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Thread: Stephen Davies Update

  1. #281

    Didn't see this posted


  2. #282
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    Buy big eye glasses next time at Walmart. Lol

  3. #283
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    My family have donated $10,000 to Dr Davies research from Beijing , China .We hope we will do more for his work.

    Shishi

  4. #284
    Senior Member poonsuzanne's Avatar
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    Hi Shi Shi,

    This is very supportive and generous of your family!!!

    Let's continue to fight together for effective therapies for spinal cord injuries. The more efforts we will gather the faster the therapies will arrive. Nothing and no one can stop or discourage me from going forward!

    Thanks again!
    Your friend Suzanne
    Suzanne

  5. #285
    Can you estimate the time frame for realistic human chronic application? I hope it's not 15+ years. What can we do to speed the trials up?


    http://www.eurekalert.org/pub_releas...-rsh030804.php
    Misaligned scar tissue that forms at spinal cord injuries physically blocks nerve regeneration and contains molecules called chondroitin sulfate proteoglycans that inhibit nerve fiber growth. Decorin inhibits the action of pro - inflammatory molecules released in spinal cord injuries, called transforming growth factors, which are thought to promote the formation of scar tissue.


    Researchers in the study infused decorin directly into the injury site in rats with a mini-pump system, which used silica cannulas 160 microns in diameter. Because the cannulas were so small, they did not contribute to the formation of scar tissue. Using a high-powered laser scanning microscope and protein chemistry to analyze tissue samples, Davies and co-workers were able to show that decorin infusion reduced inflammation, scar formation and the levels of some proteoglycans by 80-95 percent allowing nerve fibers (called axons) to grow across spinal cord injuries in just four days.
    Last edited by Malibu; 04-25-2008 at 11:49 AM.

  6. #286
    Dr Davies,

    Can you elaborate on this excert found at wikipedia - I am not sure what to make of it.

    http://en.wikipedia.org/wiki/Decorin


    Decorin appears to influence fibrillogenesis, and also interacts with fibronectin, thrombospondin, the complement component C1q, epidermal growth factor receptor (EGFR) and transforming growth factor-beta (TGF-beta).


    In some publications, decorin has been shown to enhance the bioactivity of TGF-beta 1, in other publications, TGF-beta 1's bioactivity has been shown to be inhibited. Because of this, it is believed the primary function of decorin lies in certain aspects of regulation during the cell cycle.
    Infusion of decorin into experimental rodent spinal cord injuries has been shown to suppress scar formation and promote axon growth.
    Decorin has been shown to have anti-tumorigenic properties in an experimental murine tumor model and is capable of suppressing the growth of various tumor cell lines. There are multiple alternatively spliced transcript variants known for the decorin gene. It is a candidate gene for Marfan syndrome.[1]

  7. #287
    My concern is with the TGF's sequestering. Does Decorin limit TGF's? If so, wouldn't this cause inflammation the same way that Marfan does?


    http://en.wikipedia.org/wiki/Marfan_syndrome

    Marfan syndrome is caused by mutations in the FBN1 gene on chromosome 15,[7] which encodes a glycoprotein called fibrillin-1, a component of the extracellular matrix. The Fibrillin 1 protein is essential for the proper formation of the extracellular matrix including the biogenesis and maintenance of elastin fibers. The extracellular matrix is critical for both the structural integrity of connective tissue but also serves as a reservoir for growth factors.[4] Elastin fibers are found throughout the body but are particularly abundant in the aorta, ligaments and the ciliary zonules of the eye, consequently these areas are among the worst affected.


    A transgenic mouse has been created carrying a single copy of a mutant fibrillin 1, a mutation similar to that found in the human fibrillin 1 gene that is known to cause Marfan syndrome. This mouse strain recapitulates many of the features of the human disease and promises to provide insights into the pathogenesis of the disease. It has been found that simply reducing the level of normal fibrillin-1 causes a Marfan-related disease in mice.[8]
    Transforming growth factor beta (TGFβ) plays an important role in Marfan syndrome. Fibrillin-1 indirectly binds a latent form of TGFβ keeping it sequestered and unable to exert its biological activity. The simplest model of Marfan syndrome suggests that reduced levels of fibrillin-1 allow TGFb levels to rise due to inadequate sequestration. Although it is not proven how elevated TGFb levels would be responsible for the specific pathology seen with the disease, an inflammatory reaction releasing proteases that slowly degrade the elastin fibers and other components of the extracellular matrix is known to occur. The importance of the TGFb pathway was confirmed with the discovery of a similar syndrome Loeys-Dietz syndrome involving the TGFβR2 gene on chromosome 3, a receptor protein of TGFβ.[9] Marfan syndrome has often been confused with Loeys-Dietz syndrome, because of the considerable clinical overlap between the two syndromes.[10]




    If Docorin dissolves scar tissue, then isn't this like Marfan syndrome?


    l

  8. #288
    Senior Member Jesse's Mom's Avatar
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    I check often hoping to see a post from Dr. Davies yet see nothing. Although I realize he must be very busy it is quite distressing to not hear anything since Jan 29th. Does anyone know what is going on with his work?

  9. #289
    Quote Originally Posted by Jesse's Mom
    I check often hoping to see a post from Dr. Davies yet see nothing. Although I realize he must be very busy it is quite distressing to not hear anything since Jan 29th. Does anyone know what is going on with his work?
    He has posted twice within the last 2 weeks that I know of. They're in
    the W2W '08 thread. Look up his post history.

  10. #290
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    Jesse's Mom

    Buck Nastier is right Dr. Davies was at W2W even though he was ill at the time, 103 F fever. I want you to know that I also go to Carecure many times each day looking for any posts from Dr. Davies.

    I understand that Dr. Davies has to be very careful about what research information he releases prior to publication. He needs to publish to get funding and if he discusses publicly his research results the journals won't publish the information. I suspect that Dr. Davies would love to share more with us but he knows that he can't. This is my understanding of the situation if someone can shed more light on this I'll be watching.

    Roger

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