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Thread: Jerry Silver and Other Discussion from ChinaSCINet Update

  1. #131
    Senior Member khmorgan's Avatar
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    Quote Originally Posted by lynnifer View Post
    Really? I thought it was much sooner than that.
    I think "a few weeks" is a good estimate. See:

    http://www.google.com/url?sa=t&rct=j...55534169,d.eWU

  2. #132
    Would it not be possible that a 10 year post chronic spinal cord may have made changes over time to breakdown a portion of the gilia scar barrier that was originally developed?

    Yes, indeed, the scar does change over time. It becomes thinner and its associated inhibitory proteoglycan extracellular matrices become more restricted to the cell surfaces. In some very severe contusive injuries, Schwann cells eventually invade through the dorsal portion of the scar and enter the core of the lesion. It is unknown how they do this. Schwann cells are extremely growth promoting and they provide a scaffold for axonal growth, mostly of sensory axons from the roots, that can pass through the scar wall and into the core of the lesion. This phenomenon demonstrates that the scar is not totally but only relatively impenetrable. However, the presence of axons in the lesion core does not mean that scar does not exist but, rather, that over time the scar changes and one of these changes is that Schwann cell invasion occurs. However, axons do not pass completely through the lesion as Wise suggests but only into the lesion core where they remain trapped and functionally useless.

  3. #133
    Quote Originally Posted by 6 Shooter View Post
    From my reading of CareCure over the last 6 years, I tend to believe that both Jerry and Wise are correct in thier observations and statements relating to their observations. Both have convincing arguments and support for their statements.

    One main variable between the "chronic" mouse/rat model and the human chronic model seems to be time. A chronic mouse/rat is considered chronic after 20+ days or so. A human is considered chronic after several years. It is visually obvious that both the mouse/rat and humans loose sensory and motor function immediately after SCI injury. The spinal cords in both try to wall off the injury site. Inflamation and necrosis occurs in both. Above, Jerry described the damage done to the spinal cord in great detail.

    In Jerry's 20+ day chronic model, he has the advantage of seeing slices of mouse/rat spinal cords under powerful microsopes before and after treatments. Dr. Young does not have that opportunity as the humans are still living. Dr. Young does have the opportunity to view human spinal cords during surgery. However, portions of the treated human's spinal cords are not viewable under a microscope as the patients are still alive. So, Dr. Young has structured a battery of tests to observe patients and score changes observed in the body.

    Would it not be possible that a 10 year post chronic spinal cord may have made changes over time to breakdown a portion of the gilia scar barrier that was originally developed? That may partially explain Dr. Young's posts about the motor changes in Christopher Reeves at 3+ years post injury. That would also explain some of the positive changes observed with the UCB cell transplants in the China studies.
    6 Shooter, irrespective of the timeframe for chronics as it really is irrelevant in the context of what you're saying, I think that this is a really good point that you make and look forward to hearing what the specialists (i.e. Wise and Jerry, not Paolo) have to say. I hope this doesn't just get burried in a discussion about the definition of a chronic.

    Clayton
    "Wheelie Wanna Walk!"

  4. #134
    Quote Originally Posted by Le Type Fran├žais View Post
    Dr. Young and Dr. Silver,

    I ask this with the utmost respect and no intention of stirring stife, but speaking of the existence of this scar tissue, how can two scientists come away with different opinions on the existence of something that should be quite evident?

    Todd
    I have been studying this structure for most of my scientific career. I have had a long standing NIH grant entitled "Regeneration beyond the glial scar" for nearly 30 years. If one simply reads the literature , uses the proper techniques and does the right experiments there is no doubt that scar exists. Indeed, the scar is well known by neurosurgeons who attempt to aspirate away non-invasive brain tumors that are surrounded by scar. They, aspirate until they push up against a tough tissue border that is the surrounding scar. By the way, contrary to what Wise suggests, there is no need for fibroblasts to create the tough scar. If you'd like, read my 2004 Nature Reviews Neuroscience review. Regeneration beyond the glial scar : Article : Nature Reviews ...
    http://www.nature.com/nrn/journal/v5...l/nrn1326.html - Similar
    Review. Nature Reviews Neuroscience 5, 146-156 (February 2004) | doi : 10.1038/nrn1326 ... the glial scar. Jerry Silver1 & Jared H. Miller1 About the authors ...

    Here is another reference:


    Glial scar
    From Wikipedia, the free encyclopedia
    Glial scar formation (gliosis) is a reactive cellular process involving astrogliosis that occurs after injury to the Central Nervous System. As with scarring in other organs and tissues, the glial scar is the body's mechanism to protect and begin the healing process in the nervous system. In the context of neurodegeneration, formation of the glial scar has been shown to have both beneficial and detrimental effects. Particularly, many neuro-developmental inhibitor molecules are secreted by the cells within the scar that prevent complete physical and functional recovery of the central nervous system after injury or disease. On the other hand, absence of the glial scar has been associated with impairments in the repair of the blood brain barrier.[1]

    Contents [hide]
    1 Scar components
    1.1 Reactive astrocytes
    1.2 Microglia
    1.3 Endothelial cells and fibroblasts
    1.4 Basal membrane
    2 Beneficial effects of the scar
    3 Detrimental effects of the scar
    4 Primary scar molecular inducers
    4.1 Transforming growth factor β (TGF-β)
    4.2 Interleukins
    4.3 Cytokines
    4.4 Ciliary neurotrophic factor (CNTF)
    4.5 Upregulation of nestin intermediate filament protein
    5 Suppression of glial scar formation
    5.1 Olomoucine
    5.2 Inhibition of Phosphodiesterase 4 (PDE4)
    5.3 Ribavirin
    5.4 Antisense GFAP retrovirus
    5.5 Recombinant monoclonal antibody to transforming growth factor-β2
    5.6 Recombinant monoclonal antibody to interleukin-6 Receptor
    6 References
    Last edited by jsilver; 01-03-2013 at 09:27 PM.

  5. #135
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    Dr. Silver,
    Do you foresee any positive results in an Asia A complete injury ever regaining their bowel and blatter function back in the next decade? I would be happy to finish my life out with regaining these functions. I appreciate your comments.

  6. #136
    Senior Member khmorgan's Avatar
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    Quote Originally Posted by jsilver View Post
    ...
    Here is another reference:


    Glial scar
    From Wikipedia, the free encyclopedia
    Glial scar formation (gliosis) is a reactive cellular process involving astrogliosis that occurs after injury to the Central Nervous System. As with scarring in other organs and tissues, the glial scar is the body's mechanism to protect and begin the healing process in the nervous system. In the context of neurodegeneration, formation of the glial scar has been shown to have both beneficial and detrimental effects. Particularly, many neuro-developmental inhibitor molecules are secreted by the cells within the scar that prevent complete physical and functional recovery of the central nervous system after injury or disease. On the other hand, absence of the glial scar has been associated with impairments in the repair of the blood brain barrier.[1]
    From Wikipedia: http://en.wikipedia.org/wiki/Scar

    Scars are areas of fibrous tissue (fibrosis) that replace normal skin after injury. A scar results from the biological process of wound repair in the skin and other tissues of the body. Thus, scarring is a natural part of the healing process. With the exception of very minor lesions, every wound (e.g. after accident, disease, or surgery) results in some degree of scarring. An exception to this is animals with regeneration, which do not form scars and the tissue will grow back exactly as before.
    Scar tissue is the same protein (collagen) as the tissue that it replaces,[1] but the fiber composition of the protein is different; instead of a random basketweave formation of the collagen fibers found in normal tissue,[1] in fibrosis the collagen cross-links and forms a pronounced alignment in a single direction.[1] This collagen scar tissue alignment is usually of inferior functional quality to the normal collagen randomised alignment. For example, scars in the skin are less resistant to ultraviolet radiation, and sweat glands and hair follicles do not grow back within scar tissue.[2] A myocardial infarction, commonly known as a heart attack, causes scar formation in the heart muscle, which leads to loss of muscular power and possibly heart failure. However, there are some tissues (e.g. bone) that can heal without any structural or functional deterioration.
    As I think Dr. Young has said many times, he does not deny the existence of the necrosis tissue, he just prefers not to call it "scar" tissue because of the confusion that it causes lay people, like myself.

  7. #137
    Quote Originally Posted by khmorgan View Post
    From Wikipedia: http://en.wikipedia.org/wiki/Scar

    As I think Dr. Young has said many times, he does not deny the existence of the necrosis tissue, he just prefers not to call it "scar" tissue because of the confusion that it causes lay people, like myself.
    Oh, but you are wrong here. He does deny that in the absence of fibroblasts in the CNS there is scar. Thus, he denies that gliosis (astrocyte only behavior) can form a barrier. There are no fibroblasts in the brain or spinal cord normally, so in the absence of a penetrating injury that freely allows them into the CNS compartment from the meninges, it has been thought that few fibroblasts enter the CNS. So the astrocytes have taken over the job in the CNS of walling off inflammation. When fibroblasts do enter CNS in large numbers then the scar that is made by astrocytes becomes even more impenetrable because fibroblats produce a myriad of additional inhibitory molecules and the reactive astrocytes wall them off as well with a membranous structure called basal lamina. If you or Wise wish to call what the astrocytes do something other than "scar' that is no problem but you will not be able to communicate with the rest of the world where use of the word scar is more flexible. In the end, the important point is that reactive astrocytes contribute to regeneration failure in the CNS in a big way and they have to be overcome, removed or altered somehow to get regeneration to occur especially at chronic stages. Until data is presented, there is no evidence that UMBCs or lithium are capable of overcoming scar or the inhibitory molecules associated with it.

  8. #138
    Quote Originally Posted by JoeMonte View Post
    Dr. Silver,
    Do you foresee any positive results in an Asia A complete injury ever regaining their bowel and blatter function back in the next decade? I would be happy to finish my life out with regaining these functions. I appreciate your comments.
    While we can't study bowel function in rodents after SCI, because bowel activity in them is little affected by SCI, we are focusing on urinary function which is considerably altered. Indeed, the urinary system seems to be a most accessible system for repair after SCI, since the brainstem nuclei that control urination have a remarkably high intrinsic capacity for long distance regeneration once we give them a bridge across the lesion and the good news is that this can occur even at chronic stages after injury. In addition, we are using either a complete transection or a most severe contusive injury as our models, which is like ASIA A. Please view my 2nd presentation at the recent W2W to see what progress we have made. I have learned that it is coming online soon. I remain highly optimistic that the answer to your question is "yes". We are certainly working as hard and fast as we can to make this a reality.

  9. #139
    Quote Originally Posted by khmorgan View Post
    I think "a few weeks" is a good estimate. See:

    http://www.google.com/url?sa=t&rct=j...55534169,d.eWU

    Yes i see it was last up dated in 2002 The surprising thing then was they where working on rats . Their is only so many rats stories we can take Hopefully we are moving on
    AS I SIT HERE IN MY CHAIR . I LOOK OUT UPON THE GROUND .I WONDER WILL I EVER GET UP AND WALK A ROUND ??


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  10. #140
    Quote Originally Posted by jsilver View Post
    While we can't study bowel function in rodents after SCI, because bowel activity in them is little affected by SCI, we are focusing on urinary function which is considerably altered. Indeed, the urinary system seems to be a most accessible system for repair after SCI, since the brainstem nuclei that control urination have a remarkably high intrinsic capacity for long distance regeneration once we give them a bridge across the lesion and the good news is that this can occur even at chronic stages after injury. In addition, we are using either a complete transection or a most severe contusive injury as our models, which is like ASIA A. Please view my 2nd presentation at the recent W2W to see what progress we have made. I have learned that it is coming online soon. I remain highly optimistic that the answer to your question is "yes". We are certainly working as hard and fast as we can to make this a reality.
    The video is online now in the educational video library from the Working 2 Walk 2012 Album.

    http://u2fp.org/educate/

    Last edited by GRAMMY; 01-07-2013 at 03:52 AM.

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