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Thread: Stephen Davies Update

  1. #411
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    Your report put tears in my eyes. Thank you Dr. Davies for this report. Keep up the good work.

    Thanks to all who are moving forward on this research despite all the diffuculties you face.

  2. #412
    Quote Originally Posted by Steven Edwards
    Naive stem cells are ones that haven't been differentiated to their desired state before transplantation.
    Thanks Steven. Would this therefore mean that there would be a strong possibility that people who will take part in the China umbilical cord trial shall end up having more pain?

  3. #413
    Senior Member poonsuzanne's Avatar
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    Quote Originally Posted by betheny
    Suzanne, have you met Dr Davies before? If not, you 2 are in for a mutual treat! I love it when nice people meet each other, esp if they bond over important work as the 2 of you surely will.
    Betheny,

    Many thanks for your kind words!!

    I have met Dr. Davies once at the W2W 08. He is a young and devoted SCI scientist full of potentials and is a gentleman too. I did not have enough chance to speak to him at the W2W as he was busily attending the W2W with full dedication, and he was quite sick too at that time.
    Suzanne

  4. #414
    Quote Originally Posted by zokarkan
    Thanks Steven. Would this therefore mean that there would be a strong possibility that people who will take part in the China umbilical cord trial shall end up having more pain?
    zokarkan, worsening of neuropathic pain is a risk that must be considered with all treatments. We have some evidence suggestion that methylprednisolone given at the time of transplant may prevent development of neuropathic pain and will be testing this in our clinical trial with cord blood mononuclear cell transplants.

    Wise.

  5. #415
    Quote Originally Posted by Wise Young
    We have some evidence suggestion that methylprednisolone given at the time of transplant may prevent development of neuropathic pain and will be testing this in our clinical trial with cord blood mononuclear cell transplants.

    Wise.
    Hello Wise, this could be great, I have more neuropathic pain every year, this is making my blood pressure goes higher and higher and I hope this will not kill me.. I really hope the sci community is sufficiently aware about the risks of neuropathic pain with stem cells transplantation.
    Anyway, do we know if it's the presence of GDAsCNTF itself that's generating neuropathic pain?.. or does it generated some kind of bad plasticity process inside the spine?.. Why does spasms and neuropathic pain increase with time?..Does that mean that level of GDAsCNTF inside the spine increases with time too?.. What about reducing the amount of GDAsCNTF around the injury?..
    Thanks
    G78

  6. #416
    Congratulations on your team's findings Dr Davies. At a time when there seem to be a lot of new injuries occuring, it is very encouraging to get news that could one day reverse all this damage and suffering.

  7. #417
    Dr. Davies first off I want to thank you for your persistence in pursuing your quest for a cure. I can't begin to express my appreciation for your thoughtfulness and your wanting to help all of us who are in desperate need of a cure. I know that you are going to succeed in you research for finding a curative therapy to help us walk again. I can't help but wonder though why I'm not getting any feedback on the subject of how to join or be a part of a clinical trial. I know you suggested a timeline of 2-3 years for the trials to begin. I spoke to you at W2W2 and you told me that with the continuation of physical therapy I would be a good candidate to participate. Since then I've been in aquatic therapy and other PT programs. I'm just asking you to please let me know how I would know how to find out when they would start and how to apply. Thanks again for you time and efforts.

  8. #418
    Hello everyone, I just want to make the point that medical science is not like chemistry. You cannot add this to stop that or add two things and predict an outcome. It is more like genetics. Not Mendelian genetics, which is very simplistic, but more like polymorphic genes with factors like penetrances, expressivity. What I am trying to say, is that when medical science formulates a treatment the results vary from person to person and from species to species. If the treatment works on the mice 50% effectively, it may work on a humans 10%. If you use a technique on mice and it works 80% we cannot explain why it didn't work as well on the 20% and why the results vary from mouse to mouse. Spinal cord regeneration will vary from animal studies to human clinical trials and in human clinical trials that will vary from person to person. So simply saying GDAsCNTF equals pain may not necessarily be true. You will see terms like, ''strongly indicates''. Or the term ''evidence suggests.'' Even terms like ''indicates''. The bottom line is we cannot make the body do what we wanted to do 100% of the time and we don't know why. We can only go by if there is a statistical difference is between using nothing and using something and the percent of effectiveness it has. I to wish it were black and white that if you did a series of steps that would result in the outcome that we predicted. Unfortunately it doesn't work that way and that is why we need clinical trials at extreme testing because they were so many unknowns we can never be sure that anything is safe. That is why we have lawyers that advertise to get clients to come in that have side effects from various medications.

    That being said, great job Dr. Davies and we cannot wait for phase 1 especially if you can get and grow the cells from the patients own cells.
    Last edited by jhope; 09-22-2008 at 05:51 PM.

  9. #419
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    It is basic science, which is very good, since some bother to do studies like basal research on the injured spinal cord, for maybe possible future therapies.

    Peoples around the world should be ‘jumping’ up and down for the few basic SCI researchers around the world bothering with this complicated field of research.

  10. #420
    Quote Originally Posted by Leif
    Davies. Great going further on for this quest, and as you wrote Lars Olson studies from Karolinska research helped which by you’re study seems to be valid, but the Karolinska Nobel institute bunch should look at studies like yours to move basic research to the clinics, but are they, really? I do not think so, they get millions after millions, and research and research, -I say give money on focused research, and as for SCI research I think this is valid, these days. Like you’re study might show one can focus on SCI and not solely focus on basic research in general. So thanks for that.


    Isn’t plasticity known as for example like brain strokes for the different synapses connections and grids to learn new usage, meaning already some existing neuronal grids exists, by making detours or otherwise, by some existing networks, to make connections (obviously like in the real injured cord does not happen)? And if not existing neighbouring connections in the cord to help out, how does one create a good neuronal grid at the injury site and other lost dead long wire connections in the chronic injured cord to send ascending and descending signals communicating signals in this grid to restore it, when the rest of the even close grid in the cord are destroyed, like for example long axons controlling motomovement say in legs in the human body to reconnect when controlling neurons in the grey matter is destroyed? How will one go by such scientific quests to overcome such hurdles, growing back long paths of axons in the human body, and replacing neuronal motoneuronal cells, -what could a scientific strategy be as for this? Difficult questions, still.
    Hi Leif,
    You've asked some good questions, many of which I have already answered to a large extent in my previous posts. If you don't mind I'd rather you took a quick read of my old posts than for me to write what would have to be an extensive reply. In particular I would read my more recent posts about decorin and its ability to not only make the environment of the injured spinal cord more supportive of axon growth but that it can also directly increase the ability of adult neurons to grow axons (by up to 14.4 fold) in the presence of high levels of multiple inhibitory molecules (myelin and scar associated CSPGs) that are known to be present in the injured spinal cord.

    I have many years experience with transplanting neurons into the injured adult nervous system and although my work showed there are guidance cues for directing the growth of axons from transplanted adult neurons in the pathways of the brain (Davies et al Nature 1997) and spinal cord (Davies et al., J Neuroscience 1999), these old studies also showed that the axons failed to grow across scar tissue that had high levels of CSPG inhibitory molecules. This is the reason why I turned my attention to developing technologies such as decorin and GDAs that can greatly improve the the ability of severed axons and those growing from transplanted neurons to grow within the environment of the injured spinal cord.

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