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Thread: Dr. Jerry Silver: Latest chronic SCI research results featured at Cleveland

  1. #71

    intermittent hypoxic therapy

    Quote Originally Posted by tomsonite View Post
    Hi Dr. Silver,
    1. When it comes to chronic vs. acute SCI, I know Gordon Mitchell (and others) theorize that the response to intermittent hypoxia has to do with inflammation - he (and others I believe) have shown that IH alone produces more pronounced responses for certain behaviors in a chronic vs. acute SCI model. What is your take on that? And, does reduced inflammation in chronic SCI vs. acute play a role for the specific results you're showing, or does it have more to do with the perineuronal net?


    2. I'm sure you are aware of the work by Randy Trumbower, Zev Rymer and others examining IH in humans with incomplete SCI showing an improvement in voluntary lower body strength as well as walking function after an single bout of IH. Is there any reason to believe the respiratory results you present would NOT occur in other systems controlled by alpha moto-neurons and skeletal muscle (hands, walking, bowel & bladder, etc)?


    3. You mention that ISRT is working on a controlled AAV vector to deliver ch'ase, and that it can be "turned off" when improvements plateau - could you elaborate on that? It was my understanding that AAV's can't necessarily be turned off.


    4. You mentioned that IH + ch'ase produced tonic activity in 1/3 of the animals, though that may wane over time - concurrently, you showed earlier in the presentation how the perineuronal net comes back naturally after a period of being reduced with ch'ase. Is it possible that ch'ase let too much serotonin "get through", so to speak, after IH, causing this augmented activity in those animals? Is there perhaps an optimal combination of ch'ase and IH that we could figure out so that we can minimize the chances of that response occurring?

    5. You mention specific targets to deliver ch'ase to at different parts of the spinal cord to target specific behaviors. Does this mean that it wouldn't be enough to deliver ch'ase just to the site of an injury, but rather we'd need to inject ch'ase all along the cord to allow for a period of plasticity to occur?


    6. Lastly, is this work published yet? I'd love to read a full report.
    *********

    Hi, saw your post and want to tell you I rented IHT equipment for a month from hypoxico.com and it seemed to help at first, but I could never get down to 80 percent saturation level in 90 secs. It took 4 min with lever full open or not. Then it suddenly made me vulnerable to a bad cold bug and wiped out my energy, had to refill my 4ap prescription just to walk with my walker. Tried it twice after cough gone and second time I started coughing bad, throat hurting. I never get sick, have an incomplete sci at c/4. What your post suggests is that IHT works best if you have inflammation or something like that, is that right? Do you have a link for me? Thanks!

  2. #72
    Quote Originally Posted by FellowHawkeye View Post
    *********

    Hi, saw your post and want to tell you I rented IHT equipment for a month from hypoxico.com and it seemed to help at first, but I could never get down to 80 percent saturation level in 90 secs. It took 4 min with lever full open or not. Then it suddenly made me vulnerable to a bad cold bug and wiped out my energy, had to refill my 4ap prescription just to walk with my walker. Tried it twice after cough gone and second time I started coughing bad, throat hurting. I never get sick, have an incomplete sci at c/4. What your post suggests is that IHT works best if you have inflammation or something like that, is that right? Do you have a link for me? Thanks!
    I just replied to you in another thread...according to animal research, IH works best when you do NOT have inflammation (i.e., for people with chronic rather than acute injuries).
    What device were you using? What percentage of O2 were you using and how many intervals were you doing? There is no need to get down to 80% O2 sat necessarily, where did you get that number? The fact that you were breathing low O2 for 4 min (as opposed to 1 min on 1 min off for half an hour, as current literature suggests) might have caused your issues. Did you do 4 min of low O2 for multiple intervals in a row?

  3. #73
    Quote Originally Posted by 6 Shooter View Post
    Dr. Silver, in your rat models, have you been able to determine how long it takes before the gllal begins to form and prevent neuron and axon passage through the barrier?

    Seems to me that this glial scar formation would begin to separate the acute stage of SCI from the chronic.
    The molecular components of glial scarring begin to form almost immediately after injury. The inhibitory proteoglycans of the scar are stimulated as soon as the blood brain barrier is broken. One of the triggers of proteoglycan production by reactive astrocytes is Transforming Growth Factor beta (TGFb) that is bound to fibrinogen. This compound rapidly leaks out of the blood into the CNS following damage. The physically obstructive components of the scar such as glial hypertrophy, changes in alignment of the glia perpendicular to the injury and pericyte migration to the lesion edge to form the fibroblastic component of the scar take several weeks to occur.

  4. #74
    Wow. Thanks for the detailed response. Very interesting.

    In your studies, is this process aggravated or sped up by swelling in the area surrounding the lesion? Is this process retarded by cooling (maybe continuous) the surrounding area to reduce swelling? Have read your posts on ch'ase and the peptide. So promising and great work to reverse the course of this horrible affliction.

  5. #75
    Quote Originally Posted by 6 Shooter View Post
    Wow. Thanks for the detailed response. Very interesting.

    In your studies, is this process aggravated or sped up by swelling in the area surrounding the lesion? Is this process retarded by cooling (maybe continuous) the surrounding area to reduce swelling? Have read your posts on ch'ase and the peptide. So promising and great work to reverse the course of this horrible affliction.

    Edema occurs after injury as fluids exit the vasculature into the astrocyte end feet that closely abut all the vessels in the CNS. The astrocytes swell as they fill with water. There is a special water channel that astrocytes produce that is called aquaporin 4. Actually blocking this channel helps to lessen edema in the brain or spinal cord after trauma. I don't know of any data that directly links edema to subsequent scar formation. However, cooling can help control edema somewhat but the major impact of cooling is on the inflammatory system, which , in turn, does have a major role in triggering scar. The scar is an essential event that helps to wall off areas of inflammation in an attempt to protect the remaining fragile tissue from inflammatory mediated secondary damage.

  6. #76
    Dr. Silver , Hi, would you please check the PM I sent you and see if you can reply . Thanks

  7. #77
    Dr. Silver,
    By my understanding, high peptide dosage safety (non-established yet)
    and Viral delivery method for Ch'ase (exact procedure non exsisting - yet)
    shouldn't be obstacles to design Human trial - or you have to wait for them
    along with large animal trial results?
    If results from UK Ch'ase dog trial shows Ch'ase effectivnes - would this be enough
    so you can come closer to the human trial, or we still need to see primates trial
    prior to the human trial??

    Do you see any progress, any promising contacts, that might
    accelerate movement toward human trial with Ch'asee + Peptide + IH or Rehab, so far?

    BTW, must be hard on you when you come so close to possible cure
    and would like to help so many desperate people but you need to keep
    your scientific, precise calculating shield on...
    You are already Hero to sharing all of this with us!!!

    Please let us know how we can help?
    www.MiracleofWalk.com

    Miracles are not contrary to nature, but only contrary
    to what we know about nature
    Saint Augustine

  8. #78
    Quote Originally Posted by comad View Post
    Dr. Silver,
    By my understanding, high peptide dosage safety (non-established yet)
    and Viral delivery method for Ch'ase (exact procedure non exsisting - yet)
    shouldn't be obstacles to design Human trial - or you have to wait for them
    along with large animal trial results?
    If results from UK Ch'ase dog trial shows Ch'ase effectivnes - would this be enough
    so you can come closer to the human trial, or we still need to see primates trial
    prior to the human trial??

    Do you see any progress, any promising contacts, that might
    accelerate movement toward human trial with Ch'asee + Peptide + IH or Rehab, so far?

    BTW, must be hard on you when you come so close to possible cure
    and would like to help so many desperate people but you need to keep
    your scientific, precise calculating shield on...
    You are already Hero to sharing all of this with us!!!

    Please let us know how we can help?
    Dear Comad,

    Thanks for your questions and your very kind personal comment. I am keeping my fingers crossed about the dog trial
    and at the same time being cautiously optimistic. I believe the chondroitinase being used for this trial is a heat stabilized
    version that allows the enzyme to remain active at body temperature for a longer time than the regular enzyme. I do not
    know at what spinal level the enzyme is being delivered nor how much is being delivered. The third generation, regulated, virus delivered
    enzyme will be most potent and has the ability to spread much further up and down the spinal cord. So even if the current trial
    is not efficacious, I will be disappointed but far from giving up. Of course, if the dog trial shows positive effects then I would imagine
    that the pace could move rather rapidly to humans without the need for primate experiments. We are doing all we can to move our peptide toward
    the clinic.

  9. #79
    This may be a stupid question but is this "peptide" taken orally, or is it injected into the injury site on the spinal cord? Also is chase planned to be used alone or is it to be a part of the peptide?

  10. #80
    Quote Originally Posted by JamesMcM View Post
    This may be a stupid question but is this "peptide" taken orally, or is it injected into the injury site on the spinal cord? Also is chase planned to be used alone or is it to be a part of the peptide?
    Watch 23:00 https://www.youtube.com/watch?v=TRlqbDNqSYc

    It's injected.

    A peptide is a short protein. Taking it orally would probably decompose it into aminoacids.
    Debating on CareCure is like participating in the special-olympics. You may win, but you're still disabled.

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