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Thread: Jerry Silver and Other Discussion from ChinaSCINet Update

  1. #71
    Quote Originally Posted by lunasicc42 View Post
    I have never commented on this for fear of getting it wrong but I came to think that wise doesn't disagree that something is there, he just has an issue about calling it a "scar" by his understanding of the definition of the word "scar"
    But what I Honestly admit, is that, everytime he attempts to explain exactly why he doesn't like to call it a "scar"... He explains a "matrix of gliosis" or something to that effect. I Honestly think: "isnt that just another way of saying 'scar'? "

    I might be confused

    I've wondered if it's just semantics, myself; maybe the argument
    is over the word "scar" vs "gliosis." But they're also debating
    whether it's necessary to remove sections of spinal cord or not.
    Wise, to my knowledge, doesn't remove anything from the cord.

    I just don't understand how both can have successful animal studies
    with a totally different opinion on a fundamental issue.

  2. #72
    Quote Originally Posted by Buck503 View Post
    I've wondered if it's just semantics, myself; maybe the argument
    is over the word "scar" vs "gliosis." But they're also debating
    whether it's necessary to remove sections of spinal cord or not.
    Wise, to my knowledge, doesn't remove anything from the cord.

    I just don't understand how both can have successful animal studies
    with a totally different opinion on a fundamental issue.
    That's what is confusing and frustrating for me... One is saying regeneration isn't possible without dealing with the scar at chronic time periods and the other is saying, wrong, it is possible and early indications of these human trials seem to point towards just this.
    Honestly... I don't think there's much more to say until we see at least the next update on the data, hopefully showing explicitly both the white matter growth and the extent of walking, whether posted here or published in a journal... Without the data to help as an arbiter, it's all speculation.

  3. #73
    Have a contused chronic sci at C3/4, use walker for short distances in apartment, feel normal sensation except right toes and somewhat fingers, never had pain after neck healed from fusion surgery, big inflammation response mostly uncurtailed, take no meds, very healthy, spasticity progresses since second year after a second fall after ear surgery (otoslerosis). My question is do I have a scar or much of one? Couldn't autologous stem cell therapy perk up my spinal cord? Thanks!

    Jan

  4. #74
    NOTE - Been walking with walker ever shorter distances since 5 and a half months at RIC in Chicago. I'm big on nutrition, been a vegan for over a decade, eating natto now for its Vitamin K2 (and protein) and supplementing with lithium orotate.

    Jan

  5. #75
    Quote Originally Posted by ay2012 View Post
    Anyone else as distressed over this as I am? I know that in science there is room for vigorous disagreement, even between voices as important in spinal cord injury research as Dr.'s Young and Silver...but for them to be so clearly opposed over such a fundamental issue. Has any animal study in a complete, chronic model shown regeneration and/or return of function simply by injecting stem cells into the lesion and without explicitly trying to deal with the "scar"? If yes, then the above statement seems less worrisome. If not, well....
    Ay,

    the scar issue has been a source of frustration for me since the beginning.
    In fact was one of the first reasons I was told for which there is no regeneration after SCI.
    Soon after my SCI I have found CareCure and I started to hear what Wise thinks about the scar and I have believed him for a while.
    Nevertheless everytime I have had the opportunity to talk with a doctor or a researcher I have asked what they think about the scar. Turns out, in my exoerience, that most doctors and researchers believe the scar is a problem to deal with in order to get significsant recovery especially in case of severe SCI.
    The arguments Wise has in support of his position have become weaker year after year at my eyes while arguments I hear that support the idea that the scar is a problem have become stronger especially as the scar has been studied more in details.

    What is more disturbing to me is that very few researchers have been studing the scar closely (probably because chronic SCI is still considered hopeless by most of the researchers).
    If the scar had been studied by more people in the past, likely we would be much closer to a real effective therapy to recover functions for people with chronic SCI.

    Paolo
    In God we trust; all others bring data. - Edwards Deming

  6. #76
    Quote Originally Posted by Solan View Post
    Good point
    Solan,

    could you check with the spinal unit in Oslo to see if/when they are planning to start clinical trials with UCB cells?

    Paolo
    In God we trust; all others bring data. - Edwards Deming

  7. #77
    If Dr. Silver is correct, then we are screwed. I am a dentist. I have watched surgery in my residency. It is barbaric and damaging to tissue. If you go into a spinal cord and remove anything, you will be worse or die. The access and violation of the integrity tissues and of millions of axons will be worse then your original injury. You want to re recover again? If their was an antibody that could remove this "SCAR TISSUE" then maybe. Ripping muscle tendons an every layer of the spinal cord exposing it to infection and foreign cells and bacteria in unfathomable to me.
    This is after ripping everything out to get to the spinal cord.
    http://www.youtube.com/watch?v=HoWWRQfWYTo
    Han: "We are all ready to win, just as we are born knowing only life. It is defeat that you must learn to prepare for"

  8. #78
    Quote Originally Posted by Fly_Pelican_Fly View Post
    Basic science is very different to translational science which in turn is very different to a clinical study. You cannot expect a single researcher to be responsible for a therapy from discovery to bedside. To expect that is ridiculous.

    Also note that the nature of beast (science can be glacial) is that any science at clinical study stage will likely be objectively analysed by researchers that are working upon lines of science that are one or two generations down the line at basic/translational stages.

    If and when Ch'ase gets to the clinic, Hans Keirstead or Murray Blackmore may debate the weaknesses of the enzyme or the viral vector delivery. If PTEN/SOCS3 gets to the clinic, Reggie Edgerton may question whoever the principal investigator is for the trial about the type of rehabilitative component being used in the trial.

    May the debate continue - it's healthy. It happens at scientific meetings. It happens at symposiums. Why shouldn't it happen here? If we suppress it, more of our well-informed advocates will leave this forum as they have done recently.
    .....
    In God we trust; all others bring data. - Edwards Deming

  9. #79
    Jerry,

    I am aware of Michael Sofroniew's studies. In fact, the thrust of his laboratory's work is very much in line with our own. For example, in an important 2004 paper (abstract below), they reported that mild and moderate stab wounds of the spinal cord do not produce much tissue loss but severe crush or contusion injuries produce areas that are devoid of astrocytes. They concluded that reactive astrocytosis is good and that reactive astrocytes protect tissue and preserve function after spinal cord injury. We also consider these astrocytes to be good for the spinal cord.

    I have looked at hundreds of contused rat spinal cords. Many axons enter the injury site from surrounding tissues. If there really were a barrier to axons entering the injury site, why are we seeing all these axons? I am not saying that glial scars do not exist. I just don't think that it is present in most contused spinal cords. In very severe spinal cord contusions where there is massive tissue loss and cells invading from outside the central nervous system will result in a cavity. Reactive glial cells can and do surround such cavities. Glial scars do form when one does a hemisection or transection of the spinal cord without carefully closing the dura. However, in a majority of 12.5 mm and 25.0 mm weight drop contusions of the rat spinal cord, we simply do not see a tight glial barrier that you describe.

    Finally, we have seen many axons entering the injury site after injury. In 2001, Hill, et al. did a followup study of the kinds of axons that enter the injury site. Yes, I am aware that they call the injury site a "cavity" but they also characterize this "cavity" as being filled with a loose matrix of tissue and that even corticospinal tract (CST) axons penetrate into the "lesion matrix" over long periods of as long as 8 months and that reticulospinal tracts penetrate into the matrix over that same period of time.

    Wise.

    1. Faulkner JR, Herrmann JE, Woo MJ, Tansey KE, Doan NB and Sofroniew MV (2004). Reactive astrocytes protect tissue and preserve function after spinal cord injury. J Neurosci 24: 2143-55. Department of Neurobiology, University of California, Los Angeles, California 90095-1763, USA. Reactive astrocytes are prominent in the cellular response to spinal cord injury (SCI), but their roles are not well understood. We used a transgenic mouse model to study the consequences of selective and conditional ablation of reactive astrocytes after stab or crush SCI. Mice expressing a glial fibrillary acid protein-herpes simplex virus-thymidine kinase transgene were given mild or moderate SCI and treated with the antiviral agent ganciclovir (GCV) to ablate dividing, reactive, transgene-expressing astrocytes in the immediate vicinity of the SCI. Small stab injuries in control mice caused little tissue disruption, little demyelination, no obvious neuronal death, and mild, reversible functional impairments. Equivalent small stab injuries in transgenic mice given GCV to ablate reactive astrocytes caused failure of blood-brain barrier repair, leukocyte infiltration, local tissue disruption, severe demyelination, neuronal and oligodendrocyte death, and pronounced motor deficits. Moderate crush injuries in control mice caused focal tissue disruption and cellular degeneration, with moderate, primarily reversible motor impairments. Equivalent moderate crush injuries combined with ablation of reactive astrocytes caused widespread tissue disruption, pronounced cellular degeneration, and failure of wound contraction, with severe persisting motor deficits. These findings show that reactive astrocytes provide essential activities that protect tissue and preserve function after mild or moderate SCI. In nontransgenic animals, crush or contusion SCIs routinely exhibit regions of degenerated tissue that are devoid of astrocytes. Our findings suggest that identifying ways to preserve reactive astrocytes, to augment their protective functions, or both, may lead to novel approaches to reducing secondary tissue degeneration and improving functional outcome after SCI.
    2. Hill CE, Beattie MS and Bresnahan JC (2001). Degeneration and sprouting of identified descending supraspinal axons after contusive spinal cord injury in the rat. Exp Neurol 171: 153-69. Department of Neuroscience, The Ohio State University, Columbus, Ohio 43210, USA. Contusive spinal cord injury (SCI) results in the formation of a chronic lesion cavity surrounded by a rim of spared fibers. Tissue bridges containing axons extend from the spared rim into the cavity dividing it into chambers. Whether descending axons can grow into these trabeculae or whether fibers within the trabeculae are spared fibers remains unclear. The purposes of the present study were (1) to describe the initial axonal response to contusion injury in an identified axonal population, (2) to determine whether and when sprouts grow in the face of the expanding contusion cavity, and (3) in the long term, to see whether any of these sprouts might contribute to the axonal bundles that have been seen within the chronic contusion lesion cavity. The design of the experiment also allowed us to further characterize the development of the lesion cavity after injury. The corticospinal tract (CST) underwent extensive dieback after contusive SCI, with retraction bulbs present from 1 day to 8 months postinjury. CST sprouting occurred between 3 weeks and 3 months, with penetration of CST axons into the lesion matrix occurring over an even longer time course. Collateralization and penetration of reticulospinal fibers were observed at 3 months and were more extensive at later time points. This suggests that these two descending systems show a delayed regenerative response and do extend axons into the lesion cavity and that the endogenous repair can continue for a very long time after SCI.
    Last edited by Wise Young; 12-30-2012 at 11:07 PM.

  10. #80
    Quote Originally Posted by paolocipolla View Post
    Ay,

    the scar issue has been a source of frustration for me since the beginning.
    In fact was one of the first reasons I was told for which there is no regeneration after SCI.
    Soon after my SCI I have found CareCure and I started to hear what Wise thinks about the scar and I have believed him for a while.
    Nevertheless everytime I have had the opportunity to talk with a doctor or a researcher I have asked what they think about the scar. Turns out, in my exoerience, that most doctors and researchers believe the scar is a problem to deal with in order to get significsant recovery especially in case of severe SCI.
    The arguments Wise has in support of his position have become weaker year after year at my eyes while arguments I hear that support the idea that the scar is a problem have become stronger especially as the scar has been studied more in details.

    What is more disturbing to me is that very few researchers have been studing the scar closely (probably because chronic SCI is still considered hopeless by most of the researchers).
    If the scar had been studied by more people in the past, likely we would be much closer to a real effective therapy to recover functions for people with chronic SCI.

    Paolo
    Most of the studies of "glial scar" have been done in animal models where penetrating wounds of the spinal cord have been done on the spinal cord. A lot of people are pontificating on glial scars without having studied spinal cord contusions, which constitute a majority of human spinal cord injuries.

    Wise.

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