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Thread: Stephen Davies Update

  1. #311
    Banned adi chicago's Avatar
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    Quote Originally Posted by Stephen Davies
    This is a tough question to answer as there could be several reasons, some of them unrelated to the OEG cells, that might have caused the onset of neuropathic pain. The surgery itself may have induced inflammation that in turn caused the neuropathic pain. However, one big question is what types of cells are actually within what is being called an OEG transplant. It is my understanding that Dr. Lima in particular thinks that the benefits he claims to have seen in patients are due to "stem cell"-like cells within the mixed bag of olfactory neuroepithelium cells that are transplanted. A recent paper form the Olson group in Sweden clearly showed that transplantation of "naive" human neural stem cells into spinal cord injured rats resulted in relatively modest recovery and robust neuropathic pain. My lab has also been investigating which stem cell-like cells (or cells that can be derived from stem cells or neural precursor cells) result in neuropathic pain after transplantation to spinal cord injuries (the paper is in review so say no more on a public forum).

    Whether any of the cell types that are being proposed for clinical trial here in the US or elsewhere promote neuropathic pain (which can take up to more than a year to manifest) is a vitally important question for all of us (including Geron) that propose conducting SCI clinical trials. It is not enough for a lab or company to state that we waited say 9 months after a treatment and the rats looked "fine". Sensitive tests are required to see the early signs of neuropathic pain in rats. Not all rats that are used in SCI studies even have the ability to develop neuropathic pain like humans do. Remember, rats only live a couple of years or so whilst a person that has received a cell transplant treatment for an SCI will have to live with all the long term effects of the therapy for many years i.e. much more time for severe pain to develop.

    Some with a severe SCI may say hey, I'll take the risk and already have. This is a personal choice everyone is rightfully entitled to make. However it must also be remembered what a huge set back it will be to the whole field of stem cell technology for SCI repair if a premature clinical trial is conducted that results in many patients having severe pain problems. As many of you who attended W2W already know, I think we can however have the gains and avoid the pain, if we use "stem cell" technology in the right ways to repair an SCI.
    Thank you very much dr.Davies ,i appreciate your response.
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  2. #312
    Senior Member lynnifer's Avatar
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    Dr Davies or Schmeky, does this sound similiar to the work already being done?

    SOX9 in the article sounds like Decorin.

    http://www.robarts.ca/news.php?id=251

    Dr. Arthur Brown – Targeting the protein SOX9 to alter scar gene expression and to promote regeneration after spinal cord injury - $782,455

    If so, this is the kind of double research stuff that makes me mad!
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  3. #313
    Senior Member Schmeky's Avatar
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    Lynnifer,

    Just reading the attached article I read the word "inhibition", which to me indicates acute. However, I am by no means an expert.
    Last edited by Schmeky; 05-27-2008 at 12:15 PM.

  4. #314
    Quote Originally Posted by lynnifer
    SOX9 in the article sounds like Decorin.

    http://www.robarts.ca/news.php?id=251

    Dr. Arthur Brown – Targeting the protein SOX9 to alter scar gene expression and to promote regeneration after spinal cord injury - $782,455
    It's not duplicate, so no need to be angry. SOX9 [may] promote glial scar formation after injury, as suggested by Schmeky, whereas Decorin degrades the glial scar after it has already formed (among other things).

    ETA:

    The failure of the adult injured spinal cord to support axonal regeneration is in part attributed to the glial scar. Reactive astrocytes constitute a major cellular component of the glial scar and are heterogeneous with respect to the extracellular matrix proteins that they secrete. Astrocytes may produce antiregenerative molecules such as chondroitin sulphate proteoglycans (CSPGs) or proregenerative molecules such as laminin and fibronectin. While many different CSPGs are expressed after spinal cord injury (SCI) they all rely on the same enzymes, xylosyltransferase-I and -II (XT-I, XT-II) and chondroitin 4-sulfotransferase (C4ST) to add the repulsive chondroitin sulfate side chains to their core proteins. We show that XT-I, XT-II, and C4ST are part of a CSPG biosynthetic gene (CBG) battery. Using primary astrocyte cultures and quantitative PCR we demonstrate that TGFbeta2, PDGF, and IL-6 induce the expression of CBGs, laminin and fibronectin by several-fold. We further show that over-expression of the transcription factor SOX9 also strongly induces the expression of CBGs but does not increase the expression of laminin or fibronectin. Correspondingly, SOX9 knock-down in primary astrocytes causes a decrease in CBG and an increase in laminin and fibronectin mRNA levels. Finally, we show that the in vivo expression profiles of TGFbeta2, PDGF, IL-6, and SOX9 are consistent with their potential roles in differentially regulating CBGs, laminin and fibronectin gene expression in the injured spinal cord. This work suggests that SOX9 levels may be pivotal in determining the balance of pro- and anti-regenerative extracellular matrix molecules produced by astrocytes. (c) 2007 Wiley-Liss, Inc. (Source)
    Last edited by Steven Edwards; 05-27-2008 at 09:32 AM.
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  5. #315
    Senior Member lynnifer's Avatar
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    Thanks guys! You're in the top ten of the most intelligent at CareCure in my opinion!
    Roses are red. Tacos are enjoyable. Don't blame immigrants, because you're unemployable.

    T-11 Flaccid Paraplegic due to TM July 1985 @ age 12

  6. #316
    Dr. Davies, I've been following your work and met you at the working2walk seminar in D.C. I know that you have been using decorin first on acute sci's and I'm wondering where you stand now on using decorin on chronic sci's. And I have aone more question on injuries. I've only been hurt for a year and 3 days and I still don't know whats the difference between having an acute injury and having a chronic injury. If anyone can tell me that I would greatly appreciate it.

  7. #317
    Senior Member kate's Avatar
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    Quote Originally Posted by wysong417
    I've only been hurt for a year and 3 days and I still don't know whats the difference between having an acute injury and having a chronic injury. If anyone can tell me that I would greatly appreciate it.
    wysong, acute injuries are brand new -- less than 48 hours The next phase is called subacute, which lasts another couple of weeks. Anything after that is chronic.

    Those time frames might not be exact, but they're close.

  8. #318
    Thank you, I never knew what the definitions were but now I do.

  9. #319
    Hi Everyone,
    Sorry I haven't posted in a while. I have been full on in the lab and then took a quick break visiting my Mum in the UK. Good news is I have a new SCI related Decorin publication in the journal Neurobiology of Disease which is now currently available online at:

    http://dx.doi.org/10.1016/j.nbd.2008.06.009 .

    This paper basically shows that decorin can directly boost (by up to ~15x) the ability of adult neurons to grow axons (nerve fibers) in the presence of high levels of inhibitory molecules found in SCI scar tissue (CSPGs) and myelin (MAG, NOGO, OMgp). This is really great news for chronic SCI as our new data shows that in addition to altering the formation of scar tissue, i.e "lowering the hurdle" that axons must cross at sites iof injury, decorin can also effectively:
    1. render growing axons insensitive to remaining CSPGs at the injury site,
    2. render growing axons insensitive to myelin associated inhibitors in the white matter pathway beyond the injury (where axons must grow for long distances up and down the cord), and,
    3. allow axons to grow within the inhibitory CSPGs that are normally found within target gray matter where the axons must finally make connections in order to support recovery.

    Thus decorin can act as a combination therapy in itself by supressing scar formation and boosting the ability of neurons to grow axons within spinal cord environments full of different types of inhibitors.

    Before anyone asks yes chronic sci experiments to test the effects of decorin on regeneration and recovery are ongoing in the lab. Remember, to conduct chronic SCI experiments you have to first wait for the injured cord to be chronic enough i.e. post injury time points ranging from 6 months to a year. You also have to properly characterize what is happening in chronic SCI (which we are doing) so as to have a baseline with which to compare the effects of a treatment. In this way you can better understand the mechanism by which a treatment such as decorin is working. Understanding mechanism allows you to further improve how a treatment is best given for optimum results, particularly if you want to go to clinical trial.

    Sox-9...Not the same as decorin at all. Knowing that a particular molecule may be involved in scar formation, and having a pharmaceutical grade molecule like decorin that you can infuse and that has multiple beneficial effects, are two entirely different concepts. Whether Sox-9 has an effect on decorin levels in the injured cord or vice versa is an interesting question we may look at.

    Okay back to the lab.

    Stephen.

  10. #320

    Great News

    Thankyou Dr. Davies for your continued work, the fantastic news in this latest publication can only prove that you are moving towards a treatment that can lead to significant returns.

    As with all publications I can only assume that this published material is lagging behind (please correct me if I am wrong) what is happening in the lab at this very moment, which only makes me and I'm sure everybody else very excited.

    Once again thank you for all your efforts and may the successes keep on coming!

    BR

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