the awful positions he and his colleagues had taken for us patients. Among several instances where a lay person like me had him utterly outflanked, he was completely UNAWARE OF MATTMAN's work. He wanted to borrow my copy of her textbook! I was astounded that someone making critical medical policy at the highest levels of this county had not even read a book referenced in virtually every other book I have read on the subject of Lyme disease.
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Veny W. Musum
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edj2001
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Posted: Sat Dec 27th, 2008 20:37 |
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I just completed a Cell Culture Biotechnology class and became aware of the problems associated with cell culture contamination especially by Mycoplasma. Of course this is in-vitro but it is interesting to see how the bacteria are able to infect the cells.
Take a look at the following report. There are specific references to Mycoplasma contamination.
Ryan J PhD., “Understanding and Managing Cell Culture Contamination”, Corning Incorporated Life sciences
http://catalog2.corning.com/Lifesciences/media/pdf/cccontamination.pdf
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Shari Gold
Member in Phase 3
| Joined: | Sat Dec 27th, 2008 |
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Posted: Wed Dec 31st, 2008 07:56 |
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Hi Dr. Marshall....
Just curious about this article that I just found on my web browser.
Have you read any of this in any of your recent research .. and what do you think about the team using "ferrets" for the in vivo portion of the experiment????
Best,
Shari Gold
Full article:
http://news.aol.com/health/article/researchers-solve-1918-flu-mystery/289681
Re:... solving the riddle of the 1918 flu pandemic
(excerpt from Yahoo browser story)
"We wanted to know why the 1918 flu caused severe pneumonia," Kawaoka said in a statement.
They painstakingly substituted single genes from the 1918 virus into modern flu viruses and, one after another, they acted like garden-variety flu, infecting only the upper respiratory tract.
But a complex of three genes helped to make the virus live and reproduce deep in the lungs.
The three genes -- called PA, PB1, and PB2 -- along with a 1918 version of the nucleoprotein or NP gene, made modern seasonal flu kill ferrets in much the same way as the original 1918 flu, Kawaoka's team found.
Most flu experts agree that a pandemic of influenza will almost certainly strike again. No one knows when or what strain it will be but one big suspect now is the H5N1 avian influenza virus.
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Dr Trevor Marshall
Research Team
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Posted: Wed Dec 31st, 2008 14:57 |
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Shari,
I have no idea whether ferrets are a good analog of man's immune system, nor whether the isolated flu genes behave the same way when transfected as they did in the native flu organism. Studies like this are of little value until they lead to tangible results.
I had a series of discussions with Nobel Laureate Peter Doherty about a year ago. He has spent the last decade trying to find a vaccine for the HIV virus. He made it clear to me that the behavior of a virus, which is an organism which derives most of its genes from its host, is extremely complex, and extremely variable. Based on those discussions, I feel that this ferret research seems a bit simplistic, but I may be wrong.
You will find previous discussion here about the 1918 Flu, there has been a persuasive hypothesis advanced that TB was involved as well as a virus.
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vwmusum
Member
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Posted: Wed Dec 31st, 2008 15:07 |
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Hi Dr. Marshall,
I was following up on my Dec. 27th post. One essential part of my post asks:
"What are there differences for the lay person between Inter Phagocytic, Metagenomic, Microbiota and CWD L-forms, mycoplasm and other rarely understood In-Vivo bacteria?"
It would be very helpful to gain your understanding of what seems to the lay person (much less medical professionals and microbiologists) a confusing list of all these often referred to bacterial forms. This would include those listed above in addition to the “Bio Films” Dr. Alan Macdonald has pioneered the discovery of and any other important forms you feel need to be defined and understood by all.
Is all the micro-bio nomenclature describing essentially the same thing? That seems unlikely again to the lay person. It would be VERY helpful to gain a deeper understanding of this. I believe that would allow us all much better insight into what we with chronic illness are up against and what the MP is so successful at overcoming.
Despite reading extensively on the subject, I would most gratefully defer to you. Based on my conversations with numerous medical professionals, I believe this understanding; especially from someone of your knowledge and ability to bring clarity to any subject would be vital in moving the discussion and wider understanding forward.
Would it be possible to list ALL these major various, rarely understood, or widely recognized forms and provide a short definition of each class or group?
We are all indebted to you Dr. Marshall and thank you very much.
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Veny W. Musum
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Dr Trevor Marshall
Research Team
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Posted: Wed Dec 31st, 2008 17:36 |
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What you are seeing is an incremental advance in understanding.
Alan McDonald is still looking for species, but microbiologists now realize that species mean very little. The key thing is the way that the genomes interact.
See, for example, this video from the Metagenomics 2006 conference:
http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/doolittle.rm
(W. Ford Doolittle from Dalhousie University (Canada))
Please try and work through my Keynote at the World Gene Congress for the details of why it is the genomes that matter, and not the species:
http://www.vimeo.com/2585394
Hence the Metagenomic Microbiota has to be the focus of Science as we move forward, and not the physical shape of the microbial communities. Remember that L-forms were discovered by Emmy Kleinberger-Nobel in 1934. A lot of things have happened since then
http://marshallprotocol.com/forum39/6844.html
Happy New Year to all...
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vwmusum
Member
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Posted: Sun Jan 4th, 2009 17:07 |
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Hi Dr. Marshall,
I believe I am starting to grasp the magnitude of the Marshall Protocol. Is it possible almost EVERYONE in one level or another has some degree of Inter Phagocytic, Metagenomic, Microbiota?
Should the 2 blood tests for Vit. D and the 1,25 Vit. D metabolite be as common as a cholesterol screening?
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Veny W. Musum
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Dr Trevor Marshall
Research Team
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Posted: Sun Jan 4th, 2009 17:23 |
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Yes and Yes.
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vwmusum
Member
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Posted: Sun Jan 4th, 2009 21:34 |
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WOW!!!
I am more motivated than ever to help with your work.
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Veny W. Musum
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