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Thread: Jerry Silver and Other Discussion from ChinaSCINet Update

  1. #351
    Dr. silver,
    Hi, would you please go and read the new post on cure page Title " spinal research (ISRT): update" by fly_pelican_fly and see what you think of that research about CHAS . Thank you

  2. #352
    Quote Originally Posted by Wise Young View Post
    Here is the full paper Lu, et al. 2012 that I referred to in my last post.
    I find this interesting from the paper:

    "Several lines of evidence support the observation that axons
    have regenerated in this study: (1) regenerating axons emerge
    from the midportions of the graft in the lesion site, where spared
    axons are unlikely to be located; (2) axons exhibit irregular trajectories,
    often with abrupt turns, rather than existing in tightly
    linear bundles typical of spared axons
    ;
    ..."(pg. 8216).

  3. #353
    Quote Originally Posted by kz View Post
    Dr. silver,
    Hi, would you please go and read the new post on cure page Title " spinal research (ISRT): update" by fly_pelican_fly and see what you think of that research about CHAS . Thank you
    KZ, I believe Jerry is part of the Ch'ase+ISRT steering committee.

    See: http://www.spinal-research.org/wp-co.../Programme.pdf

  4. #354
    Dr. silver,
    Hi, would you please go and read the new post on cure page Title " spinal research (ISRT): update" by fly_pelican_fly and see what you think of that research about CHAS . Thank you

    I was extremely excited to read this. This is really wonderful news. I think they are finally going to do this.

  5. #355
    Quote Originally Posted by NowhereMan
    axons exhibit irregular trajectories,
    often with abrupt turns, rather than existing in tightly
    linear bundles typical of spared axons;

    Yes, precisely!!! This type of haphazard axonal patterning is typical of truly re-growing axons. Everyone in the regeneration biology community, except Wise, understands the importance of this basic concept. This is exactly the argument I raised when I questioned the validity of Wise's DTI data and his conclusions that axons had regenerated in his patients. I hope he is paying close attention to this exchange between you and I.

    from my post #124 "Truly regenerating axons NEVER grow in tightly aligned bundles. Regeneration in the adult is not like the fasciculated axon growth that occurs in the embryo. Indeed, the presence of aligned bundles of axons passing in the vicinity of a cord lesion is always suggestive of spared axons."
    Last edited by Wise Young; 01-31-2013 at 07:55 AM.

  6. #356
    Quote Originally Posted by jsilver View Post
    Yes, precisely!!! This type of haphazard axonal patterning is typical of truly re-growing axons. Everyone in the regeneration biology community, except Wise, understands the importance of this basic concept. This is exactly the argument I raised when I questioned the validity of Wise's DTI data and his conclusions that axons had regenerated in his patients. I hope he is paying close attention to this exchange between you and I.

    from my post #124 "Truly regenerating axons NEVER grow in tightly aligned bundles. Regeneration in the adult is not like the fasciculated axon growth that occurs in the embryo. Indeed, the presence of aligned bundles of axons passing in the vicinity of a cord lesion is always suggestive of spared axons."
    Jerry,

    I edited the your post so that the quotes show...

    Axons grow in bundles during development, a process called fasciculation, aided by expression of the L1 cellular adhesion molecule by axons. The fact that almost all the axons in the spinal cord are organized into tracts indicates that axons can grow in bundles. Likewise, axons in peripheral nerves grow in bundles. Just because axonal growth appears to be dispersed and haphazard in animal studies, it does not mean that bundled growth cannot occur under certain circumstances. In fact, such types of growth is desirable.

    We did the DTI to assess the location of the white matter in the spinal cords. The results were surprising. *Every* one of five spinal cords of ASIA A subjects that we were able to image successfully with DTI, we saw a clear gap in the fiber tracts between the rostral and caudal spinal cord. In two of these patients, we saw the fiber tracts approach each other, overlap, and even bundles of fibers that extend long distances into the proximal and distal spinal cord.

    In any case, we think that this is sufficiently promising to see if we can repeat this in a phase III randomized clinical trial in larger numbers of subjects. We are of course also still following the subjects for over one year in hopes that neurological scores correlate with these findings. Finally, we are currently cleaning up and analyzing the 6-12 month data from 20 subjects that were transplanted in Kunming with intensive locomotor training.

    Wise.

  7. #357
    Wise

    "Just because axonal growth appears to be dispersed and haphazard in animal studies, it does not mean that bundled growth cannot occur under certain circumstances. In fact, such types of growth is desirable."

    Sure, I agree that regenerating axons can be induced to cross a lesion in the cord within tight bundles, but this occurs only when they are given an aligned scaffold or tubular prosthesis or segments of peripheral nerves to guide them. However, when such axons exit the distal end of the bridge (and this rarely happens unless you lure them out of the other side with neurotrophins or add ch'ase or strongly stimulate their intrinsic growth capacity or some combination of the three) they then instantly begin to meander again. So the presence of a very long bundled thing extending long distances beyond a lesion in your patients will be interpreted by all those who do this for a living or read the relevant literature, as spared fibers and will have a hard time accepting these structures as regenerating axonal bundles. Even if they might be axonal then they will be considered to have been spared but somehow their visualization with DTI has changed over time. As I mentioned earlier if you can show that such rectilinear bundles continue to elongate at their distal tips over extended periods of time then, I think, you will be in business. None-the-less, without showing convincing data using modern anatomical techniques that such unprecedented regeneration can occur in a chronic animal model using your strategy, there will always be skeptics that you have proven that long distance axonal regeneration can occur at such lengthy chronic stages in a human. As far as correlation between behavior and the presence of these structures, I thought I heard you present at Bedford that there wasn't any.
    Last edited by jsilver; 01-31-2013 at 01:10 PM.

  8. #358
    All we need now is for the Neurological scores to correlate with the findings. Patience is a virtue. Will find out more next five months.
    In any case, the dialogue between the two professors is extremely informative.
    Please Dr. Young, Keep sharing with us all the good news.

  9. #359
    Quote Originally Posted by jsilver View Post
    Thanks for citing this one from the Fehlings lab because it demonstrates nicely the role of scar associated inhibitory molecules in curtailing stem cell migration especially at chronic stages after injury. You and Wise should actually read it. Just look at the title. The authors demonstrate yet again the need for a combinatorial strategy that breaks down CSPGs (via chondroitinase) and adds a cocktail of neurotrophins to keep stem cells alive in order to allow them to escape the lesion, migrate remarkable distances and remyelinate axons. Without chondroitinase at chronic stages the stem cells remained trapped within the scar. This is not a paper about axonal regeneration to restore function but likely remyelination of axons or possibly sprouting effects.
    From attached:
    In this report, we studied the role of glycogen synthase kinase-3 (GSK-3) inactivation on neurite and axon growth from adult neurons via combined in vitro and in vivo approaches. We found that the major CNS inhibiting substrates including chondroitin sulfate proteoglycans could inactivate protein kinase B (Akt) and activate GSK-3 signals in neurons.
    Systemic application of the GSK-3 inhibitor lithium to spinal cord-lesioned rats suppresses the activity of this kinase around lesion.
    Application of GSK-3 inhibitors stimulates axon formation and elongation of mature neurons whether in presence or absence of inhibitory substrates.
    Quote Originally Posted by jsilver View Post
    None-the-less, it is a very nice paper giving hope that a proper combinatorial strategy employing stem cells can restore some useful function at chronic time points following SCI.
    Excellent!
    Treatments with GSK-3 inhibitors including a clinical dose of lithium to rats with thoracic spinal cord transection or contusion injuries induce significant descending corticospinal and serotonergic axon sprouting in caudal spinal cord and promote locomotor functional recovery.
    Our studies suggest that GSK-3 signal is an important therapeutic target for promoting functional recovery of adult CNS injuries and that administration of GSK-3 inhibitors may facilitate the development of an effective treatment to white matter injuries including spinal cord trauma given the wide use of lithium in humans.

  10. #360
    My favorite part of the paper:

    "We recently reported that pain reliever ibuprofen improved axon
    growth and functional recovery in SCI rodents when applied at a
    dose of 60 mg/kg/d, which is a higher dose than that used clinically
    as a cyclooxygenase inhibitor (Fu et al., 2007)."

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