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  • #300603
    Joe M
    Participant

        http://www.nih.gov/news/health/jun2008/niams-19.htm

    A couple of things regarding this article:

    1.  I think it highlights the difference between rheumatologists and researchers.  Often rheumies take a beating on this board for not being more familiar with the research side of medicine when that is not really their job.  

    2.  The research keeps getting more targeted.  IF they do come up with an effective drug that does not have the risk of infection or other side effects, I wonder what  critisism will be leveled against the makers of such drug?

    #315112
    John McDonald
    Participant

    Joe, if they are correct in thier auto-immune paradigm then this would be a nice breakthrough. If Brown and Marshall are correct in asserting that the “auto-immune” diseases are actually microbial infection, then this treatment would only provide temporary relief. Neither approach has yet conclusively demonstrated a permanent cure, so I welcome the research. I wish the funding authorities would spend even a fraction of this effort on probing Trevor Marshall's claims. It wouldn't take much using PCR techniques to validate or to disprove Marshall's disease model in a microbiology lab. But the current paradigm for unexplained inflammation is “auto-immune” so they won't be looking in Marshall's or Nicholson's couch cushions for spare change anytime soon. But science marches on. It took a long time for continental drift to catch on.

    #315113
    Joe M
    Participant

    Totally agree John.  All areas should be explored with equal veracity.  My guess is it will happen like most other amazing discoveries – by accident.  Someone researching the auto-immune theory will discover something TM has been saying all along and things will get on track. 

    #315114
    JBJBJB
    Participant

    I am trying to brain storm now. Could Arthritis Foundation make it like an annual conference to get the world rheumies together to present their research and treatment methods? When do call out, the conference not only just call out rheumies, but also immunologists, internal medicine doctors. Doctors can pay registration/conference fees, and the rest of the money perhaps can be donated by our patients or some organizations.

    This would definitely get a lot of attention on AP/MP/other non-traditional RA therapies.

    I understand the AF did this and had a good turn out. What I am saying is this type of conference needs to be more frequent.

    JMO

    JB 

    #315115
    Maz
    Keymaster

    [user=266]JBJBJB[/user] wrote:

    Could Arthritis Foundation make it like an annual conference to get the world rheumies together to present their research and treatment methods? When do call out, the conference not only just call out rheumies, but also immunologists, internal medicine doctors. Doctors can pay registration/conference fees, and the rest of the money perhaps can be donated by our patients or some organizations.

     

    Hi JB,

    This is exactly the kind of thing that Barbara Marx Hubbard (a housewife and mother, turned politician) described as the ideal model for politics, so that every aspect of the political process (or any process) could come together to share their particular model to enable all the various parts of the one “dog” were all speaking to the head….not just the tail, wagging the dog. Everyone at the time (70s, I think) critiqued her model harshly as being too idealistic, but she actually organised conventions and proved it could work. 🙂  She was an idealist, perhaps, but it takes a bit of idealism and vision to change current models that obviously don't work. Hubbard called it “conscious evolution.”

    Peace, Maz  

    #315116
    Joe M
    Participant

    Hi all,

    There are two big conferences of research rheumatologists that I am familiar with.  One is the annual ACR (American College of Rheumatology) conference, and the other is EULAR (European something something) that meets once a year.  There are dozens of research reports that come out of these events.  I am not sure of the dates though.

    Joe

    #315117
    Maz
    Keymaster

    Hi Joe,

    You know what I find really interesting about this study? Apart from the fact that it may hold promise as a new treatment for rheumatoid disease (though hard to tell what side-effects may be so early on…I Am Legend always springs to mind! ;))….I just thought two comments in the study seemed to be worded in such a way as to be politically correct when in fact they are pretty contradictory. In other words, these researchers have found something pretty significant about blocking the inflammation process, but seems they had to almost word it as a reassurance that the treatment would be “potentially synergistic or complementary” to existing TNF blocking treatments. Then, right below that it says they'd actually be more effective at treating autoimmune disease without breaking down the body's immune defenses. 

    “…Siegel noted that if they were to be used in rheumatic diseases, they would be a complement to strategies that block TNF because they hit a different arm of the immune system. “It could be potentially synergistic or complementary,” he said.

    … The group's findings suggest that DR3-blocking agents might be more effective at specifically treating autoimmune disease without breaking down the body's defenses against infections, a long-sought goal of researchers in the field.”

    I'm becoming a little more clued in to how these researchers have to really watch their backs when they discover something that could amount to a breakthrough in scientific understanding or risk losing funding for further study. Just seems transparently clear that in spite of the wordings, “synergistic and complementary,” that these researchers feel it would be a much more effective drug and could replace existing TNF Blockers.

    Just find that political aspect of scientific research unfortunate, really….that these guys just can't do their jobs without something potentially dogging their efforts.  

    Here's a question for you, Joe, John, or anyone: Does the DR3 surface protein mentioned in this study bear any relation to the genetic haplotype HLA DR3 or is this something quite different?

    Peace, Maz

     

    #315118
    Joe M
    Participant

    Hi Maz,

    Your question is above my head, I'm afraid I have no idea.

    On another point, my understanding of why this could by synergistic is because the DR3 protein is a receptor for TNF-a.  Kind of like the TNF doesn't have anywhere to go. 

    I also noticed “cell wall” referenced in the article.  Who knows, once they get looking at cell walls, they might find cell wall deficient buggers floating around!

    You know the saying “Any publicity is good publicity” – I feel the same way about RA research.  Any research is good because you never know what they will stumble upon.

    #315119
    Michele
    Participant

    Interesting article, Joe!

    I've begun looking at clinical rheumatologists in a different light. It helps me “forgive” them and understand they are not the “researchers” they are the clinicians. Here's a clumsy analogy:

    God = Instrument Maker
    Researcher = Instrument Technician
    Rheumatologist = Musician

    One attractive thing about Marshall's model is that he is using human mollecular modelling while the researchers in this report are still using the immune system's of mice. So how are we different than mice? Might this be a relatively important feature in research? (Building a clarinet is different than building a flute.)

    The most disconcerting thing to me about my analogy is that I compared myself to the rheumatologist! 😯

    I admittedly live in my ivory tower box previously trained in another ivory tower box. I love to look outside of my box to know how to do things better and more efficiently! But life gets full of side-attractions like chronic disease. :crying:

    So far, MP is working the way it is predicted and my pain levels are far more manageable. (But I hate the light restrictions.) 😕

    I need to go practice…

    😎

    Michele

    #315120
    Maz
    Keymaster

    [user=20]Joe M[/user] wrote:

    You know the saying “Any publicity is good publicity” – I feel the same way about RA research.  Any research is good because you never know what they will stumble upon.

    Joe, I agree and, like you, feel that some of the best findings often arrive as the result of something researchers weren't even looking for…at least that's what history has had a tendency to reveal. Just wish I had more of a scientific mind knew what all these labels meant. 😕 

    Peace, Maz

    #315121
    Joe M
    Participant

    Michele,

    I like your analogy, and am glad to hear you are doing well!

    I have long thought of this as a war.  The clinical rheumies are the front-line soldiers, doing whatever they can with the arsenal they have been given by the generals to help their patients.  They are too busy with the enemy to focus on the bigger picture.

    The generals are the drug company researchers, the NHI, and the FDA , laying the course for the future and deciding what weapons get down to the front lines.

    And then there's the general contractors, who are always looking for better guns, tanks, and missiles to provide the generals.  Their work is completely unknown to the front-line soldiers until their creations have been tested and approved by the generals. 

    _____________________________________________

    Why mice?  I found this article called “Why Mice?”

    http://www.vetmed.ucdavis.edu/Animal_Alternatives/whymice.htm

    #315122
    Michele
    Participant

    Joe,

    I sure like your analogy. It is like a battle! Great description.

    Michele

    #315123
    spacehoppa
    Participant

    Hmm, I just googled DR3 because it sounds like (vitamin) D receptor 3 doesn't it. Well, I think it possibly might be!? See below. In which case, does this mean that what these researchers have discovered is what Trevor Marshall already knows, that binding the VDR (or this part of it) helps the body to clear autoimmune diseases, without compromising the immune system?

    I may be jumping ahead of myself (as always) here. What do you guys think?

    http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1221460

    “The vitamin D(3) receptor (VDR), which is the nuclear receptor for 1alpha,25-dihydroxyvitamin D(3) [1alpha,25(OH)(2)D(3)], acts primarily as a heterodimer with the retinoid X receptor (RXR) and binds preferentially to directly repeated arrangements of two hexameric binding sites with three spacing nucleotides [DR3-type vitamin D response elements (VDREs)]. “

    VDRE here stands for DR3-type vitamin D response elements.

     

    #315124
    Michele
    Participant

    Ruth!

    You are a detailed researcher! Nice catch! I wonder if Trevor knows about this study?

    Michele

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